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作 者:刘保荣[1] 袁博[1] 慕喜喜 慕为民[1] 王重民[1]
出 处:《山西医科大学学报》2016年第6期517-521,共5页Journal of Shanxi Medical University
摘 要:目的观察大黄素对结肠癌细胞增殖的抑制作用,并探讨其可能机制。方法取人结肠癌SW620细胞,分为对照组,大黄素低浓度(30μmol/L,LD)组,中浓度(60μmol/L,MD)组,高浓度(90μmol/L,HD)组和大黄素+内质网特异性应激抑制剂4-PBA(大黄素90μmol/L、PBA8μmol/L,HD+PBA)组。各实验组细胞在培养基中对应加入相应浓度的大黄素溶液或大黄素+4-PBA溶液后培养48 h,MTT比色法观察细胞增殖,Hoechst染色法观察细胞凋亡,Western blot法检测ERS标志蛋白GRP-78、CHOP以及活化Caspase-12的表达变化。结果与正常对照组相比,LD、MD及HD组大黄素对结肠癌SW620细胞增殖的抑制率、细胞凋亡率和细胞内GRP-78、CHOP和活化Caspase-12的表达水平均显著升高(P<0.05),且呈现浓度依赖性(P<0.05);与HD组相比,HD+PBA组对结肠癌SW620细胞增殖的抑制作用、细胞凋亡以及细胞内GRP-78、CHOP以及活化caspase-12的表达水平均显著降低(P<0.05)。结论大黄素能够通过内质网应激(ERS)诱导的细胞凋亡途径抑制结肠癌细胞增殖。Objective To investigate the inhibitory effect of emodin on the proliferation of colon cancer cells and to explore its possible mechanism. Methods The human colon cancer cells of SW620 were divided into control group,low concentration of emodin(30mol / L)group(LD),middle concentrations of emodin(60 mol / L)group(MD),high concentration of emodin(90 mol / L)group(HD)and emodin(90 mol / L)plus 4-PBA(ERS inhibitor,8 μmol / L)group(HD + PBA). The SW620 cells were cultured with the corresponding concentrations of emodin or emodin plus 4-PBA. After culture for 48 h,the proliferation rate of SW620 cells was observed by MTT colorimetric method,the apoptosis of SW620 cells was observed by Hoechst staining,and the expression of endoplasmic reticulum stress(ERS)marker proteins(GRP-78,CHOP and activated Caspase-12)in SW620 cells were detected by Western blot. Results Compared with control group,the inhibitive rate of proliferation,the apoptosis rate and the expression levels of GRP-78,CHOP and activated Caspase-12 were significantly increased in a concentration dependent manner in LD,MD and HD groups(P 0. 05). Compared with HD group,the inhibitive rate of proliferation,the apoptosis rate and the expression levels of GRP-78,CHOP and activated Caspase-12 were significantly decreased in HD + PBA group(P 0. 05). Conclusion The proliferation of colon cancer cells can be inhibited by emodin through the pathway of apoptosis induced by ERS.
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