(-)-gossypol induces autophagy in Daudi cells through ERK signal pathway

倪振洪; 王滨; 丁雯; 程攀科; 连继勤; 何凤田

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(-)-gossypol induces autophagy in Daudi cells through ERK signal pathway

更新时间：2026-01-09

- (-)-gossypol induces autophagy in Daudi cells through ERK signal pathway
- Journal of Army Medical University Vol. 34, Issue 23, Pages: 2384-2387(2012)
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  CLC： R733.4;R965;R979.19
- Published：2012
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倪振洪,王滨,丁雯,程攀科,连继勤,何凤田.左旋棉酚通过ERK通路诱导Daudi细胞发生自噬及意义[J].陆军军医大学学报(原第三军医大学学报),2012,34(23):2384-2387.

　Ni Zhenhong,Wang Bin,Ding Wen,Cheng Panke,Lian Jiqin,He Fengtian.(-)-gossypol induces autophagy in Daudi cells through ERK signal pathway[J].J Amry Med Univ (J Third Mil Med Univ),2012,34(23):2384-2387.
倪振洪,王滨,丁雯,程攀科,连继勤,何凤田.左旋棉酚通过ERK通路诱导Daudi细胞发生自噬及意义[J].陆军军医大学学报(原第三军医大学学报),2012,34(23):2384-2387. DOI：

　Ni Zhenhong,Wang Bin,Ding Wen,Cheng Panke,Lian Jiqin,He Fengtian.(-)-gossypol induces autophagy in Daudi cells through ERK signal pathway[J].J Amry Med Univ (J Third Mil Med Univ),2012,34(23):2384-2387. DOI：

摘要

目的探讨左旋棉酚诱导淋巴瘤Daudi细胞发生自噬可能机制及对细胞存活率的影响。方法采用CCK-8法检测左旋棉酚在体外对Daudi细胞增殖抑制作用的影响；采用台盼蓝排斥实验检测不同处理对细胞存活率的影响；Western blot检测细胞中自噬相关蛋白LC3、ERK和磷酸化ERK的表达情况；AO染色观察经左旋棉酚处理后Daudi细胞酸性小体的变化情况。结果左旋棉酚能剂量依赖性地抑制Daudi细胞的增殖和促进细胞死亡；AO染色后经左旋棉酚处理的细胞内可观察到大量的酸性小体形成；Western blot显示左旋棉酚能显著上调自噬相关蛋白LC3Ⅱ的表达及增强磷酸化ERK的水平，抑制ERK的磷酸化能下调LC3 Ⅱ的表达；ERK抑制剂U0126及自噬抑制剂CQ和3-MA均能显著增强左旋棉酚的杀细胞效力。结论左旋棉酚可能通过ERK通路诱导Daudi细胞发生自噬，抑制ERK介导的自噬能够显著增强左旋棉酚的抗瘤效应。

Abstract

Objective To investigate the mechanism of (-)-gossypol-induced autophagy and its effect on cell viability in Burkitt lymphoma Daudi cells. Methods CCK-8 detection was used to assess the inhibitory effects of (-)-gossypol on the proliferation in Daudi cells. Trypan blue exclusion assay was used to detect cell viability during different treatments. Western blotting was used to determine the expression of LC3 Ⅱ and ERK. Acridine orange staining was used to detect the formation of acidic vesicular organelles (AVO). Results (-)-gossypol inhibited cell proliferation and induced cell death in a dose-dependent manner. Increased AVOs were noted after treatment of cells with (-)-gossypol. Western blot analysis revealed that (-)-gossypol treatment markedly upregulated LC3 Ⅱ and induced phosphorylation of ERK. Inhibition of ERK activity blocked the upregulation of LC3 Ⅱ mediated by (-)-gossypol. Inhibition of autophagy by U0126 (ERK inhibitor)

CQ and 3-MA (autophagy inhibitors) enhanced cell death mediated by (-)-gossypol. Conclusion (-)-gossypol effectively inhibits cell proliferation and induces autophagy in Burkitt lymphoma Daudi cells via ERK pathway.

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