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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 protective mechanism of nervonic acid (NA) on paclitaxel injured intestinal crypt cells. Methods Paclitaxel was used to treat IEC-6 cells and the concentration of paclitaxel IC50 was measured. The relative proliferation rate of IEC-6 cells treated with paclitaxel (IC50) with different concentrations of NA (5μmol / L, 10μmol / L, 20μmol / L) In situ nick end detection (TUNEL method) to detect DNA fragmentation. Western blotting was used to detect related protein expression. Results Paclitaxel promoted normal IEC-6 cell apoptosis. NA maintains cell morphology and maintains cell viability. TUNEL assay showed that compared with the blank control group, the apoptosis of paclitaxel group was significantly increased. Compared with the paclitaxel group, the apoptosis of NA group was significantly reduced. Compared with paclitaxel group, NAA group had lower levels of A-FABP, p-p38, Bax, Cyt C and cl-Caspase-3 and increased Bcl-2 and Bcl-2 / Bax (P <0.01). p38 no significant change (P> 0.05). Conclusions NA attenuates paclitaxel-induced apoptotic injury in intestinal crypt cells by regulating p38 pathway and Bcl-2 / Bax.