OBJECTIVE:To study the effects of nimesulide combined with oxaliplatin on transplanted tumor growth and im-mune function of rats with esophageal cancer. METHODS:Rats were randomly divided into model group(intragastrically given So-dium carboxymethyl cellulose solution+intravenously given 5% Glucose injection in tail),nimesulide group(intragastrically given 20 mg/kg),oxaliplatin group(intravenously given 13.6 mg/kg in tail)and combination group,10 in each group. Esophageal can-cer Eca109 cells were subcutaneously injected to develop transplanted tumor model. After modeling,rats in each group received rel-evant medicines by corresponding ways,once a day for ig,once every 4 d for iv in tail. Rats were sacrificed after 8 weeks,tumor volume and quality of rats were measured,tumor inhibition rate was calculated,and contents of tumor markers(CEA,CYFRA21-1,SCCAg),percentages of immune cells(CD3+,CD4+,CD8+T cells and NK cell)in peripheral blood were detected. RESULTS:Compared with model group,tumor volume and quality in other 3 groups were decreased (P<0.05);contents of tumor markers were decreased (P<0.05). Percentages of CD3+,CD4+ T cells and NK cell in nimesulide group were increased,percentages of CD8+T cell was decreased(P<0.05). Percentages of CD3+,CD4+T cells and NK cell in oxaliplatin group and combination group were decreased,percentages of CD8+ T cell was increased(P<0.05). Compared with nimesulide group and oxaliplatin group,tu-mor inhibition rate in combination group was increased(P<0.05);contents of tumor markers were decreased(P<0.05);percent-ages of immune cells were lower than nimesulide group and higher than oxaliplatin group(P<0.05). CONCLUSIONS:Nimesulide can enhance the oxaliplatin's antitumor effect on esophageal cancer,and decrease its inhibition degree on immune functions.

Aim To investigate the effect of ASIC1 a ( acid-sensing ion channel 1 a ) on the pathological change of diabetes complication liver fibrosis and the proliferation and activation of hepatic stellate cell ( HSC-T6 ) stimulated by PDGF-BB under hyperglyce-mia. Methods Diabetes rats model was established by streptozotocin ( STZ) , and liver fibrosis rats model was induced by carbon tetrachloride ( CCl4 ) . Then, the liver extent of damage and the expression of ASIC1 a were observed in the diabetic rats, liver fibrosis rats and diabetes complication liver fibrosis rats. In vitro, after pretreated with amiloride, HSC-T6 was treated with high glucose for 24 h and then stimulated with PDGF-BB for another 24 h. The proliferation and acti-vation of HSC-T6 were observed, and the expression of ASIC1a, α-SMA and collagen Ⅰ were detected by Western blot. Results Compared with the control group, rats from diabetic group induced by STZ, liver fibrosis group induced by CCl4 , and the diabetes com-plication liver fibrosis rats co-induced by STZ and CCl4 were all observed with liver damage at different levels, and tissue injury of complication group was most seri-ous. However, the expression of ASIC1a in the three model groups was significantly increased compared to the control group. ASIC1a level was most obvious in the diabetes complication liver fibrosis rats. Amiloride pretreatment significantly decreased ASIC1 a expression and inhibited PDGF-BB mediated proliferation and the expression ofα-SMA and collagenⅠin HSC-T6 under high glucose environment. Conclusion High ambient glucose aggravates HSC activation and hepatic fibrosis, and this may be related with the increasing expression of ASIC1a.