Objective: To observe the role of calcium sensitive receptor (CaSR) in the pathogenesis of diabetic liver injury. Methods: Forty Wistar rats were randomly divided into normal control group (control, n=10) and diabetes group (T1D, STZ 60 mg/kg intraperitoneal injection, n=30), and the samples were collected at the 2nd, 4th and 8th week. Rats hepatic stellate cells (HSC) were randomly divided into normal control group (Control, 10% FBS-DMEM culture, n=5), high glucose group (HG, 10% FBS-DMEM+40 mmol/L glucose, treated for 48 h, n=5) and CaSR inhibitor group (HG+Calhex 231, 10% FBS-DMEM+40 mmol/L glucose+2.5 μmol/L Calhex₂₃₁ for 48h, n=5). The body weight, blood glucose, serum glutamic oxaloacetic transaminase (AST) and alanine aminotransferase (ALT) activities were measured dynamically. The changes of liver morphology and ultrastructure were observed by HE staining and Masson staining by transmission electron microscopy. The changes of CaSR and liver fibrosis related indexes were detected by Western blot.Results: Compared with the control group, diabetic rats lost weight, while blood glucose, AST and ALT increased significantly, and the expression of CaSR, collagen Ⅰ(CO Ⅰ), collagen Ⅲ (CO Ⅲ), matrix metalloproteinase(MMP)-1, -2 and -9 increased significantly. The results of the cell model were basically the same as those in vivo. Compared with the control group, the expression of α-smooth muscle actin (α-SMA) was increased, indicating that HSC differentiated into myofibroblasts in HG group. The expression of the main components of ECM (CO Ⅰ and CO Ⅲ), and the key enzyme of ECM degradation (MMP9) were also increased, while CaSR inhibitor, Calhex₂₃₁, could reduce the above changes.Conclusion: The up-regulation of CaSR expression is involved in the occurrence of diabetic liver injury and fibrosis.

Objective:To observe the effects of dihydromyricetin (DHM) on obesity induced by high-fat diet in mice, and to explore whether its mechanism of action is related to the promotion of WAT browning. Methods: Sixty c57bl/6j mice were randomly divided into 6 groups (n=10): ①normal control group (ND group): normal feed feeding; ②Normal control + low dose DHM group (ND+L-DHM group): normal feed feeding was treated with low dose DHM (125 mg/(kg·d)); ③Normal control + high dose DHM group (ND+H-DHM group): normal feed feeding was treated with high dose DHM (250 mg/(kg·d)); ④High-fat diet group (HFD): high-fat diet; ⑤high-fat diet + low-dose DHM group (HFD+L-DHM group): high-fat diet feeding with low-dose DHM; ⑥High-fat diet + high-dose DHM group (HFD+H-DHM group): High-fat diet was treated with high-dose DHM. After 16 weeks, the mice were fasted overnight, blood samples were collected for fasting blood glucose and blood lipids, then the animals were sacrificed, body length was measured, and Lee's index was calculated. After weighing the adipose tissue in the scapula, groin and epididymis, formaldehyde fixation and HE staining were used to observe the fat cells size, immunohistochemistry was used to detect the expression of uncoupling protein 1 (UCP1). The body weight was measured every 4 weeks during the experiment.Results: Compared with the ND group, the body weight of the mice in the HFD group was increased significantly, suggesting that the obese mouse model replicated successfully. In addition, the body fat weight, fat cell diameter, Lee's index and blood glucose of the HFD group were increased significantly, and the expression of UCP1 in the adipocytes was increased. Body weight, fat cell diameter, Lee's index and blood glucose of HFD mice treated with L-DHM and H-DHM were reversed significantly, while the expression of UCP1 in adipocytes was more significantly increased; however, L-DHM and H-DHM had no significant effects on the above indicators in normal mice.Conclusion: Dihydromyricetin inhibited high fat diet induced mouse obesity; the mechanism might be associated with promoting WAT browning.

Objective: To study the effects of acute and chronic exercise on phosphatidylinositol 3-hydroxy kinase(PI3K)/protein kinase B(AKT)/glucose transporter 4(GLUT4)signaling pathway in adipose tissue of rats with type 2 diabetes mellitus (T2DM) induced by high-fat diet and low-dose streptozotocin (STZ). Methods: A total of 52 SD male rats aged 15 months were randomly divided into normal control group (13) and high-fat group (39), and fed normal and high fat diets. After 8 weeks, the body weight of the high-fat group was higher 20% than that of the normal control group. After a small dose of STZ, the blood glucose level was ＞16.7 mmol/l, and the model was successfully established. The diabetic model group was randomly divided into a diabetic control group (DC, n=13), a diabetic chronic exercise group (DCE, n=13), and a diabetic acute exercise group (DAE, n=13). The DCE group underwent an 8-week swimming exercise and the DAE group performed a one-time swimming exercise. Blood lipids, blood glucose and serum insulin levels were measured, and the contents of fat PI3K, AKT and GLUT4 proteins were determined by Western blot method.Results: The levels of body weight, blood lipids, blood glucose and insulin in the diabetic group were significantly higher than those in the normal control group (P＜0.01); high density liptein cholesterol(HDL-C) levels were decreased (P＜0.05), and the expressions of PI3K, AKT and GLUT4 protein in adipose tissue were decreased (P＜0.01). After 8 weeks of swimming training, the levels of body weight, blood lipids, blood glucose and insulin all were decreased significantly (P＜0.01); while the level of HDL-C was increased (P＜0.05), and the expressions of PI3K, AKT and GLUT4 protein were increased (P＜0.01). After acute exercise, the levels of blood lipids, blood glucose and insulin were decreased (P＜0.05); the level of HDL-C was increased (P＜0.05), and the expression levels of fat PI3K, AKT and GLUT4 were increased significantly (P＜0.05).Conclusion: ①High fat diet combined with low-dose STZ induced damage to the PI3K/AKT pathway in adipose tissue of T2DM rats reduced insulin sensitivity. ②Acute and chronic aerobic exercise can improve the disorder of glucose and lipid metabolism through PI3K/AKT pathway, and the chronic exercise is better than acute exercise.

Objective: To observe the effects of acute exhaustive exercise on the expressions of oxidative stress related enzymes in skeletal muscle of rats. Methods: Forty male SD rats were divided into 4 groups, 10 rats in each group, which were the control group (C group), exhausted exercise group (E group), exercise + PKC inhibitor group (EC group), exercise + NOX inhibitor group (EA group). Three groups of exercise rats were familiarized with treadmill running for 3 days (5 m/min, once/d, no incline), then rested for one day. EC group was injected with PKC inhibitor chelerythrine (5 mg / kg) one day before and one hour before exercise, EA group was injected with NADPH oxidase inhibitor apocynin (10 mg / kg) at the same time, group C and group E were injected with the same dose of normal saline. Three groups of exercise rats were subjected to a one-time treadmill exhaustion exercise, and the plantaris were taken after exhaustion. Reactive oxygen species (ROS) were detected by DCF fluorescent probe, NOX2, NOX4, 3-NT were analyzed by Western blot, and PKC, NOX2, NOX4 were analyzed by immunoprecipitation.Results: Compared with group C, ROS level, NOX2 and NOX4 protein expressions, PKC-NOX2 and PKC-NOX4 complex levels, and 3-NT production in group E were significantly increased (P＜0.01, P＜0.05), and ROS level was no significant difference in group EC and group EA (P＞0.05), and NOX4 protein expression in group EC was significantly increased (P ＜ 0.05). Compared with group E, ROS level, NOX2 and NOX4 protein expressions, PKC-NOX2 and PKC-NOX4 complex levels, 3-NT production were decreased significantly (P＜0.01, P＜0.05).Conclusion: Exhausted exercise induces increased expressions of NOX2 and NOX4 proteins in skeletal muscle, and PKC mediates the production of ROS by regulating NOX2.

Objective: To investigate the effects of aerobic exercise on Cdc2-like kinase (CLK2) protein expression and the fat content in liver of mice fed with high fat diet. Methods: C57BL/6 mice were distributed in normal diet, high fat diet (fed with highfat diet during 16 weeks) and trained high fat diet group (fed with high-fat diet during 16 weeks and exercised during 8 weeks),10 mice in each group. The expression of CLK2 protein in liver of each group was detected by Western blot. The fat content of liver in each group was detected by oil red O staining, and the relative genes of fat metabolism in each group were evaluated by real-time quantitative PCR.Results: The mice fed with high fat diet showed insulin resistance, the hepatic CLK2 content and fat content were increased compared to the normal diet group. Otherwise, the chronic physical exercise improved insulin resistance state, prevented the increasing of CLK2 in the liver and attenuated hepatic fat accumulation.Conclusion: Aerobic exercise could reduce the expression of CLK2 protein in the liver of mice fed with high fat diet.

Objective:To study whether the two methods of energy calculation affects the value of relative energy contribution in men’s T54 wheelchair racing events. Methods: Ten men’s T54 wheelchair racers (age (22.9±5.2) yrs、sitting height (90.9±3.2) cm、body mass (59.3±8.3) kg) participate in 1 incremental test and 4 time trials (400 m、800 m、1 500 m、5 000 m). A portable gas analyzer, polar heart rate belt and a blood lactate analyzer were used to measure VO₂ at every breath, HR and blood lactate changes. The energetic contribution was measured with phosphocreatine-lactate-oxygen(PCr-La-O₂) and maximal accumulated oxygen deficit(MAOD) methods.Results: The anaerobic and total energy portions from MAOD were lower than those from PCr-La-O₂ ( especially in 400 m: W_TOT (50.8 ±12.7) KJ vs (65.2±13.5) KJ、W_ANA (31.0±9.0) KJ vs (45.4±11.4) KJ, P＜0.05), resulting in W_AER% calculated by MAOD was generally higher than PCr-La-O₂ method (especially in 400 m : W_AER% 39.0% ±1.2% vs 30.4%±8.4 %,P＜0.05).Conclusion: The study proves that the two-calculation method causes W_AER% difference. MAOD method does lead to an overestimate of W_AER%. Recommend to use the same calculation method for diagnosis and monitoring in the longitudinal study of long-term scientific research (such as the 4-year Olympic Games),to avoiding the difference in results caused by different calculation methods, which will further influence the development of coaches’ training plans and training implementation effect.

Objective:To investigate the mRNA, protein expression levels and the phosphorylation levels of key factors in rapidly accelerated fibrosarcoma/mitogen-activated protein kinase kinase/extracellular regulated protein kinases (Raf/MEK/ERK) pathway, and to clarify the regulatory function of Raf/MEK/ERK pathway in myocardial hypertrophy. Methods: Twenty SD rats were divided into sham-operated group and model group. The myocardial hypertrophy model was established by transverse aortic constriction (TAC). At 12 weeks after TAC, blood samples were collected from the submandibular vein, and the serum was separated to detect the content of N terminal pro B type natriuretic peptide (NT-proBNP). After that, the rats were subjected to echocardiography and hemodynamic measurement. Then the pathological changes of myocardial tissue were observed. And the levels of mRNA, protein expression and the phosphorylation of key factors in Raf/MEK/ERK pathway were detected in myocardial tissue.Results: Compared with sham-operated group, left ventricular end-diastolic interventricular septal thickness (IVSd), left ventricular end-systolic interventricular septal thickness (IVSs), left ventricular end-diastolic posterior wall thickness (LVPWd) and left vebtricular end-systolic posterior wall thickness (LVPWs) in TAC model group were increased significantly (P＜0.05,P＜0.01), left ventricular end-systolic diameter (LVIDs) was decreased significantly (P＜0.01), LV Mass and LW(LV Mass/Weight)were increased significantly (P＜0.05, P＜0.01). The levels of heart rate (HR), left ventricular pressure maximal rate of rise (+dp/dtmax), left ventricular pressure maximal rate of fall (-dp/dtmax) were decreased significantly (P＜0.01). The serum level of NT-proBNP in TAC rat was increased significantly (P＜0.01). The myocardial cells in TAC model group were arranged disorderly, myocardial cell hypertrophy, cytoplasm were increased significantly, and inflammatory cells infiltrated. A large amount of collagen fibers were deposited and large area of myocardial cells were stained blue in TAC rat. The expression levels of phospho-c-Raf (Ser259) and phospho-c-Raf (Ser338) in myocardial tissue were significantly increased (P＜0.01), meanwhile the expression levels of phospho- MEK1/2(Ser217/Ser221) and phospho-ERK1/2 (Thr202/Tyr204) were also significantly increased (P＜0.01).Conclusion: The regulatory role of Raf / MEK / ERK pathway in cardiac hypertrophy may be through the activation of phosphorylation of c-raf, MEK1, Mek2, ERK1 and ERK2 at specific sites.

Objective:To investigate the probable roles of the novel C2H2 zinc finger transcription factor ZFP580 on all-transretinoic acid (ATRA)-regulated VSMCs migration and underlying mechanisms. Methods: Rat aortic VSMCs were isolated, cultured and identified. VSMCs were treated with ATRA at the concentrations of 0, 5, 10 or 20 μmol/L for 24 hours. The migration ability of VSMCs was observed in each group and compared with control group which was treated by 0 μmol/L ATRA. The mRNA and protein expression levels of ZFP580 were detected by QPCR and Western blot. ZFP580 protein expression in VSMCs was detected under ATRA stimulation when ERK inhibitor PD98059 was used to inhibit the protein expression of ERK. Adenovirus transfection technology was used to obtain VSMCs with overexpression or low expression of ZFP580, and QPCR and Western blot were used to detect the mRNA and protein levels of MMP-2, MMP-9 and ZFP580.Results: On the 10th day of VSMCs culture, immunofluorescence showed that SM22 alpha antibody, as a specific marker of smooth muscle cells, was positive. Compared to the control group, VSMCs migration was reduced by 32%, 43%, and 59% in the group of 5, 10, and 20 μmol/L ATRA pretreatment. Compared with the control group, VSMCs treated by 20 μmol/L ATRA reduced the cell migration by 49%, 36% and 22% at 24, 48 and 72 h. The mRNA and protein expression levels of ZFP580 were increased with the increase of ATRA stimulation solubility and the extension of stimulation time. ERK was increased significantly after 15 min of ATRA stimulation. Pretreatment with ERK inhibitor PD98059 (20 μmol/L) inhibited the expression of ERK protein and reduced the expression of ATRA-induced ZFP580 protein. Overexpression of ZFP580 inhibited the expressions of MMP-2 and MMP-9, whereas down-expression of ZFP580 promoted the expressions of MMP-2 and MMP-9.Conclusion: ATRA increased the expression of ZFP580 through the ERK signaling pathway, while ZFP580 was involved in ATRA's inhibition of VSMCs migration by affecting the expression of downstream MMP-2 and MMP-9.

Objective: To investigate the effects of ginsenoside Rg5 on the proliferation, cycle and invasion of gastric carcinoma cell lines, providing experimental evidence for the anti-tumor mechanism of ginsenoside Rg5. Methods: In this experimental study, the human immortalized normal gastric mucosa cell GES-1 and gastric adenocarcinoma cell lines AGS and MKN-45 were treated with Rg3 and Rg5 at the concentrations of 10, 20, 30, 40 and 50 μmol/L for 24 h, 3 parallel holes were set for each group. A cell viability test, cell cycle analysis, transwell assay, ELISA and immunoblotting were performed.Results: The viabilities of AGS and MKN-45 were suppressed by Rg3 and Rg5 in a concentration-dependent manner. The activity of Rg5 against gastric cancer cells was stronger than that of Rg3, and its toxicity to GES-1 was lower than that of Rg3. After the treatment of 20 μmol/L of Rg5 for 24 h, Rg5 could generate cell cycle S phase arresting by decreasing the CyclinA1/cyclin-dependent kinase 2 (CDK2)/proliferating cell nuclear antigen (PCNA) complex production and increasing the P21^CIPI. Rg5 inhibited the migration of MNK-45 cells by reducing the expressions of MMP2 and MMP9. WB results showed that Rg5 inhibited the proliferation and migration of gastric cancer mainly by inhibiting the expression of Notch1 protein to regulate its downstream cycle and invasion related proteins.Conclusion: These results suggest that Rg5 exhibits stronger anti-cancer activity than Rg3 in gastric cancer cells, and has higher anti-gastric cancer cell activity than Rg3 and inhibits cell proliferation and migration by regulating the Notch1 pathway.

Objective: To investigate the effects of cerium oxide (CeO₂) nanoparticles on the viabilities of nerve cells PC12 and SH-SY5Y. Methods: CeO₂ nanoparticles were synthesized, structures were characterized and properties were evaluated. PC12 cells and SH-SY5Y cells were treated with CeO₂ nanoparticles at different concentrations (1, 2.5, 5, 10, 25, 50, 75, 100, 150 μg/ml) for 24 h and the cell viability was measured by MTT assay. Then PC12 cells and SH-SY5Y cells were co-treated with CeO₂ and active oxygen scavenger NAC and the cells were stained with DCFH-DA probe for ROS. The number of cells and the fluorescence intensity were observed under a fluorescent inverted microscope. Differences were assessed by one-way ANOVA.Results: After treatment with CeO₂ nanoparticles, the viabilities of both PC12 cells (P＜0.01) and SH-SY5Y cells (P＜0.01) were decreased comparing with the control group. After staining with DCFH-DA probe, the fluorescence intensity of the nerve cells was enhanced depending on the concentration of CeO₂ nanoparticles suggesting that CeO₂ induced the generation of reactive oxygen species (ROS). The fluorescence intensity of PC12 cells was decreased after CeO₂ nanoparticles (100 μg/ml) co-treatment with active oxygen scavenger NAC. Compared with CeO₂ nanoparticles alone at 25 μg/ml (P＜0.01), 50 μg/ml (P＜0.01), 75 μg/ml (P＜0.01), 100 μg/ml (P＜0.01), the cell viability was significantly increased after co-treatment with NAC.Conclusion: CeO₂ nanoparticles has a negative effect on the viabilities of nerve cells PC12 and SH-SY5Y, and the effect might be depend on ROS.

Objective: Effects of Yiqi Huashi Tongluo Formula on oxidative stress and renal fibrosis of residual kidney were investigated in five/sixth nephrectomy rats. Methods: The rat model of chronic renal failure after nephrectomy was established by Platt method. Two weeks after the operation, the rats were randomly divided into model group, Yiqi Huashi Tongluo Formula (YHT) group, benazepril online (BH) group and sham group, with 8 rats in each group. Treatment was initiated once a day for 12 weeks after successful modeling. Animals were treated once a day with intragastric administration for 12 weeks. (Aqueous solution of free decoction granules in YHT group was 0.276 g/100 g·d. BH group benazepril hydrochloride tablet aqueous solution 0.09 mg/100 g·d gavage; sham group and model group were gavage with 1 ml/100 g normal saline). Urine was collected with a metabolic cage at the end of the 12th week, and urine protein content was detected for 24 hours. The rats were then anesthetized to extract blood from the abdominal aorta and the kidneys. The pathological changes of left kidney were observed by HE staining and Masson staining. The activity of superoxide dismutase (SOD) and the content of malondialdehyde (MDA) in kidney homogenate were determined by colorimetry. Western blot assay was used to detect the expressions of nuclear factor-erythroid 2-related factor 2 (Nrf2), kelch-like ech-associated protein-1 (Keap1), NADPH oxidase 4 (Nox4), transforming growth factor-binding 1(TGF-β1), type I collagen (Collagen1) and Nrf2 in the nucleus in renal tissue.Results: Compared with sham group, model group rats had severe glomerular injury and obvious fibrosis. Levels of Scr, BUN, MDA and 24-hour urine protein excretion, protein expressions of Keap1, Nox4, TGF-β1 and Collagen1 were significantly increased (P＜0.01), while SOD activity and Nrf2 expression were significantly decreased (P＜0.01).Compared with the model group, the degree of glomerular lesion was reduced and fibrosis was less after YHT or BH intervention, and the levels of Scr, BUN, MDA, 24-hour urine protein excretion, protein expressions of Keap1, Nox4, TGF-β1 and Collagen1 were significantly decreased (P＜0.01), while SOD activity and Nrf2 expression were significantly increased (P＜0.01).Conclusion: Through affecting the Nrf2/Keap1 signaling pathway and down-regulating the expression of TGF-β1 protein, Yiqi Huashi Tongluo Formula improved the oxidative stress damage and fibrosis degree of residual kidney in the model rats with renal failure.

Objective: To find if edaravone can play a protective role in a mouse model of pulmonary oxygen toxicity and explore the intervention mechanism. Methods: Thirty male C57BL/6 mice were randomly divided into 3 groups(Air +Vehicle, Hyperbaric oxygen(HBO) +Vehicle and HBO + Edaravone). Mice were either given edaravone (5 mg/(kg·d)) in sterilized water or a sterilized water vehicle for 3 days before oxygen exposure. Mice in HBO groups were exposed to 0.23 MPa hyperoxia (≥95% O₂) for 6 h. Lung tissues were collected and the wet/dry ratio of lung were analyzed. For histologic analysis, lung sections were stained with hematoxylin and eosin (HE). Proinflammatory cytokine levels and antioxidant enzyme activities in lungs were determined by using ELISA kits. The expression levels of pro-apoptosis protein were determined with Western blot analysis.Results: Edaravone treatment could significantly reduce lung permeability, decrease tissue pro-apoptosis protein (cleaved-caspase3) and inflammation (IL-1β). However, edaravone treatment had no effect on antioxidant enzyme activities.Conclusion: These results showed that edaravone treatment had a protective role in pulmonary oxygen toxicity through curbing inflammation and apoptosis.

Objective: To evaluate the effects of prenatal radiation of 850～1 900 MHz mobile phone on white matter in cerebellum of adult rat offspring. Methods: Pregnant rats were randomly divided into short term maternal radiation group, long term maternal radiation group and control group. Rats in short term and long term maternal radiation group were exposed to 6 h/d and 24 h/d mobile phone radiation during 1-17 days of pregnancy, respectively. The cerebellums of offspring rats at the age of 3 month(n＝8)were taken. Cell morphology in cerebellum was studied by hematoxylin-eosin (HE) staining. The expressions of myelin basic protein (MBP), neurofilament-L (NF-L) and glial fibrillary acidic protein (GFAP) in cerebellum of rat offspring were detected by immunohistochemistry and Western blot.Results: Compared to control group, the morphological changes of purkinje cells in cerebellum were obvious in rat offspring of short term and long term maternal radiation group. Compared to control group, decreased MBP and NF-L expressions and increased GFAP expression were observed in long term maternal radiation group(all P＜0.05). Compared to short term radiation group, the expressions of MBP and NF-L were down-regulated (all P＜0.05) and the expression of GFAP was up- regulated(P＜0.05) in long term radiation group.Conclusion: Prenatal mobile phone radiation might lead to the damage of myelin and axon with activity of astrocytes in cerebellum of male rat offspring, which is related to the extent of radiation.

Objective: To observe the effects of resveratrol on body composition in adult catch-up growth rats and to explore the possible mechanism. Methods: Eight-week-old male SD rats were randomly divided into 6 groups: normal controls for 4 weeks (NC4) group, caloric restriction for 4 weeks (R4) group, calorie restriction meanwhile resveratrol treatment for 4 weeks (R4E) group, normal controls for 12 weeks (NC12) group, catch-up growth (CUG) group and catch-up growth meanwhile resveratrol treatment for 8 weeks (CUGE) group. At the end of the four-week and twelve-week experimental period, the body weight, muscle and fat content of trunk and whole body, the ratio of trunk to whole body fat were detected, and at the end of twelve-week experimental period, the expression of SIRT1 in skeletal muscle and epididymal adipose tissue, and the expression of PPARγ in epididymal adipose tissue were detected.Results: Compared with NC12 group, the fat content of trunk and whole body and trunk to whole body fat ratio in CUG group were increased significantly, along with the expression of PPARγ in epididymal adipose tissue was increased significantly (P＜0.05), while the muscle content of trunk and whole body, the expression of SIRT1 in skeletal muscle and epididymal adipose tissue in CUG group were decreased significantly compared with NC12 group (P＜0.05 or P＜0.01); compared with CUG group, oral administration of resveratrol distinctly reduced the body fat content and trunk to whole body fat ratio in the CUGE groups, and the expression of PPARγ in epididymal adipose tissue of CUGE group was also significantly decreased (P＜0.05). Meanwhile, the muscle content and the expression of SIRT1 in skeletal muscle and epididymal adipose tissue in CUGE group were significantly increased compared with the CUG group (P＜0.05).Conclusion: Resveratrol can decrease body fat content, increase muscle content and improve abdominal fat accumulation in adult catch-up growth rats, and its mechanism may be associated with increasing SIRT1 expression in skeletal muscle and visceral adipose tissue, decreasing PPARγ expression in visceral adipose tissue.

Objective: To observe the regulatory effect of 6-Shogaol on Notch signal pathway in colonic epithelial cells of mice with ulcerative colitis. Methods: Forty Kunming mice were randomly divided into normal group (n=10) and model group (n=30). The model of ulcerative colitis was induced by free drinking of 2% dextran sulfate sodium salt(DSS). After 15 days, the mice were divided into model group, 6-gingerenol group and positive control group with 10 mice in each group. Normal group and model group were treated with normal saline, 6-gingerenol group was treated with 6-Shogaol 100 mg/(kg·d), positive control group was treated with sulfasalazine 100 mg/(kg·d), for 20 days. The histopathological changes of colon were observed, and the expressions of Hes-1 and Math-1protein in colonic epithelial cells were detected by immunofluorescence double labeling method. The expressions of Notch-1, Hes-1 and Math-1 mRNA in colonic epithelial tissue were detected by RT-PCR. The expressions of Notch-1, Hes-1 and Math-1 protein in colonic epithelial tissue was detected by Western blot.Results: Compared with the normal group, the expression of Notch-1 and Hes-1 protein and the relative expression of mRNA in colonic epithelium of model group were significantly increased (P＜0.01), while the relative expressions of Math-1 mRNA and protein were decreased significantly (P＜0.01). Compared with the model group, the expressions of Notch-1 and Hes-1 protein and the relative expression of mRNA in colonic epithelium of 6-Shogaol group and sulfasalazine group were decreased significantly(P＜0.01), while the relative expressions of Math-1 mRNA and protein were increased significantly(P＜0.01).Conclusion: 6-Shogaol can inhibit the over activation of Notch pathway and regulate the balance of differentiation between colonic epithelialabsorptive cell line and secretory cell line and repair damaged mucosal tissue.