基于PI3KAkt-Bcl-2通路探讨TSG-6对人瘢痕疙瘩凋亡机制的影响  

Effects of TSG-6 on Apoptosis Mechanism of Human Keloid Based on PI3KAkt-Bcl-2 Pathway

作　　者：胡银娥[1] 代淑芳[1] 魏沙沙 许丹丹 郭丽丽[2] Hu Yin'e;Dai Shufang;Wei Shasha;Xu Dandan;Guo Lili(Huaihe Hospital of Henan University,Kaifeng 475000,China;Zhengzhou University,Zhengzhou 450001,China)

机构地区：[1]河南大学淮河医院,河南开封475000 [2]郑州大学,河南郑州450001

出　　处：《中国中西医结合皮肤性病学杂志》2020年第5期397-401,共5页Chinese Journal of Dermatovenereology of Integrated Traditional and Western Medicine

基　　金：2016年河南省医学科技攻关计划项目(201602163)。

摘　　要：目的基于PI3KAkt-Bcl-2通路探讨肿瘤坏死因子-α刺激基因(TSG)-6对人瘢痕疙瘩凋亡机制的影响。方法以本院2017年8月—2018年8月通过手术治疗的56例瘢痕疙瘩患者为对象,收集其手术标本,对TSG-6过度表达细胞株(过度表达组)、TSG-6干扰细胞株(干扰组)、TSG-6过度表达对照细胞株(过度表达对照组)、TSG-6干扰对照细胞株(干扰对照组)进行构建,测定以上4组及瘢痕疙瘩成纤维细胞中PI3K、Akt、Bcl-2表达情况。结果过度表达组细胞凋亡率是36.67%,分别较过度表达干扰组的16.67%、干扰组的13.33%、干扰对照组的6.67%、瘢痕疙瘩成纤维细胞的10.00%高,差异有统计学意义(P<0.05);过度表达组细胞增殖速度较瘢痕疙瘩成纤维细胞慢,干扰组细胞增殖效应显著较其余组别高,差异有统计学意义(P<0.05),过度表达对照组、干扰对照组、瘢痕疙瘩成纤维细胞凋亡对比则差异无统计学意义(P>0.05);过度表达组PI3K、Akt、Bcl-2基因mRNA与蛋白表达均显著较干扰组、过度表达对照组、干扰对照组、瘢痕疙瘩成纤维细胞低,干扰组PI3K、Akt、Bcl-2基因mRNA与蛋白表达均较过度表达组、过度表达对照组、干扰对照组、瘢痕疙瘩成纤维细胞高,差异有统计学意义(P<0.05),过度表达对照组、干扰对照组、瘢痕疙瘩成纤维细胞对比则差异无统计学意义(P>0.05)。结论TSG-6过度表达可抑制瘢痕疙瘩成纤维细胞中PI3K、Akt、Bcl-2表达,表明TSG-6可对PI3KAkt-Bcl-2通路产生负向调控作用,促进瘢痕疙瘩成纤维细胞凋亡,进而达到抑制瘢痕疙瘩增生的效果。Objective In order to explore the effects of tumor necrosis factor-αstimulated gene 6(TSG-6)on apoptosis mechanism of human keloid based on PI3KAkt-Bcl-2 pathway.Methods Surgical specimens were collected from 56 patients with keloid who were treated by surgery in our hospital from August 2017 to August 2018.TSG-6 overexpression cell line(overexpression group),TSG-6 interference cell line(interference group),TSG-6 overexpression control cell line(overexpression control group),and TSG-6 interference control cell line(interference control group)were constructed.The expression of PI3K,Akt and Bcl-2 in four groups of cells were measured.Results The apoptosis rate of overexpression group was 36.67%,which was higher than that of over-expression interference group(16.67%),interference group(13.33%)and interfering control group(6.67%),with statistically significant(P<0.05).The expression of PI3K,Akt,Bcl-2 gene mRNA and protein in overexpression group were higher than that of the interference group,overexpression control group and interference control group,the expression of PI3K,Akt,Bcl-2 gene mRNA and protein in interference group were higher than those of the overexpression group,overexpression control group and interference control group,with statistically significant(P<0.05).But there was no significant difference between interference control group and overexpression control group(P>0.05).Conclusion The overexpression of TSG-6 can inhibit the expression of PI3K,Akt and Bcl-2 in keloid fibroblast.This suggests that TGG-6 may exert negative regulation effect on PI3KAkt-Bcl-2 pathway,promote the apoptosis of keloid fibroblast,and thereby achieve the effects of inhibiting the hyperplasia of keloid.

关 键 词：PI3KAkt-Bcl-2通路 肿瘤坏死因子-α刺激基因-6 瘢痕疙瘩 凋亡 机制 

分 类 号：R619.6[医药卫生—外科学]