摘要
目的探讨神经酸(nervonic acid,NA)对紫杉醇损伤的小肠隐窝细胞的保护机制。方法采用紫杉醇处理IEC-6细胞,检测紫杉醇IC50浓度。MTS法检测不同浓度NA(5μmol/L、10μmol/L、20μmol/L)对紫杉醇(IC50浓度)干预后的IEC-6细胞的相对增殖率。原位缺口末端检测法(TUNEL法)检测DNA断裂情况。蛋白质印迹法检测相关蛋白表达。结果紫杉醇促进正常IEC-6细胞凋亡。NA对维持细胞形态、保持细胞活力有一定作用。TUNEL法显示,与空白对照相比较,紫杉醇组细胞凋亡明显增加;与紫杉醇组细胞比较,NA组细胞凋亡明显减少。与紫杉醇组比较,NA组A-FABP、p-p38、Bax、Cyt C、cl-Caspase-3降低(P<0.01),Bcl-2、Bcl-2/Bax升高(P<0.01)。p38无明显变化(P>0.05)。结论 NA可通过调节p38通路、Bcl-2/Bax等减轻紫杉醇诱导的小肠隐窝细胞的凋亡损伤。
Objective To investigate the effect of nervonic acid （NA） on IEC-6 cell induced by paclitaxel （PTX） , including mechanism and vitality. Methods IEC-6 cell treated with PTX to detective PTX ICs0. IEC-6 cells＇ relative proliferative rates of NA in different levels （5 Ixmol/L, 10 μmol/L, 20 μmol/L） were detected by MTS assay, the expression levels of A-FABP, p38, Bcl-2, Bax, Bcl-2/Bax, CytC and cl-Caspase-3 were detected by Western blotting, and apoptotic ceils of IEC-6 were detected by TUNEL. Results PTX could encourage normal cells apoptosis. NA was characterized with biological functions such as maintenance of cell shape and vitality. TUNEL showed that PTX could promote cells apoptosis, and NA had a protective effect on IEC-6 apoptosis induced by PTX. The expressions of A-FABP, p-p38, Bax, CytC, cl-Caspase-3 were reduced and Bcl-2, Bcl-2/Bax expression were increased in NA group compared with PTX group （P 〈 0. 01 ）. There was no significant difference of p38 in two groups （P 〉 0. 05）. Conclusion NA can reduce paclitaxel-induced apoptosis of IEC-6 ceils by regulating p38 pathway and Bcl-2/Bax.
出处
《胃肠病学和肝病学杂志》
CAS
2017年第11期1268-1272,共5页
Chinese Journal of Gastroenterology and Hepatology
基金
国家自然科学基金资助项目(81302958
81373582)
广东省中医药局建设中医药强省课题资助(20131102
20151019
20151018)
