Objective: To investigate the relationship between mitochondrial DNA (mtDNA) variation and high altitude essential hypertension(HAEH) in the Chinese Tajik population. Methods: Fifty-three patients with HAEH and 46 healthy subjects were enrolled from the Chinese Tajik population. The mtDNA fragments were amplificated by polymerase chain reaction, and products were sequenced to acquire full sequence of mtDNA. The mtDNA sequences of all subjects were compared to the Cambridge sequence to explore mtDNA variations and analyze difference between HAEH and healthy controls. Online softwares were applied to predict function changes caused by positive associated mtDNA variations. Results: Compared to the control group, the frequency of haplogroup U4b was significant higher in HAEH group(P=0.023,OR=7.062,CI(95%)=1.306-38.182), and the frequencies of 8 mutations from haplogroup U4b showed a significant difference between the HAEH group and control group (all with P values below 0.05). The mt DNA15693T＞C mutation was the only missense mutation, which affected amino acid 316 in mitochondrial cytochrome b (MTCYB) by changing it from methionine to threonine. Bioinformatics analysis indicated that the mutation in MTCYB may play a biological role through affecting the second structure of protein. Conclusion: MtDNA subhaplogroup U4b is a genetic factor for HAEH in the Chinese Tajik population, and mtDNA15693T＞C mutation may be an important molecular mechanism of HAEH.

Objective: To investigate the obestatin neural projections from arcuate nucleus (ARC) to hippocampus in diabetic rats, and its effects on gastric motility and gastric emptying of rats. Methods: Diabetic model was established by fructose intake combined with streptozotocin injected intraperitoneally in healthy male Wistar rats. Diabetic rats were randomly divided into five groups: control group (NS group), 0.1, 1 and 10 pmol obestatin group, and obestatin + NBI27914 group, with 7 rats in each group. 0.5 μl saline (NS), obestatin (0.1 pmol, 1 pmol, 10 pmol) or the mixture (10 pmol obestatin + 60 pmol NBI27914) was injected into the hippocampus respectively, the gastric motility was recorded immediately after administration, and the gastric emptying was studied 15 min later. ARC-hippocampus obestatin neural pathway and ARC obestatin mRNA expression were compared between normal and diabetic rats with fluorogold (FG) retrograde tracing and immunofluorescence histochemical staining. Results: Compared with normal rats, the number of ARC FG/obestatin double labeled neurons and the expression level of ARC obestatin mRNA were decreased significantly in diabetic rats (P＜0.05); Obestatin could inhibit gastric motility and gastric emptying in a dose-dependent manner (P＜0.05~0.01) and the effects of obestatin could be partially blocked by NBI27914, an antagonist of corticotropin releasing factor receptor 1 (CRFR1) (P＜0.05). Compared with normal rats, the inhibitory effects of obestatin on gastric motility and gastric emptying were significantly decreased in diabetic rats (P＜0.05). Conclusion: There is an obestatin neural pathway between ARC and hippocampus, which participates in the regulation of gastric motility and gastric emptying in diabetic rats, and CRFR1 signal pathway is involved in this process. The damage of this neural pathway may participate in gastric motility dysfunction in early stage of diabetes.

Objective: To compare epicardial electrograms between the left atrium (LA) and pulmonary veins (PVs) dynamically at development of persistent atrial fibrillation(AF) in goats PVs. Methods: Ten female goats were instrumented with electrodes at the LA and left side PV. Sustained AF (＞24 h) was induced in the goat by rapid intermittent left atrial pacing for(9.5±2.3)days at a pacing interval of 20 ms for 1 s with a maximum output of 6.0 V, followed by a 2-s period without pacing. Characteristics of PVs and LA epicardial electrograms were analyzed in the development of AF. Results: With prolonged stimulation, the duration of AF was prolonged, complex fractionated atrial electrograms(CFAEs) in LA and was increased gradually, PVs had more CFAEs than LA all the time. When induced AF lasted for more than 24 h, CFAEs in PVs became sustained approximately (2.7%±3.6% vs 92.6%±6.4%, at onset of AF vs AF lasted for more than 24 h, P＜0.05), and the ratio of CFAEs in PVs was more than that in LA (92.6%±6.4% vs 72.8%±5.3%, P＜0.05). Conclusion: The epicardial CFAEs are in specific area, which increase along with electrical remodeling. The epicardial CFAEs may play an important role in the maintenance of AF in this model.

Objective: To investigate the effects of novel BimunoGalactooligosaccharides (B-GOS) on cognitive behavior and depression of APP/PS1/tau Alzheimer's disease transgenic mice. Methods: Five-month-old male APP/PS1/tau AD transgenic mice and C57BL/6J control mice were divide into C57+Vehicle group, C57+B-GOS group, APP/PS1/tau+Vehicle group and APP/PS1/tau+B-GOS group, with 10 mice in each group. After continuous administration of B-GOS for 5 months, the cognitive behavior and depressive mood changes of mice in each group were detected by open field experiment, new object recognition experiment, Y maze experiment, Morris water maze experiment, tail suspension test, forced swimming test and conditioned fear experiment, respectively. Results: ①Open field experiment: the percentage of activity time in the central area of open field in APP/PS1/tau+Vehicle group mice was significantly lower than that in C57+Vehicle group mice (P＜0.01), and was remarkably increased after B-GOS intervention (P＜0.05). ② New object recognition experiment: the new object recognition index (NOI) of APP/PS1/tau+Vehicle group mice was significantly lower than that of C57+Vehicle group mice (P＜0.01), and was observably increased after B-GOS intervention (P＜0.05). ③ Y maze experiment: the spontaneous alternation correct rate of APP/PS1/tau+Vehicle group mice was notably lower than that in C57+Vehicle group (P＜0.01), and was distinctly increased after B-GOS intervention (P＜0.01). ④ Classical water maze experiment: the escape latency of APP/PS1/tau+Vehicle group mice on the 4th and 5th days was significantly longer than that of C57+Vehicle group mice (P＜0.01), which was markedly shortened after B-GOS intervention (P＜0.05). During the space exploration phase, the percentage of swimming time in the target quadrant and the times of crossing the platform in APP/PS1/tau+Vehicle group mice were significantly lower than those in C57+Vehicle group mice (P＜0.01), which were notably increased after B-GOS intervention (P＜0.01). ⑤ Tail suspension test and forced swimming test: the percentage of immobility time in APP/PS1/tau+Vehicle group mice was dramatically higher than that in C57+Vehicle group mice (P＜0.01), and was obviously reduced after B-GOS intervention (P＜ 0.01). ⑥ Conditioned fear experiment: before conditioned stimulus (CS), the freezing ratio of mice in each group had no statistical difference (P＞0.05). After CS, the freezing ratio of APP/PS1/tau+Vehicle group mice was significantly lower than that of C57+Vehicle group mice (P＜0.01), and was notably increased after B-GOS intervention (P＜0.01). Conclusion: B-GOS could reverse the cognitive behavioral impairment of APP/PS1/tau mice and alleviate their depression to a large extent.

Objective: This article mainly studies the effects of miR-125b-5p on the proliferation and apoptosis of human hemangioma endothelial cells HemECs. Methods: RT-qPCR was used to detect the expressions of miR-125b-5p and MCL-1 mRNA in HemECs and collateral cells of human hemangioma endothelial cells. HemECs were selected and divided into control group, miR-NC group, miR-125b-5p mimic group, miR-125b-5p inhibitor group, pc-MCL-1 group, miR-125b-5p+ pc-MCL-1 group, 9 multiple holes in each group. . HemECs were transfected with 100 nmol · L^-1 of miR-NC, miR-125b-5p mimic, miR-125b-5p inhibitor, pc-MCL-1 plasmids separately or in combination. MTT method was used to detect the proliferation of HemECs. The apoptosis of HemECs was detected by flow cytometry. Dual luciferase report was used to to detect targeting relationship. The relative expression levels of Ki67, PCNA, cleaved caspase-3, Bax, Bcl-2, p-p70s6k/ p70s6k, p-AKT/AKT, and p-mTOR/mTOR proteins were detected by Western blot. Results: By comparing the expression levels of miR-125b-5p in hemangioma tissues and cells, HemECs cell lines with obvious down-regulation effects were selected for follow-up experiments. Compared with the control group, the proliferation of HemECs and the expressions of Ki67 and PCNA in the miR-125b-5p mimic group were decreased significantly (P＜0.01). The apoptotic rate of HemECs and the expression levels of cleaved Caspase-3 and Bax were increased significantly, while the expression of Bcl-2 was decreased significantly (P＜0.01). The expression levels of p-AKT/AKT, p-mTOR/mTOR and p-p70S6K/p70S6K were down-regulated significantly (P ＜0.01); the proliferation of HemECs and the expressions of Ki67 and PCNA in the miR-125b-5p inhibitor group were increased significantly (P ＜0.01); the apoptosis rate and the expressions of cleaved Caspase-3 and Bax were decreased significantly, and the expression of Bcl-2 was increased (P＜0.05, P＜0.01). miR-125b-5p targeted down-regulation of MCL-1. Compared with miR-125b-5p mimic group, the proliferation of HemECs and the expressions of Ki67 and PCNA in miR-125b-5p+ pc-MCL-1 group were increased significantly (P＜0.01), the apoptosis rate of HemECs and the expressions of cleaved Caspase-3 and Bax were decreased significantly, while the expression of Bcl-2 was increased (P＜0.01). The expressions of p-AKT/AKT, p-mTOR/mTOR, and p-p70S6K/p70S6K was also increased significantly (P＜0.01). Conclusion: miR-125b-5p inhibits the proliferation of human hemangioma endothelial cells and induces apoptosis. The mechanism may be related to the targeted down-regulation of MCL-1 expression and inhibition of AKT/mTOR pathway activation.

Objective: In this study, human gastric cancer MGC-803 cells were treated with betulinic acid at different concentrations to investigate its effect on cell autophagy. Methods: The human gastric cancer MGC-803 cells were divided into 4 groups, each group was set with 3 replicate. The control group was not treated with betulinic acid, the other three groups were added with final concentration of 10,20,30 mg/L betulinic acid, respectively. Cells were treated with betulinic acid for 48 h,qRT-PCR was applied to detect the effect of betulinic acid on mRNA expressions of autophagy-related genes in human gastric cancer MGC-803 cells. Western blot was performed to determine the protein expressions of cell autophagy-related genes after drug treatment. Immunofluorescence was used to detect the localization and expression of LC3 protein in MGC-803 cells after drug treatment. Results: Compared with the control group,in the concentration range of 10~30 mg/L, the mRNA expression of LC3 and Beclin-1 in human gastric cancer MGC-803 cells treated with betulinic acid were increased significantly, the expressions of Beclin-1 and LC3-Ⅱ protein were also increased significantly, while the expression of LC3-Ⅰ protein was decreased significantly. Among them, betulinic acid at the concentration of 30 mg/L showed the best effects. In addition, betulinic acid induced the LC3 protein in MGC-803 cells to form spot aggregates in the cytoplasm. Conclusion: At the concentrations of 10~30 mg/L, betulinic acid can induce autophagy in human gastric cancer MGC-803 cells.

Objective: To investigate the effect of betulinic acid on the proliferation of human gastric cancer MGC-803 cells in vitro. Methods: Human gastric cancer MGC-803 cells were divided into 4 groups, each with 3 multiple holes. Control cells add betulinic acid at a concentration of 0 μg /ml, and the other three experimental groups were added with final concentration of 10, 20, 30 μg/ml Betulinic acid respectively. Cells in each group were incubated in a 5% CO₂ incubator for 48 hours, and the Giemsa staining method and trypan blue exclusion method were used to detect the effect of betulinic acid on the cell clone formation rate and growth inhibition rate; EdU method and flow cytometry were used to detect cell proliferation and cell cycle changes; qRT-PCR and Western blot were used to detect the expressions of cell cycle regulators CCNB1 and CCND1. Results: Compared with the control group, the clone formation rate of human gastric cancer MGC-803 cells was significantly reduced (P＜0.01), the growth inhibition rate was significantly increased, and the cell proliferation ability was significantly decreased (P＜0.01); with the increase of betulinic acid concentration in each experimental group the proportion of cells in the G1 phase was gradually decreased, and the number of cells in S phase was increased significantly (P＜0.01); the mRNA and protein expression levels of cell cycle regulators CCNB1 and CCND1 were decreased significantly, and the 30 μg/ml betulinic acid treatment group performed best. Conclusion: At a final concentration of 10～30 μg/ml, betulinic acid can reduce the proliferation of human gastric cancer MGC-803 cells, inhibit cell growth, and down-regulate the expression of CCNB1 and CCND1 to block human gastric cancer MGC-803 cells in the S phase.

Objective: To explore the apoptosis of human gastric cancer MGC-803 cells induced by toosendanin(TSN) and its mechanism. Methods: The human gastric cancer MGC-803 cells were divided into 5 groups, each group was set with 3 replicate. Fluorouracil (5-FU) and 0 nmol/L toosendanin (TSN) were used as positive control and negative control, respectively. The other three groups were treated with toosendanin at the final concentrations of 30, 50, and 70 nmol/L, respectively. After 48 h of treatment with toosendanin, the morphology of the cells were observed under laser confocal microscopy. Flow cytometry was used to detect the mitochondrial membrane potential, and enzyme-labeled assays were used to detect the activities of Caspase-3 and Caspase-9. The mRNA and protein levels of Bcl-2, Bax, Cyt c and APAF-1 were measured by qRT-PCR and Western blot. Results: Compared with the 0 nmol/L TSN group, after the human gastric cancer MGC-803 cells were treated with toosendanin at the concentrations of 30, 50, and 70 nmol/L for 48 h, the cell volume shrinkage, nucleus cleavage and chromatin morphological changes were observed under the microscope. The activities of Caspase-3 and Caspase-9 were increased significantly (P＜0.05), while the mitochondrial membrane potential was decreased significantly (P＜0.05). In addition, the mRNA and protein expression levels of Bax, Cyt c and APAF-1 were increased significantly (P＜0.05), while the mRNA and protein expression levels of Bcl-2 were decreased significantly (P＜0.05). Conclusion: Toosendanin up-regulates the expressions of Bax, Cyt c and APAF-1, down-regulates the expression of Bcl-2 gene, enhances the activities of caspase-3 and caspase-9, and induces the apoptosis of human gastric cancer MGC-803 cells.

Objective: To investigate the effect of TGF-β1/Smad signaling pathway on the apoptosis of HepG2 cells under endoplasmic reticulum stress (ERS). Methods: An ERS model was established firstly. Human hepatocellular carcinoma HepG2 cells were treated with 3 μmol/L tunicamycin (TM) for 24 h to induce ERS. Cells were divided into 6 groups, each with 3 replicate holes, and the experiment was repeated 3 times. The 6 groups included untreated group, TM group (3 μmol/L TM treatment group), TM + NC group(3 μmol/L TM + si-TGF-β1 negative control group), TM + si-TGF-β1 group(3 μmol/L TM + si-TGF-β1 group), TM + pEX-3 group(3 μmol/L TM + plasmid control group), and TM + TGF-β1 pEX-3 group(3 μmol/L TM + TGF-β1 overexpressed plasmid group). HepG2 cells were transfected with TGF-β1 small interfering RNA (TGF-β1 si-RNA) and TGF-β1 overexpressed plasmids (TGF-β1 pEX-3) by Lipofectamine. Twenty-four hours after transfection, RT-qPCR and Western blot were used to detect the expression of TGF-β1 and p-Smad2 in HepG2 cells of each group. CCK-8 and flow cytometry were used to analyze changes in the proliferation inhibition rate and apoptosis rate of HepG2 cells in each group. Results: Compared with the untreated group, the expressions of TGF-β1 and p-Smad2 in TM group were significantly reduced (P＜0.05). Compared with the TM group, the expressions of TGF-β1 and p-Smad2, as well as the cell proliferation inhibition rate and apoptosis rate in TM + si-TGF-β1 group were obviously decreased (P＜ 0.01), while the expressions of TGF-β1 and p-Smad2, cell proliferation inhibition rate and apoptosis rate of TM + TGF-β1 pEX-3 group were significantly increased (P＜0.01). Conclusion: The TGF-β1/Smad signaling pathway was inhibited in hepatocellular carcinoma HepG2 cells under ERS, when this pathway was activated, the apoptosis rate of HepG2 cells under ERS was increased significantly.

Objective: To investigate the protective effects and mechanisms of the polysaccharide from Balanophora involucrata HK.f (BIH) on liver injury induced by D-galactose in rats. Methods: Sixty male SD rats were randomly divided into 5 groups: the control group (n=12), the D-gal group (n=12), the BIH-L treatment group (D-gal+50 mg/kg BIH, n=12), the BIH-M treatment group (D-gal+100 mg/kg BIH, n=12), and the BIH-H treatment group (D-gal+200 mg/kg BIH, n=12). The rats were injected into the back of the neck with D-gal of 100 mg/kg/d subcutaneously except for the control group. The BIH treatment group were divided into BIH-L group (50 mg/(kg·d)), BIH-M group (100 mg/(kg·d)), and BIH-H group (200 mg/(kg·d)), respectively. The rats in the BIH group were intragastrically administrated with the relative BIH solution, while the rats in the control and D-gal group were treated with saline solution for 42 days. The serum contents of ALT, AST and DBIL c were tested by automatic biochemical analyzer, the content of MDA was determined by thiobarbital acid method and the SOD activity was detected by xanthine oxidase method. Expressions of Caspase-3, Bax, and Bcl-2 in liver were measured by Western blot, and morphological changes by HE staining and immunohistochemistry. Results: The serum contents of ALT, AST and DBIL in the D-gal group were significantly increased compared with those in Con group (P＜0.01) and were decreased in the BIH group as compared with the D-gal group (P＜0.01). Cell apoptosis, the Caspase-3 and Bax levels, and the MDA content in the D-gal group were increased compared with those in the control group (P＜0.01). And BIH treatment could attenuate these effects induced by D-gal. Meanwhile, the Bcl-2 level and SOD activity in the BIH group were increased compared with that in the D-gal group (P＜0.05, 0.01). Conclusion: BIH can protective liver injury through reducing cell apoptosis and inhibiting oxidative stress.

Objective: To study the alleviating effects of curcumin on splenic inflammation in overtraining rats by regulating toll-like receptor 4 (TLR4)-p38 mitogen-activated protein kinase (p38 MAPK)/nuclear factor-kappa B (NF-κB) signaling pathway. Methods: Male Wistar rats of 7-week old were divided into control group (C group, 12), overtraining model group (OM group, 11), curcumin + overtraining model group (COM group, 14). C Group did not undergo any exercise intervention. OM and COM group underwent 8-week incremental load swimming training. During the training, rats in the COM group were treated with 200 mg/ (kg·d) curcumin in the volume as 5 ml/kg, and the other groups were treated with an equal volume of 0.5 % sodium carboxymethylcellulose. 24 hours after the last training, the spleen index was calculated by weighing, the pathological changes of the spleen were observed by light microscopy, and the biochemical indicators of blood and spleen were detected. Results: After 8-week incremental load swimming training, the splenic structure in C group was normal under light microscope; the spleen index of OM group was significantly lower than that of C group (P＜0.01) and pathological changes of inflammation were obvious; the spleen index of COM group was significantly higher than that of OM group (P＜0.05) and pathological changes of inflammation were alleviated. Compared with C group, in OM group, the serum levels of corticosterone (Cor), NF-κB, tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and TLR4 expression rate on splenic monocytes surface, splenic TNF-α, IL-6 were increased (P＜0.05 or P＜0.01), the expressions of p38 MAPK, phosphorylated p38 mitogen-activated protein kinase (p-p38 MAPK) and NF-κB in spleen were increased (P＜0.05 or P＜ 0.01); serum testosterone (T), serum and splenic interleukin-10 (IL-10) were decreased (P＜0.01). Compared with OM group, in COM group, serum levels of Cor, NF-κB, TNF-α, IL-6 and TLR4 expression rate on splenic monocytes surface, splenic TNF-α, IL-6 were decreased (P＜0.05 or P＜0.01), the expressions of p38 MAPK, p-p38 MAPK and NF-κB in spleen were decreased (P＜ 0.05); serum T, serum and splenic IL-10 were increased (P＜0.05). The trend of T/Cor ratio between groups was consistent with testosterone change. Conclusion: The 8-week incremental load swimming training aggravated inflammation of spleen in rats, led to pathological inflammatory changes. Curcumin supplementation during training can down-regulate expressions of TLR4-p38 MAPK/NF-κB signaling pathway-related proteins, thereby maintaining a dynamic equilibrium between pro-inflammatory/anti-inflammatory cytokines, protecting the spleen.

Objective: To investigate the effects of different intensities of aerobic exercise on the morphology of the atrioventricular node and the expressions of vascular endothelial growth factor (VEGF), vasoactive intestinal peptide (VIP) and synaptophysin (Syn) in rats. Methods: Three-month-old SD rats were randomly divided into 3 groups: quiet control group (C), moderate-intensity aerobic exercise group (AE), and high-intensity aerobic exercise group (FE), each with 8 rats. The moderate-intensity aerobic exercise and high-intensity aerobic exercise rat models were rats established by using 8-week treadmill training ways. Results: Compared with the quiet control group, in the moderate-intensity aerobic exercise group, the atrioventricular nodule muscle fibers were evenly distributed, with smaller gaps, a sense of transparency, and collagen tightly wraps around the atrioventricular nodules. The intercalary disc had a clear structure and complete connection, and the capillary tube wall was relatively clear. Thick elastic fibers were more developed, the expression levels of VEGF and VIP in the atrioventricular node were increased significantly (P＜0.05), and there was no significant change in the expression of Syn. In the high-intensity aerobic exercise group, the atrioventricular nodule muscle fibers were unevenly distributed and arranged abnormally, connection between cells were disordered, and vacuolated. The intercalary disk was twisted, circling and overlapping, fuzzy, discontinuous, and extremely dilated. The wall was thick and the endothelial cells were arranged sparsely and disorderly. Moreover, high-intensity aerobic exercise significantly inhibited the expressions of VEGF, VIP, and Syn (P＜0.05). Conclusion: Aerobic exercise training of different intensities has obvious effects on the morphology and structure of the atrioventricular node and the expressions of VEGF, VIP and Syn. Moderate aerobic exercise can maintain and promote the normal morphology and structure of the atrioventricular node, while high-intensity aerobic exercise can damage the morphology and structure of the ventricular node, which is presumably closely related to the arrhythmia induced by high-intensity exercise.

Objective: To investigate the effects of glutamine on exercise-induced fatigue, skeletal muscle oxidation and liver cell apoptosis in rats. Methods: Twenty SPF grade SD rats aged at 8 week and weight from 180 to 220 g, were divided into control group and glutamine-treated group after one week of feeding, 10 rats in each group. The rats in the glutamine group were treated with glutamine at the dose of 1.0 g/(kg·d)by intragastric administration, and the rats in control group were administrated with equal volume of normal saline. After 7 days, the exhaustion test was conducted, the content of glutathione (GSH) was detected by high-performance liquid chromatography. Superoxide dismutase (SOD), malondialdehyde (MDA), lactic acid (2-hydroxypropanoic acid (LD) were detected by enzyme-linked immunosorbent assay, and the creatine kinase(CK) was detected by electroluminescence. Activities of CK, Lactate dehydrogenase (LDH), and expression levels of Bcl-2 and Bax mRNA were detected by fluorescence quantitative RT-PCR. Results: The duration of exhaustion in the glutamine group was greater than that in the control group (P＜0.05). The serum glutathione level in the glutamine group was lower than that in the control group (P＜0.05). After exhaustion, the levels of GSH, SOD and MDA in serum and skeletal muscle of the glutamine group were higher than those of the control group significantly differences (P＜ 0.05). The serum Bax mRNA level in the glutamine group was lower than that in the control group significantly (P＜0.05). The serum bcl-2 mRNA level in the glutamine group was higher than that in the control group significantly (P＜0.05). Conclusion: Glutamine can effectively alleviate exercise-induced fatigue in rats, reduce the oxidation degree of skeletal muscle, and decrease the apoptosis rate of liver cells.

Objective: To investigate the effect of different arterial occlusion pressure and intermittent time on KAATSU-loaded deep-squat exercise on the characteristics of thigh muscle activation, find out the suitable relative value of personal blood pressure limit causing the maximum activation, and to provide some theoretical basis and practical reference for athletes to carry on the KAATSU Training scientifically. Methods: Ten elite male players were recruited, four kinds of external pressure condition with 0% arterial occlusion pressure (AOP), 40%AOP, 50%AOP, 60%AOP, respectively, were performed with 30%1RM(One repetition maximum)intensity of intermittent and continuous KAASTU-loaded deep-squat exercise. Wave plus wireless surface electromyography instrument was used to collect the surface EMG signals of the lower thigh muscle group. Root mean square (RMS) calculation was used to estimate muscle activity level. The normalized RMS values of the anterior thigh group and posterior thigh group were calculated by RMS of MVC, two-factor ANOVA analysis of variance were used to explore the effect of the activation of various muscle on external express and intermittent mode, to analyze the discrepancy during different external pressure. Results: ①A two-factor analysis of variance showed that different %AOP had significant effect on the normalized values of RMS of muscle measured by KAATSU deep-squat exercise(P＜0.05), but intermittent mode had no significant effect on the standard value of RMS of muscle(P＞0.05). The interaction of external pressure and intermittent mode on muscle RMS was not significant(P＞0.05); ②The normalized RMS values of Rectus Femoris, Vastus Medialis, Vastus Lateralis, Biceps Femoris, Semitendinosus were significantly increased (P＜0.05)in 50% AOP pressure condition during intermittent and continuous exercise; ③ The normalized RMS values of RF and VL were significantly increased(P＜0.05)in 50% AOP pressure condition during intermittent and continuous exercise. The %MVC values of Vastus Medialis and Semitendinosus were significantly increased(P＜0.05)in 60% AOP pressure condition during intermittent exercise. Conclusion: This study further verified that 50% AOP pressure can significantly improve the optimal activation quadriceps and posterior thigh groups and produce the best training effect for the high level handball players. It can not only promote the coordinated development of the agonist and antagonist, but also avoid overloading and prevent hamstring injury. At the same time, the intermittent mode is recommended to adopt the decompression intermittent mode.

Objective: To investigate the effects of interleukin 11 (IL-11) antagonist on bleomycin (BLM)-induced pulmonary fibrosis in mice. Methods: C57BL/6 mice were randomly divided into the control group, IL-11 antagonist group, BLM group, and BLM + IL-11 antagonist group (30 in each group). Mice in the BLM group and BLM + IL-11 antagonist group were injected with BLM at the dose of 1.5 mg/kg to induce pulmonary fibrosis. The IL-11 antagonist IL-11 Rα FC (2.5 mg/kg) was administered via the tail vein to the mice in the IL-11 antagonist group and BLM + IL-11 antagonist group every 3 days from the BLM injection. The survival status of the mice was observed. On the 21^st day after modeling, HE staining, Masson staining, and Ashcroft score were used to evaluate the degree of pulmonary fibrosis. The content of hydroxyproline (HYP) in lung tissue was determined by the alkaline hydrolysis method. The gene and protein expressions of Collagen I, Collagen III, and α-SMA in lung tissues were detected by real-time PCR and Western blot, respectively. TGF-β1 content in lung tissue was determined by enzyme-linked immunosorbent assay. Results: Compared with the control group, BLM reduced the survival rate, destructed the lung tissue, and increased the gene and protein expressions of Collagen I, Collagen III, α-SMA, and the content of TGF-β1 in lung tissue. While, IL-11 Rα Fc treatment improved the survival rate of BLM-induced pulmonary mice, reduced pathological changes, and hydroxyproline content in lung tissue. IL-11 Rα Fc also reduced Collagen I, Collagen III, and α-SMA mRNA and protein expression in the lungs of BLM-treated mice, as well as TGF-β1 content. Conclusion: The IL-11 antagonist alleviates BLM-induced pulmonary fibrosis in mice, which provides a new idea for the clinical treatment of pulmonary fibrosis.

Objective: To investigate the effects of huaihuasan and baitouweng formular on acute radiation proctitis (ARP) in rats. Methods: Forty clean grade SD rats were randomly divided into control group, model group, mesalazine group and formula group. Except the control group, all the other three groups received 6 MV-20 GY dose of X-ray irradiation in the pelvic cavity, and the rat model of acute radiation proctitis was established. The rats were given daily gavage intervention with the corresponding drugs after mold formation. According to the adult clinical equivalent dose (body surface area), the control group and the model group were given 10 ml/kg saline daily, the Mesalazine group was treated with Mesalazine solution at the dose of 0.27 g/kg, and the Formular group was given (0.91 g/kg) respectively for 14 days. All rats were killed on the 14th day after administration. To evaluate the general situation of the rats, HE staining was used to observe the pathological changes in the rectal tissues of the rats. The contents of intercellular adhesion molecule-1 (ICAM-1) and vascular adhesion molecule-1 (VCAM-1) were detected by Elisa, and the expression of NF-κb P65 in the tissues were detected by Western blot. Results: Compared with the model group, in the mesalazine group and the formular group, the clinical symptoms and intestinal mucosal healing of rats were improved significantly, the expression level of NF-κB P65 protein in the rectal tissues and the serum contents of ICAM-1 and VCAM-1 were decreased with statistically significant differences (P＜0.05). Conclusion: Huaihuasan and baitouweng formular can reduce NF-κB, ICAM-1 and VCAM-1 to improve symptoms and rectal mucosal injury in ARP rats.

Objective: To investigate the molecular protective mechanisms of Huangqi decoction inhibiting the apoptosis of renal cells in the ¹²C⁶⁺ radiation brain model rats. Methods: Fifty Wistar rats were randomly divided into five groups: normal control group, radiation alone model group, Huangqi decoction (high-dose, middle-dose and low-dose ) groups. The normal control group and the radiation alone group were treated with saline10 ml/(kg·d) by gavage, the Huangqi decoction treatment groups were treated with Huangqi decoction at the doses of 4.5, 9 and 18 g/(kg·d) by gavage respectively. After 7 d, except mice in normal control group, the brain of the rats in radiation alone model group, high-dose, middle-dose and low-dose Huangqi decoction group were radiated by 4 Gy ¹²C⁶⁺ ion once. The rats were killed by the femoral artery after irradiation 7 d. The pathomorphism changes of renal tissue were observed by HE, the IL-6 level in serum was detected by ELISA, the gene expressions of Bcl-2, Bax and caspase-3 in renal tissue were assessed by RT-PCR, and the protein expressions of Bcl-2, Bax, caspase-3 and NF-κB in renal tissue were analyzed by immunehistochemical staining. Results: Compared with normal control group, the body weight and kidney index were decreased significantly, the expression of Bcl-2 in renal tissue was decreased significantly, the serum content of IL-6 was increased obviously, and the expressions of Bax, caspase-3 and NF-κB in renal tissue were increased significantly in the radiation alone model group (P＜0.01). The mesangial cells proliferated obviously, interstitial vessels of renal tubules were dilated and congested obviously, the lumen of renal tubules was narrow and irregular in the radiation alone model group. As compared with the radiation alone model group, the body weight and the kidney index were increased obviously in high-dose Huangqi decoction group, the gene and protein expressions of Bcl-2 in renal tissue were increased significantly in Huangqi decoction intervention group(P＜0.05 or P＜0.01). whereas, the protein expressions of Bax and caspase-3 in renal tissue were decreased significantly in middle-dose and high-dose Huangqi decoction group, the serum content of IL-6 was decreased obviously, the gene expressions of Bax and caspase-3 in renal tissue were decreased significantly and the protein expression of NF-κB in renal tissue was decreased significantly in Huangqi decoction intervention group(P＜0.05 or P＜0.01). The proliferation of mesangial cells was improved and the contour of renal tubules was clear in high-dose huangqi decoction group. Conclusion: High-dose of huangqi decoction has protective effect on kidney in rats induced by ¹²C⁶⁺ radiation brain, the mechanism may be related to the regulation of Bcl-2/NF-κB signal pathway.

Objective: To investigate the effects and mechanisms of massage on the depressive behavior of rats with chronic stress. Methods: The rats were subjected to chronic unpredictable mild stress for 21 days and then treated with massage for 14 days. They were divided into the following groups: blank control group, model group, massage group and fluoxetine group, with 10 rats in each group. The important acupoints of bladder meridian were massaged for 10 minutes every day (with an interval of 2 minutes, 2 times in total). Body weight, open field test, sucrose intake test and water maze test were used to evaluate the behavioral changes. The expressions of Erk/p-ERK (Extracellular signal-related kinases/Phosphorylation extracellular signal-related kinases) and BDNF in prefrontal cortex were detected by Western Blot. Results: The body weight, open field sucrose intake test and water maze data of the model group were significantly lower than those of the Control Group (P＜0.01), and the contents of p-ERK and BDNF protein in prefrontal cortex were decreased significantly (P＜0.01). The body weight, open field test, sucrose intake test and water maze test data of rats in massage group and fluoxetine group were significantly higher than those in model group(P＜0.01). The contents of p-ERK and BDNF in frontal cortex were increased significantly (P＜0.05, P＜0.01), especially in fluoxetine group (P＜0.01). Conclusion: Massage may increase the phosphorylation level of ERK protein in hippocampus and prefrontal cortex, activate ERK signaling pathway, promote the expression of BDNF, and improve the depression behavior of chronic stress rats.

Objective: To investigate the effects of estrogen receptor α (ERα) gene overexpression on bone metabolism and calcium and phosphorus metabolism in ovariectomized osteoporosis mice, and to provide experimental basis for targeted gene therapy of osteoporosis. Methods: Thirty SPF female mice were randomly divided into sham operation group, model group and ERα overexpression group with 10 mice in each group. After the model was established, the ERα overexpression group was transfected with recombinant adenovirus vector carrying mouse ERα gene by intraspinal injection. The model group was transfected with empty virus, and the sham operation group was not treated. The expression of ERα gene in bone tissue of mice was detected by quantitative Real-time PCR (qRT-PCR). Bone mineral density (BMD) of mouse femur was measured after modeling. Trabecular number (Tb.N), trabecular thickness (Tb.Th), trabecular segregation (Tb.Sp), bone volume fraction (BV/TV) and biomechanical strength of femur were measured by micro-CT scanning. Serum levels of calcium (Ca), phosphorus (P), osteocalcin (BGP) and alkaline phosphatase (ALP) were measured by automatic biochemical analyzer. The expressions of tissue inhibitor of metalloproteinases 1 (TIMP-1) and monocyte chemotactic protein 1 (MCP-1) in bone homogenate were detected by Immunohistochemistry. Results: Compared with sham operation group, the expression level of ERα gene in bone tissue of model group was decreased significantly, the levels of BMD, BV/TV, Tb. Th, maximum load, rigidity coefficient, Ca and P were decreased, while the levels of Tb. Sp, BGP and ALP were increased significantly (P＜0.05). Compared with the sham operation group, the expression level of TIMP-1 protein in the bone tissue of the model group was significantly decreased, while that of MCP-1 protein was increased, while that of the ERα overexpression group was increased while that of MCP-1 was decreased (P＜0.05).The levels of ERα gene expression, BMD, BV/TV, TB. Th, maximum load, rigidity coefficient, Ca and P in the ERα overexpression group were significantly higher than those in the model group, while Tb. Sp, BGP and ALP were significantly lower (P＜0.05). Compared with the sham operation group, mean optical density of TIMP-1 in the bone tissue of the model group was significantly decreased, while that of MCP-1 was significantly increased, and that of the ERα overexpression group was significantly increased while that of MCP-1 was significantly decreased (P＜0.05). Conclusion: ERα gene overexpression can improve osteoporosis by regulating bone mineral density, bone parameters, bone metabolism, calcium and phosphorus metabolic indicators and the expression levels of TIMP-1 and MCP-1 in tissues.