甲壳素衍生物调控瘢痕疙瘩中TSG-6/PI3K/AKT通路表达的临床研究

Clinical Study of Chitin Derivatives Regulating the Expression of TSG-6/PI3K/Akt Pathway in Keloid

目的:甲壳素衍生物调控瘢痕疙瘩中肿瘤坏死因子α刺激基因6(TSG-6)/磷酸肌醇-3-激酶(PI3K)/丝苏氨酸蛋白激酶-B(AKT)通路表达的作用。方法:选择2020年1月-2021年10月笔者医院接受手术切除的76例瘢痕疙瘩患者为研究对象,根据术前是否使用甲壳素衍生物分为甲壳素组(n=41)和对照组(n=35)。手术后,收集瘢痕疙瘩组织,采用免疫组化法检测增殖细胞核抗原(PCNA)的阳性表达率;采用TUNEL法检测细胞凋亡率;采用western blot检测TSG-6、p-PI3K、p-AKT、鼠双微基因2(MDM2)、B淋巴细胞瘤-2基因(Bcl-2)、裂解型caspase-3(Cleaved caspase-3)的表达水平;采用酶联免疫吸附法检测肿瘤坏死因子-α(TNF-α)、IL-1β、IL-6的含量。结果:甲壳素组瘢痕疙瘩组织中PCNA阳性表达率、p-PI3K、p-AKT、MDM2、Bcl-2的表达水平、TNF-α、IL-1β、IL-6的含量低于对照组(P<0.05),细胞凋亡率、TSG-6及Cleaved caspase-3的表达水平高于对照组(P<0.05)。结论:甲壳素衍生物可调控瘢痕疙瘩中的细胞增殖及凋亡,这一作用与调控TSG-6/PI3K/AKT通路有关。

Objective To study the effect of chitin derivatives in regulating tumor necrosis factor alpha stimulatedgene-6(TSG-6)/phosphatidylinositol 3 kinase(PI3K)/serine protein kinase-B(AKT)pathway expression in keloid.Methods 76 patients with keloid who underwent surgical resection in our hospital from January 2020 to October 2021 were selected as the research object and divided into chitin group(n=41)and control group(n=35)according to whether to use chitin derivative before operation.After operation,keloid tissues were collected.The positive expression rate of PCNA was detected by immunohistochemical method,the apoptosis rate was detected by TUNELmethod,and the expression levels of TSG-6,p-PI3K,p-AKT,mouse double microgene 2(MDM2),B cell lymphoma-2 gene(Bcl-2)and cleaved caspase-3 were detected by Western blot,tumor necrosis factor-α(TNF-α),IL-1β,IL-6 content were detected by enzyme-linked immunosorbent assay.Results In chitin group,the positive expression rate of PCNA,the expression levels of p-PI3K,p-AKT,MDM2,Bcl-2 and the contents of TNF-α,IL-1β,IL-6 were lower than those in the control group(P<0.05),and the apoptosis rate and the expression level of TSG-6 and cleaved caspase-3 were higher than those in the control group(P<0.05).Conclusion Chitin derivatives regulate cell proliferation and apoptosis in keloid,which is related to the regulation of TSG-6/PI3K/Akt pathway.