| Objective:The aim of this study was to investigate the effect of adipose derived stem cell(ADSCs)combined with ginsenoside Rgl of mice with dextran sulfate sodium(DSS)induced inflammatory bowel disease.Methods:75 Male C57BL/6J mice aged 8 weeks were purchased from Nanjing Medical University(Nanjing,China)and housed under controlled temperature,humidity,and light cycle conditions.and then mice were divided into control group,DSS group,Rg1 group,ADSCs group and ADSCs+Rg1 group,with 15 mice in each group,inflammatory bowel disease was induced by one cycles of 3.0%DSS for seven days followed by 7 days of drinking water.The IBD mice were orally administered 20 mg/kg ginsenoside Rg1 from day 1 onward for 14 days and monitored daily,on days 4th,and 7th of the study(with DSS administration initiated on day 1 and to day 14th),ADSCs were administered by tail vein injection at 1×106 cell dose of per IBD mouse in 200 ml normal saline(NS).The body weight,stool consistency,and stool bleeding were recorded.At the end of treatment,animals were sacrificed and samples were collected and subjected to pathological section,inflammation scores.The levels of lymphocyte Treg and Th17 cells in spleen were detected by flow cytometry.Inflammatory response was determined by measuring the levels of different inflammatory mediators in the serum.The inflammatory cytokines IL-6,IL-10,IL-17A,and TNF-α were assessed by ELISA.Results:(1).Compared with the control group,the weight of the DSS group decreased significantly.After interventions,compared with the DSS group,the weight of the mice in the Rg1 group,the ADSCs group and the ADSCs+Rg1 group increased(P<0.05).(2).Compared with the control group,the length of colon was obviously decresed in the DSS group,and the length of colon increased significantly in ADSCs group,Rg1 group,and ADSCs+Rg1 group(P<0.05).(3).Pathological sections of the colon in the DSS group shown destruction of the intestinal mucosa severely,infiltration of inflammatory cells,and significantly increased inflammation score.Compared with the DSS group,the mucosa was repaired in the ADSCs group,Rg1 group,and ADSCs+Rg1 group,with less inflammatory cell infiltration and decreased inflammation score(P<0.05).(4).TNF-α,IL-6,and IL-17A level in mice was significantly lower than that in the DSS group in all treatment groups,with the most significant reduction in ADSCs+Rg1 group,and the decrease was more significant in the ADSCs group than in the Rg1 group(P<0.05),the level of IL-10 was significantly higher in all treatment groups than in the DSS group,with the most significant increase in ADSCs+Rg1 group(P<0.05),the level of IL-10 in the ADSCs group was increased than Rg1 group,but there was no statistical difference(P<0.05).(5).Flow cytometry shown that Treg cells in treatment groups were significantly higher than those in the DSS group,and the increase was more significant in the Rg1 group(P<0.05);there was no significant statistical difference between the ADSCs+Rg1 treatment group and the Control group(P>0.05).(6).flow cytometry shown that Th17 cells were significantly decreased after ADSCs and Rg1 treatment compared with the DSS group,and the decrease was more significant with the ADSCs+Rg1 group(P<0.05),there was no statistically significant difference between the ADSCs+Rg1 group and Control group(P>0.05).Conclusion:ADSCs and ginsenoside Rg1 may play important roles in the treatment of IBD by regulating the immune balance and inflammatory response of Treg and Th17 in model mice. |