Objective: To explore whether targeting phosphoglycerate kinase 1 (PGK1) can enhance the sensitivity of BRAF^V600E mutation melanoma cells to vemurafenib.Methods: The methods of cell biology, molecular biology and pharmacology(MTT assay, Western blot, FCM, Colongenic assay) were used in this study.Results: ① Silencing of PGK1 expression increased the efficacy of vemurafenib in melanoma cells, as evidenced by greater killing in the tumor cells subjected to combined treatment of vemurafenib with siPGK1; ②The mechanism of enhanced sensitivity of melanoma cells to vemurafenib was associated with activation of apoptotic signaling pathway.Conclusion: Targeting of PGK1 may represent a novel strategy of sensitizing melanoma cells to vemurafinib.

Objective: To explore the effects of hyperpolarization-activated cyclic nucleotide-gated channels 2(HCN2) in the formation of peripheral neuropathic pain in rats.Methods: Twenty-four healthy adult rats were divided into two groups randomly(n=12):the sham group rats were only isolated the left L4, L5 spinal nerve, the spinal nerve ligation(SNL) group was separated the spinal nerve and performed the corresponding ligation. The behavioral experiments were tested 7 days after operation; The model rats were randomly divided into 3 groups(n=6):① negative group(Saline), intra-plantar injection of saline in left hindpaws; ② positive group(gabapentin, GBPT), intraperitoneal injection of gabapentin; ③ experimental group(ZD7288), intra-plantar injection of ZD7288 in left hindpaws. The behavioral experiments were tested before injection and 1 h, 4 h, 24 h and 48 h after injection; Obtaining the dorsal root ganglion(DRG) of the control group (before operation), sham group and the SNL group(n=6), using qPCR and Western blot to analyze the mRNA and protein of HCN2 in rats' DRG.Results: The rat model of neuropathic pain was successfully established. Compared with saline group, GBPT group and ZD7288 group could significantly reduce the symptoms of neuropathic pain in rats after injection 1 h (P<0.01), and there was no difference between GBPT group and ZD7288 group. Compared with control group and sham group, the expression of HCN2 mRNA in SNL group's DRG was significantly increased (P<0.01), and the expression of HCN2 channel protein was also increased significantly (P<0.05).Conclusion: HCN2 is involved in the development of peripheral neuropathic pain and is likely to be a potential new target for the treatment of neuropathic pain.

Objective: To investigate the effect of β-sheet breaker peptide H102 on APP associated secretase in the hippocampus brain regions of APP/PS1 double transgenic mice(AD mice).Methods: Thirty 6-month-old APP/PS1 double transgenic mice were randomly divided into AD group and H102 group, a group of C57BL/6J mice with the same age, number and background was set as controls(n=15). H102 (5.8 mg/kg) 5 μl was infused by intranasal administration to mice in H102 treatment group, and equal volume of blank solution of H102 was given to mice in control group and AD group. The ability of spatial reference memory was tested by Morris water maze after 30 days of treatment. And then immunohistochemistry tests and Western blot were used to detect the content of α-secretase (ADAM10, ADAM17), β-secretase (BACE1), γ-secretase (PS1, APH1a, PEN2) in the hippocampus brain regions.Results: Compared with the control group, the expression of BACE1, PS1, PEN-2 and APH1-a protein in the hippocampus of AD group were significantly increased, ADAM10, ADAM17 protein expression were significantly reduced (P<0.05); Compared with the model group, H102 could significantly improve the spatial learning and memory ability of AD mice, significantly decreased the expression of BACE1, PS1, PEN-2 and APH1-a protein in the hippocampus, significantly increased the expression of ADAM10 and ADAM17 protein(P<0.05).Conclusion: β sheet peptides blocked H102 can reduce the formation of Aβ in the hippocampus brain area, improve the activity of α-secretase in the hippocampus brain region, decrease the activity of β-and γ-secretase, improve the learning and memory ability of AD mice.

Objective: To investigate the effects of silencing miRNA378^* on apoptosis, endoplasmic reticulum stress and calumenin of cardiomyocyte with coxsackie virus B3 (CVB3) infection.Methods: Primary cultured suckling mouse myocardium were divided into control group (normal cell), coxsackie virus infection group (normal cell and coxsackie virus B3), miRNA378^* control group (normal cell +coxsackie virus B3+miRNA378^* empty plasmid), miRNA378^* silencing plasmid group(normal cells + coxsackie virus B3 + miRNA378^* silencing plasmid). Four groups of cells were transfected, infected and treated in CO₂ incubator at 37℃. The α-SMA protein, cell apoptosis rate, calumenin, glucose regulated protein 78 (GRP78), activation transcription factor 6(ATF6) and transcription factors c/ebp homologue protein (CHOP) in endoplasmic reticulum were analyzed.Results: By detecting α-SMA protein, the isolated suckling mouse ventricular myocardium were confirmed. TUNEL detection of different groups of ventricular cell apoptosis found that coxsackie virus group of ventricular myocytes apoptosis was significant. Compared with the coxsackie virus infection group of myocardial cells, miRNA378^* silencing plasmid expression of cardiomyocyte apoptosis cells significantly reduced(P<0.01). The expressions of GRP78, ATF6 and CHOP were increased compared with those infected by Coxsackie virus infection (P<0.01), while the expressions of calumenin were decreased (P<0.01).Conclusion: CVB3 infected myocardial cells effected miRNA378^* expression. It can trigger endoplasmic reticulum stress and activates signaling pathway factor and increase myocardial cell apoptosis.>

Objective: To investigate the effects of adiponectin(ADP) postconditioning against myocardial ischemia/reperfusion injury(MIRI) in rats and role of ADP/PI3K/Akt pathway in ADP postconditioning.Methods: SD rat was connected to ventilator by tracheal intubation under anesthesia, then left anterior descending coronary artery (LAD) was threaded between left auricle and pulmonary artery cone after exposing heart by surgery. MIRI model was induced by ligation of LAD for 30 min and the following reperfusion for 120 min. Rats were divided randomly into 5 groups (n=12):① Sham group:LAD was threaded without ligation; ② MIRI group; ③ADP group (ADP postconditioning) were subjected to intravenous injection of ADP when LAD ligation for 10 min and the ligation held for 20 min after that, then reperfusion for 120 min; ④ ADP+LY294002 group were subjected to injection of ADP and LY294002 when LAD ligation for 10 min, the other steps were the same as ADP group; ⑤ LY294002 group were subjected to injection of LY294002 when LAD ligation for 10 min, the other steps were the same as ADP group. Titers of lactate dehydrogenase(LDH) and cardiac troponin I(cTnI) in plasma were observed, expressions of PI3K, Akt, phosphorylated-Akt(p-Akt), ADP mRNA, ADPR1 mRNA and PI3k mRNA in myocardial tissue were measured.Results: Compared with sham group, the levels of LDH and cTnI in MIRI group were increased (P<0.05); Compared with MIRI group, the levels of LDH and cTnI in ADP group were decreased (P<0.05); Compared with ADP group, the levels of LDH and cTnI were increased in LY294002 applying groups(P<0.05). Compared with MIRI group, the expressions of PI3K, p-Akt, ADP mRNA, ADPR1 mRNA and PI3K mRNA were increased in ADP group (P<0.05), the above mentioned 5 parameters in LY294002 applying groups were decreased(P<0.05).Conclusion: ADP postconditioning could reduce MIRI in rats, the protective effect might have relation to ADP/PI3k/Akt pathway.

Objective: To observe the effect of AdipoRon, an adiponin receptor agonist, on insulin sensitivity in mouse myoblast cell line (C2C12) and to explore its mechanism.Methods: C2C12 was induced to differentiate into myoblasts by using horse serum. Then the cells were divided into 6 groups (9 double wells):blank control group, high dose AdipoRon group, low dose AdipoRon group, insulin group and the low dose AdipoRon with PI3K inhibitor (phosphatidylinositol 3 kinase) group and the insulin with PI3K inhibitor group. After cultured for 12 h, the supernatant was collected and glucose consumption was measured. Cell proliferation was tested by using CCK8. In the 6-well plate, C2C12 was induced to differentiate into myoblasts. The drug was incubated for 12 h and the mRNA level of GLUT4 was detected by RT-PCR.Results: Compared with the blank control group, the levels of glucose consumption in high dose AdipoRon group, low dose AdipoRon group and insulin group was increased significantly (P<0.05). After adding PI3K inhibitor, the levels of glucose consumption in the above mentioned three groups were not different from that in blank control group. high dose AdipoRon group, low dose AdipoRon group and insulin group had proliferation, but only the insulin group was statistically significant (P<0.05). Compared with the control group, the levels of GLUT4 mRNA in AdipoRon high dose group, low dose AdipoRon group and insulin group were all higher than those in control group (P<0.05). After adding PI3K inhibitor, GLUT4 mRNA level was not statistically significant compared with blank control group.Conclusion: AdipoRon can increase the consumption of glucose without affecting cell proliferation, which may play a role in improving insulin sensitivity, but the specific mechanism remains to be further studied.

Objective: To observe the effects of dihydromyricetin(DHM) on cognitive dysfunction and expression of brain derived neurotrophic factor(BDNF) protein in hippocampus of type 2 diabetic mice(T2DM).Methods: Forty C57BL/6J mice were randomly divided into two groups, normal control group (n=8):normal diet feeding; T2DM model group (n=32):high-glucose and high-fat combined with 100 mg/kg streptozocin(STZ) treatment (five mice died during modeling and three failed). Twenty-four diabetic mice were modeled successfully and divided into three groups (T2DM group, T2DM+L-DHM group and T2DM+H-DHM group). Three groups mice were fed with high-glucose and high-fat diet, and treated with equal volume of normal saline, 125 mg/(kg·d) DHM or 250 mg/(kg·d) DHM for 16 weeks respectively. The control mice were fed with normal diet and treated with equal volume of saline (once a day, gavage) for 16 weeks. After 16 weeks, the body weight and fasting blood glucose were measured, intraperitoneal glucose tolerance test and related behavioral experiment were performed. Finally, the expression of BDNF protein in hippocampus of mice was detected by Western blot.Results: The model of type 2 diabetes mellitus was established successfully with high-glucose and high-fat combined with 100 mg/kg STZ. After 16 weeks, the body weight of T2DM group was significantly decreased, the fasting blood glucose was significantly increased and the glucose tolerance was significantly abnormal compared with the normal control group. Compared with T2DM group, the body weight of T2DM+DHM groups mice was increased, while the levels of fasting blood glucose were decreased. And H-DHM could significantly improve the abnormal glucose tolerance of T2DM mice. Behavior test results showed that the ability of learning and memory of T2DM mice was significant decreased compared with control group, but these phenomena were improved in T2DM+DHM groups mice, and T2DM+H-DHM group was more obvious. Western blot analysis showed that the expression of BDNF protein in hippocampus of T2DM group was significantly lower than that of control group, while T2DM+DHM group was significant increased compared with T2DM mice.Conclusion: Dihydromyricetin can improve the cognitive dysfunction in type 2 diabetic mice. The mechanism may be through hypoglycemic effect and activation of BDNF protein expression in hippocampus.

Objective: To establish type 2 diabetic model in rats complicated with hypertension.Methods: Sixty five SD male rats were divided into normal control group, 1%NaCl water-treated group, 20 mg/kg STZ-1% NaCl-treated group, 30 mg/kg STZ-1%NaCl-treated group and 40 mg/kg STZ-1% NaCl-treated group according to random digit table(n=13).Except that rats in the normal control group were fed with ordinary diet, rats in the other groups were fed with high-fat diet for 4 weeks, then maintained with free access to rat chow and 1% NaCl drinking water for 9 weeks. In addition, rats in streptozotocin(STZ) groups were received STZ at a different dose(20 mg/kg, 30 mg/kg, 40 mg/kg)respectively by intraperitoneal injection at the end of the fourth week. The experimental period lasted 13 weeks. During the study, the general condition, body weight, average food intake, blood glucose, blood pressure, blood lipids and plasma insulin levels of each rat were tested.Results: After STZ injection, tests showed body weight was significantly reduced (P<0.05), average food intake and fasting/random blood glucose level were increased significantly (P<0.05); blood pressure was obviously risen (P<0.05)and the average value of systolic blood pressure was reached 150 mmHg into hypertensive stage at the 4^th week and stable at 150~170 mmHg for five weeks(before the end of experiment); the level of plasma insulin was higher significantly (P<0.05), the level of plasma triglyceride(TG)was descended significantly (P<0.05)at the 13^th week of the experimental period, each of which was only in 30 mg/kg STZ-1% NaCl-treated rats and 40 mg/kg STZ-1% NaCl-treated rats as compared with non-treated rats or 1% NaCl water-treated rats.Conclusion: The method that the rat was fed with high-fat diet for 4 weeks, then, received intraperitoneal injection of 30~40 mg/kg STZ combined with feeding 1% NaCl drinking water, which can induce insulin resistance in rats with type 2 diabetes mellitus and hypertension.

Objective: To study the effects of p38 mitogen-activated protein kinase (p38MAPK) signal transduction pathway inhibitor SB203580 on the inflammatory reaction and lung water clearance, and to explore the role of p38MAPK in acute lung injury, to provide new way for p38MAPK inhibitor -SB203580 intervene fat embolism syndrome induced lung injury.Methods: Twenty-four adult male SD rats were randomly assigned to normal control group (OA group) (n=8), oleic acid-induced lung injury group (OA group, n=8)and SB203580 pretreatment group (n=8). OA-group was administered oleic acid (0.20 ml/kg) via right jugular vein; In SB203580-group, SB203580(5 mg/kg) was injected via jugular vein, followed 30 min before by OA infusion; At the 4 hours animals were sacrificed. Arterial blood gas, the wet/dry weight(W/D)of the right lower lung were examined, lung index(LI), pulmonary permeability index(PPI) and levels of tumor necrosis factor α(TNF-α) in bronchoalveolar lavage fluid(BALF) were examined. The expressions of p38MAPK and phospho-p38MAPK (p-p38MAPK) were determined by Western blot and immunohistochemical method. Pathological changes of the lung tissue were examined with light microscrope.Results: Compared to control group, arterial oxygen partial pressure (PaO₂) and PaO₂/FiO₂ were decreased in the animals of OA-group, while right lower lung wet/dry ratio, lung index, PPI, levels of TNF-α in BALF and the protein expression of p-p38MAPK were increased significantly (P<0.01). The pathological changes were observed significantly in injured lung tissue. Compared to OA-group, those indexes were improved in SB203580 pretreated group.Conclusion: p38MAPK signal transaction path mediated inflammatory response process and played an important role in acute lung injury. SB203580 could inhibit the expression of inflammatory cytokines, reduce lung edema, protect lung tissue of rats from OA-induced lung injury obviously. Therefore, inhibition of p38MAPK activity provides a new way for the clinical treatment of fat embolism syndrome induced lung injury.

Objective: To observe the abnormality of the electrocardiogram (ECG) and the characteristics of arrhythmia in the early stage of older pregnant women and to record the late outcome of atrial and ventricular arrhythmia.Methods: Two hundrend and ninty pregnant women were divided into 3 groups by age under 35 group, 35~39 group and 40~45 group. The ECG waveform was analyzed systematically when the patients were subjected to routine ECG examination and abnormal changes of ECG were collected and recorded, including ST segment changes, various arrhythmias, etc. Then the recovery and deterioration rate of atrial, ventricular arrhythmia was recorded.Results: The incidence of arrhythmia in 35~39 group and 40~45 group was significantly higher than under 35 group (P<0.05); the incidence of abnormal ST section in 35~39 group and 40~45 group was significantly higher than under 35 group(P<0.05); and the incidence of widened QRS wave in 40~45 group was higher than under 35 group (P<0.05). The incidence of sinus tachycardia, sinus irregularityand atrial premature beats in 35~39 group and 40~45 group was obviously lower than that under 35 group (P<0.05); the incidence of Paroxysmal supraventricular tachycardia in 40~45 group was obviously higher than under 35 group (P<0.05) and the incidence of ventricular premature beat and atrial fibrillation in 35~39 group and 40~45 group was significantly higher than under 35 group (P<0.05). The recovery rate of atrial arrhythmia in 40~45 group was obviously lower than under 35 group (P<0.05);the exacerbation rate of trial and ventricular arrhythmia in 40~45 group was obviously higher than over 35 group (P<0.05). The incidences of IUGR in 35~39 group and 40~45 group with abnormal ECG was obviously higher than under 35 group and 35~39 group with normal ECG; The incidences of fetal distress in 35~39 year-old group and 40~45 year-old group with abnormal ECG was obviously higher than under 35 group(P<0.05).Conclusion: There is a positive correlation between the old age and the incidence of arrhythmia in the early stage of pregnancy, and old age factors can reduce the recovery rate but increase the incidence of deterioration of arrhythmia. And older pregnant women with abnormal ECG have undesirable effect to perinatal infant.

Objective: To investigate the effect of the miR-21 and its target mRNA in renal tubular epithelial mesenchymal transformation (EMT) model induced by transformation growth factor-β1(TGF-β1) in human renal tubular epithelial (HK-2) cells.Methods: HK-2 cells were divided into 6 groups:normal control group, TGF-β1 group, miR-21 mimic negative group, miR-21 mimic group, miR-21 inhibitor negative group and miR-21 inhibitor group. EMT model was established in HK-2 cells induced by 4 ng/ml TGF-β1. The level of miR-21, the mRNA and protein expression of EMT related factors were detected. MiR-21 mimic plasmid and miR-21 inhibitor plasmid were transfected into HK-2 cells that treated with TGF-β1 respectively using liposome transfection technique. Observe the impact of overexpression or inhibition expression of miR-21 on the mRNA and protein expression of EMT related factors and PTEN.Results: ①Compared with the normal group, the level of miR-21 was significantly increased in model group (P<0.05), the mRNA and protein expression levels of epithelial cells marker E-cadherin was significantly decreased (P<0.01), while the mRNA and protein levels of mesenchymal cells marker α-SMA was significantly increased (P<0.05,P<0.01). ②Compared with the miR-21 mimic negative group, the level of miR-21 in miR-21 mimic group increased significantly (P<0.01), the mRNA and protein expression levels of PTEN and E-cadherin decreased significantly (P<0.05,P<0.01), the mRNA and protein levels of α-SMA increased significantly (P<0.05,P<0.01). Compared with the miR-21 inhibitor negative control group, the level of miR-21 in miR-21 inhibitor group decreased significantly (P<0.01), the mRNA and protein expression levels of PTEN and E-cadherin increased significantly (P<0.05,P<0.01), the mRNA and protein levels of α-SMA decreased significantly (P<0.05,P<0.01).Conclusion: MiR-21 may play an important role in EMT induced by TGF-β1 in HK-2 cells and regulate the expression of EMT related factors its target gene PTEN.

Objective: To study the effects of aerobic interval training (AIT) on renal cluster of differentiation 40 (CD40) expression in rats with myocardial infarction (MI) and its possible mechanism.Methods: Thirty-six rats were randomly divided into three groups (n=12):Sham, MI and MI with AIT (ME) groups. The MI model was established by ligation of the left anterior descending coronary artery. Treadmill training was performed five times a week for 8 weeks (AIT:60 min/day with 10 min of warm-up at 10 m/min and 50 min of exercise at 25 m/min 7 min interspersed with 3 min at 15 m/min). After training, cardiaorenal function and renal tissue remodeling were evaluated. The changes of CD40, high-sensitivity C reactive protein(hs-CRP), TNF-α, IL-6, p-NF-κBp65, blood urea nitrogen (BUN) and serum creatinine (sCr) were determined.Results: Compared with the sham group, MI significantly increased left ventricular end-diastolic pressure (LVEDP) and decreased left ventricular systolic pressure (LVSP) and left indoor pressure change rate peak (dp/dtmax) in the MI group, concomitant with the increase in renal collagen volume fraction (CVF), which was reversed by AIT in the ME group. Moreover, compared with the sham group, CD40 was largely dispersed within the cytoplasm of renal tubule cells in the MI group. Meanwhile, the expressions of renal CD40 mRNA and protein, the levels of serum and renal hs-CRP, TNF-α and IL-6, the phosphorylation of NF-κBp65 (p-NF-κBp65) and the levels of sCr and BUN were obviously increased in the MI group. Compared with the MI group, AIT decreased the expressions of renal CD40 mRNA and protein, the levels of serum and renal hs-CRP, TNF-α and IL-6 and the expression of p-NF-κBp65, as well as decreased the levels of sCr and BUN in the ME group.Conclusion: AIT reduces the expressions of renal CD40 protein and mRNA, inhibits NF-κB signaling pathway, and then decreases the levels of inflammatory factors thereby improve the renal dysfunction after MI.

Objective: To study the effect of different intensity exercise on skeletal muscle fiber myosin heavy chain(MHC) subtype transformation and CaN/NFATc1 signaling pathways.Methods: Twenty-four Male SD rats (2-month old) were randomly divided into normal control group (NC), moderate intensity exercise group (ME, grade 5°, speed 18 m/min), heavy intensity exercise group (HE, grade 10°, 26.8 m/min). The rats in exercise groups were treated with treadmill training for eight weeks. The type I and type Ⅱ muscle fibers were determined by ATPase staining method. MHC subtype was separated by SDS-PAGE. The activity of CaN was determined by colorimetric method. The content of NFATc1 protein in skeletal muscle was detected by immune imprinting technology.Results: ①Skeletal muscle fiber density changes:the type I and Ⅱ fiber number density of quadriceps in ME group were increased significantly (P<0.05), but in HE group, only the type Ⅱ fiber surface density was increased significantly (P<0.05). The type I fiber number density of soleus in ME and HE group was increased significantly (P<0.05). ②The changes of fibers MHC subtype percentage in skeletal muscle:the percentages of MHC I and type Ⅱa of quadriceps in ME group were increased (P<0.05), while the percentage of MHC Ⅱb was decrease (P<0.05). The percentage of MHC I in soleus was increased, while the percentages of MHCⅡa and Ⅱb were decreased. ③The activity of CaN and the content of NFATc1 protein in ME group were increased significantly (P<0.05).Conclusion: The heavy and moderate intensity exercise may induce skeletal muscle MHC type transforming from fast to slow. At the same time, the activity of CaN and the expression of NFATc1 protein are increased accompanying the changes of skeletal muscle fibers subtype.

Objective: To observe the effects of core strength training on the body balance of middle-aged men, which could provide evidence for improving the body balance and reducing the risk of falls in the middle-aged men.Methods: Sixteen 50~60 years old men were randomly divided into experimental group (core strength training, n=8) and control group(n=8). Intermittent core strength trainings were used for dynamic and static training, push-pull training and unarmed lower limb strength training by suspension ropes and yoga mat. The time for training was 50~60 min/day, 4~5 times/week for a total of 10 weeks. The men in control group remained their original living habits. We measured the ability of body static balance and dynamic balance before and after the core strength training.Results: ① Compared with before exercise training, both closed single foot standing time and the body dynamic balance were increased significantly in the experimental group after exercise training(P<0.01)(10.63±1.69 s vs 9.00±2.27 s; 77.38±10.94 vs 89.50±5.53). ② Compared with before exercise training, star excursion balance test(SEBT) values were significantly increased in the left leg(the right leg support) in eight directions and the right leg(the left leg support)in six directions (P<0.01).Conclusion: Ten-week core strength training can significantly increase the body static and dynamic balance in the middle-aged men.

Objective: To investigate the effects of the Traditional Chinese Medicine berberine on blood lipid and antioxidation ability in hyperlipoidemic model rats.Methods: Ten rats were randomly chosen as control group, and other rats were used to establish hyperllipemia rat models. Successfully molding rats were randomly divided into model group, berberine low dose group(100 mg/kg), medium dose group(200 mg/kg), high dose group(300 mg/kg), and xuezhikang group(200 mg/kg), 10 rats in each group. Each rat received gavage per day continually for 30 days. Diacylgycerol acyltransferase (DGAT), 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA), hepatic triglycerides lipase (HTGL), cholesterol 7a-hydroxylase (CYP7A), triglyceride (TG), total cholesterol (TC), low density lipoprotein (LDL), high-density lipoprotein (HDL), malondialdehyde (MDA), glutathion peroxidase (GSH-Px) and superoxide dismutase (SOD) levels were monitored.Results: The Traditional Chinese Medicine berberine could obviously decrease the liver coefficient and the contents of TC, TG, LDL-C and increase the serum content of HDL-C in hyperlipoidemia rats. The Traditional Chinese Medicine berberine decrease the levels of MDA, DGAT, HMG-CoA and increase the activities of HTGL, CYP7A, SOD and GSH-Px in liver tissue.Conclusion: The Traditional Chinese Medicine berberine could decrease the blood lipid level and prevent the lipid peroxidation damage in hyperlidemia rats.

Objective: To investigate the effects of etanercept on collagen induced arthritis rats.Methods: The rheumatoid arthritis model was established via subcutaneous injection of bovine type Ⅱ collagen, and the effects of etanercept was compared through three groups:①the normal control;②arthritis model treated with saline;③arthritis model treated with etanercept (0.5 mg/kg, intraperitoneal injection) with 10 rats in each group;group②and group③ were selected by arthritis index (≥ 2)and grouped randomly. The body weight and toe volume were measured at just before and during treatment weekly. Rats were sacrificed after 4 weeks of treatment, and the serum levels of tumor necrosis factor α(TNF-α), angiopoietin-1(Ang-1), IL-1β, IL-6 and IL-8 were tested by ELISA. Nuclear factor-kappa B(NF-κB) levels and subcellular locations in toe muscles were test by Western blot.Results: Etanercept significantly relieved inflammation of rheumatoid arthritis, lowered the TNF-α and relative inflammatory factors levels compared with saline treatment (P<0.05). The results of Western blot showed that etanercept significantly suppressed the nuclear location of NF-κB p105/p50 caused by inflammation.Conclusion: The anti-inflammatation effect of etanercept may be related to its activity in inhibiting the activation of TNF-α/NF-κB pathway.

Objective: To investigate the effects of Caulis Sinomenii (traditional Chinese medicine) on electrophysiological character of sciatic nerve trunk of toad.Methods: Forty toads were randomly divided into four groups:Ringer's solution (as a control group) and three experimental groups were treated with 0.20, 0.10, 0.05 g/ml Caulis Sinomenii decoction, each group was soaked for 15 and 30 min respectively. The conduction velocity, amplitude and threshold intensity of the sciatic nerves from each group were measured by RM6240C Physiological signals recording system.Results: Compared with the control group, the conduction velocity in high dose group was significantly decreased(P<0.01), the amplitude of the action potential in medium and high dose groups were lower(P<0.01); but the threshold intensity of the nerve trunk action potential in high dose group was increased significantly compared with that in control group (P<0.01).Conclusion: The Caulis Sinomenii decoction can reduce the excitability sciatic nerve stem of toad and block the conduction of the action potential, which may play important roles in inhibiting of sciatica.

Objective: To evaluate the effect of dexmedetomidine(Dex) on renal injury induced by lung ischemia/reperfusion(I/R) in mice.Methods: Fifty healthy SPF male C57BL/6J mice, weighing 20 g~24 g,aged 8~10 weeks,were randomly divided into five groups(n=10 each):sham operation group(sham group),lung ischemia/reperfusion group(I/R group), lung ischemia/reperfusion and normal saline group (NS group), dexmedetomidine group(Dex group), dexmedetomidine and atipamezole group (DA group). Lung ischemia/reperfusion model was established by occlusion of the left pulmonary artery for 30 min followed by 180 min reperfusion in mice. In Dex and DA groups, dexmedetomidine 20 μg/kg and dexmedetomidine 20 μg/kg plus atipamezole 250 μg/kg were injected intraperitoneally respectively at 30 min before establishment of the model, isopyknic normal saline instead of Dex were injected intraperitoneally in NS group. After the experiment the mice were killed and plasma IL-1 beta and tumor necrosis factor α(TNF-α) concentration were detected by ELISA; the renal tissues were harvested to observe ultra structure under electron microscope.Results: Compared with sham group, the concentrations of IL-1β and TNF-α in other groups were increased significantly and the structure damages of renal tissues observed under electron microscope in other groups were more serious than those of sham group. Compared with I/R group, NS groups and DA group, the concentrations of IL-1β and TNF-α in Dex group were significantly lower(P<0.05)and the structure damages of renal tissues observed under electron microscope in Dex group were slighter.Conclusion: Dexmedetomidine pretreatment can attenuate renal injury induced by lung ischemia/reperfusion and the mechanism may be related to inhibition of inflammatory responses.