基于p38MAPK-PPARγ/NF-κB信号通路探讨消肿止痛合剂对血管内皮细胞bEND-3凋亡的影响  

Discussion on Effect of Xiaozhong Zhitong Mixture(消肿止痛合剂)on bEND-3 Apoptosis of Vascular Endothelial Cells Based on p38MAPK-PPARγ/NF-κB Signaling Pathway

作　　者：朱克玉 宋渊[2] 梁旭东 沈稼轩 张团庄 乔靖 刘涛 ZHU Keyu;SONG Yuan;LIANG Xudong;SHEN Jiaxuan;ZHANG Tuanzhuang;QIAO Jing;LIU Tao(Gansu University of Chinese Medicine,Lanzhou 730000,Ganxu,China;Gansu Provincial Hospital of Traditional Chinese Medicine,Lanzhou 730000,Ganxu,China)

机构地区：[1]甘肃中医药大学,甘肃兰州730000 [2]甘肃省中医院,甘肃兰州730000

出　　处：《辽宁中医杂志》2024年第4期149-152,I0002,共5页Liaoning Journal of Traditional Chinese Medicine

基　　金：国家自然科学基金地区项目(81860863)。

摘　　要：目的从细胞及信号通路层面探讨消肿止痛合剂对皮瓣缺血再灌注损伤中血管内皮细胞凋亡的影响。方法血管内皮细胞bEND-3培养。TNF-α体外细胞凋亡诱导模型建立并将细胞分为:p38MAPK抑制剂组、PPARγ抑制剂组、NF-κB抑制剂组、模型对照组、空白组。微丝绿色荧光探针观察细胞骨架微丝。RT-PCR法检测血管内皮细胞bEND-3细胞中p38MAPK、PPARγ、IκBα、NF-κBmRNA的表达。结果空白组中p38MAPK、PPARγ、IκBα、NF-κB的表达量无明显差异,模型对照组中p38MAPK与NF-κB的表达量最高,与模型对照组相比,p38MAPK抑制剂组bEnd.3细胞中p38MAPK与NF-κB的表达被抑制,PPARγ、IκBα表达量升高(P<0.05);PPARγ抑制剂组中PPARγ、IκBα、NF-κB的表达被抑制,p38MAPK表达量升高(P<0.05),NF-κB抑制剂组中p38MAPK与NF-κB的表达被抑制,IκBα与PPARγ的表达量升高(P<0.05);与空白组相比,p38MAPK抑制剂组与NF-κB抑制剂组中p38MAPK、PPARγ、IκBα、NF-κB的表达量升高(P<0.05),PPARγ抑制剂组中p38MAPK与NF-κB表达量明显升高,PPARγ、IκBα表达被抑制(P<0.05)。结论消肿止痛合剂可抑制bEND-3细胞凋亡,其机制与影响可能与p38MAPK-PPARγ/NF-κB信号通路有关。Objective To investigate the effect of Xiaozhong Zhitong Mixture(消肿止痛合剂)on the apoptosis of vascular endothelial cells in ischemia-reperfusion injury of skin flap at the cellular and signaling pathway levels.Methods Vascular endothelial cells bEnd.3 were cultured.Tumor necrosis factor-α(TNF-α)induced apoptosis model was established and cells were divided into mitogen-activated protein kinases(p38MAPK)inhibitor group,peroxisome proliferator-activated receptorγ(PPARγ)inhibitor group,nuclear factor kappa-B(NF-κB)inhibitor group,model control group and blank group.Cytoskeletal microfilaments were observed with green fluore scent probe.The mRNA expressions of p38MAPK,PPARγ,nuclear factorκB inhibitor(IκBα)and NF-κB invascular endothelial cells bEnd.3 were detected by RT-PCR.Results The expression levels of p38MAPK,PPARγ,IκBαand NF-κB in the blank group were not significantly different and the expression levels of p38MAPK and NF-κB in the model control group were the highest.Compared with those of the model control group,the expression levels of p38MAPK and NF-κB in bEnd.3 cells in the p38MAPK inhibitor group were inhibited.The expression levels of PPARγand IκBαincreased(P<0.05).The expressions of PPARγ,IκBαand NF-κB were inhibited,and the expression of p38MAPK was increased in PPARγinhibitor group(P<0.05)while the expressions of p38MAPK and NF-κB were inhibited,and the expressions of IκBαand PPARγwere increased in NF-κB inhibitor group(P<0.05).Compared with those of the blank group,the expression levels of p38MAPK,PPARγ,IκBαand NF-κB in p38MAPK inhibitor group and NF-κB inhibitor group were increased(P<0.05)and the expression levels of p38MAPK and NF-κB in PPARγinhibitor group were significantly increased.The expressions of PPARγand IκBαwere inhibited(P<0.05).Conclusion Xiaozhong Zhitong Mixture can inhibit bEnd.3 cell apoptosis.

关 键 词：消肿止痛合剂 bEND-3细胞 信号通路 皮瓣 

分 类 号：R285[医药卫生—中药学]