肖李,王广,练高建,李程悦,龚慧芳,王俊涵,苏泽红.黄芩苷通过激活JNK/p38 MAPK通路诱导ALL Reh细胞凋亡.[J].中南医学科学杂志.,2023,(3):325-329.
黄芩苷通过激活JNK/p38 MAPK通路诱导ALL Reh细胞凋亡
Baicalin induces ALL Reh cell apoptosis via JNK/p38 MAPK pathway activation
投稿时间:2022-12-17  修订日期:2023-03-29
DOI:10.15972/j.cnki.43-1509/r.2023.03.003
中文关键词:  ALL  细胞凋亡  黄芩苷  Reh细胞  活性氧  JNK/p38 MAPK [
英文关键词:ALL  apoptosis  baicalin  Reh cell  ROS  JNK/p38 MAPK
基金项目:湖南省自然科学基金面上项目(2019JJ40243);湖南省教育厅生态环境与人类重大疾病防治重点实验室支持项目(20K107);湖南省大学生创新创业训练计划(S20211055530)
作者单位E-mail
肖李 南华大学衡阳医学院 生物化学与分子生物学研究所,湖南衡阳 421001 e-mail为2854765632@qq.com,e-mail为zehongsu@qq.com 
王广 南华大学衡阳医学院 生物化学与分子生物学研究所,湖南衡阳 421001  
练高建 南华大学衡阳医学院 实验动物学部,湖南衡阳 421001  
李程悦 南华大学衡阳医学院 实验动物学部,湖南衡阳 421001  
龚慧芳 南华大学衡阳医学院 生物化学与分子生物学研究所,湖南衡阳 421001  
王俊涵 南华大学衡阳医学院 生物化学与分子生物学研究所,湖南衡阳 421001  
苏泽红 南华大学衡阳医学院 生物化学与分子生物学研究所,湖南衡阳 421001 e-mail为2854765632@qq.com,e-mail为zehongsu@qq.com 
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中文摘要:
      目的探究黄芩苷对急性淋巴细胞白血病(ALL)细胞株Reh增殖和凋亡的影响及c-Jun氨基蛋白激酶(JNK)/p38丝裂原活化蛋白激酶(p38 MAPK)通路在其机制中的作用。 方法黄芩苷处理或联合活性氧(ROS)清除剂NAC共处理Reh细胞;流式细胞术检测细胞凋亡、胞内ROS水平和线粒体膜功能(MMP);免疫荧光实验观察凋亡细胞的数目及其形态变化。Western blotting免疫印迹检测Reh细胞内凋亡蛋白和信号通路蛋白的表达水平。 结果与对照组比较,黄芩苷组Reh细胞增殖被抑制,细胞凋亡率、促凋亡蛋白、ROS、JNK和p38磷酸化水平显著上升,抗凋亡蛋白表达下调,MMP明显受损(P<0.01)。NAC清除ROS后明显恢复细胞增殖,JNK和p38磷酸化水平明显下降,Survivin表达恢复(P<0.01)。 结论黄芩苷经激活JNK/p38 MAPK通路活化Caspase3/7,诱导Reh细胞凋亡。
英文摘要:
      AimTo investigate the effects of baicalin on the proliferation and apoptosis of acute lymphoblastic leukemia (ALL) cell line Reh, and the role of c-Jun N-terminal kinase (JNK)/p38 mitogen-acti-vated protein kinase (p38 MAPK) pathway in its mechanism. MethodsReh cells were treated with baicalin or in combination with reactive oxygen species (ROS) scavenger NAC. Flow cytometry was utilized to measure cell apoptosis, intracellular ROS levels, and mitochondrial membrane potential (MMP). Immunofluorescence was employed to observe the number and morphological changes of apoptotic cells. Western blotting was used to assess the expression levels of apoptotic proteins and signaling pathway proteins in Reh cells. ResultsCompared to the control group, baicalin treatment led to inhibited Reh cell proliferation, elevated rates of apoptosis, levels of pro-apoptotic proteins, ROS, and phosphorylation of JNK and p38, as well as reduced expression of anti-apoptotic proteins, and significant MMP damage (P<0.01). Treatment with NAC, a ROS scavenger, significantly restored cell proliferation, with a reduction in phosphorylation levels of JNK and p38, and restored expression of Survivin (P<0.01). ConclusionBaicalin activates the JNK/p38 MAPK pathway, leading to the activation of Caspase3/7 and induction of apoptosis in Reh cells.
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