摘要
目的:探究紫草素调节SOCS1/JAK2/STAT3信号通路对脂多糖(LPS)诱导的胰腺腺泡细胞炎症反应和凋亡的影响。方法:体外培养大鼠胰腺腺泡细胞AR42J,将si-NC、si-SOCS1转染至AR42J细胞中,然后给予LPS和/或高剂量紫草素处理。将未转染的细胞分为Control组、LPS组、低/中/高剂量紫草素组(L/M/H-紫草素组)(除Control外,均给予LPS处理),将转染的细胞分为si-NC组、si-SOCS1组、H-紫草素+si-NC组和H-紫草素+si-SOCS1组(均给予LPS处理)。ELISA检测炎性因子白细胞介素1β(IL-1β)、肿瘤坏死因子α(TNF-α)表达水平;CCK-8法检测细胞活力;流式细胞术检测细胞凋亡;Western blotting检测细胞中SOCS1/JAK2/STAT3信号通路相关蛋白表达情况。结果:与Control组比较,LPS组AR42J细胞中IL-1β、TNF-α水平和细胞凋亡率升高,OD450值降低(P<0.05);与LPS组比较,L-紫草素组、M-紫草素组、H-紫草素组AR42J细胞中IL-1β、TNF-α水平和细胞凋亡率均降低,OD450值升高,且H-紫草素组降低/升高更明显(P<0.05)。与Control组比较,LPS组AR42J细胞中SOCS1蛋白减少,p-JAK2、p-STAT3蛋白增加(P<0.05);与LPS组比较,H-紫草素组AR42J细胞中SOCS1蛋白增加,p-JAK2、p-STAT3蛋白减少(P<0.05),si-SOCS1组AR42J细胞中SOCS1蛋白减少,p-JAK2、p-STAT3蛋白增加(P<0.05);与H-紫草素组比较,H-紫草素+si-SOCS1组AR42J细胞中SOCS1蛋白减少,p-JAK2、p-STAT3蛋白增加(P<0.05)。结论:紫草素能够抑制LPS诱导的AR42J细胞炎症反应和凋亡,增强细胞活力,可能通过调节SOCS1/JAK2/STAT3信号通路而实现。
Objective:To explore the impacts of shikonin on lipopolysaccharide(LPS)-induced inflammation and apoptosis of pancreatic acinar cells by regulating SOCS1/JAK2/STAT3 signaling pathway.Methods:Rat pancreatic acinar cells AR42J were cultured in vitro,the cells were transfected with si-NC and si-SOCS1,then treated with LPS and/or high-dose shikonin.The untransfected cells were divided into Control group,LPS group,and low/medium/high-dose shikonin group(L/M/H-shikonin group)which were treated with LPS except Control,and the transfected cells were divided into si-NC group,si-SOCS1 group,H-shikonin+si-NC group and H-shikonin+si-SOCS1 group which were all treated with LPS.The expression of inflammatory factors interleukin 1β(IL-1β),tumor necrosis factorα(TNF-α)was detected by ELISA,the cell viability was determined by CCK-8 method,the apoptosis was detected by flow cytometry,and the expression of SOCS1/JAK2/STAT3 signaling pathway-related proteins were analyzed by Western blotting.Results:Compared with the Control group,the levels of IL-1β,TNF-α and apoptosis rate in AR42J cells in the LPS group increased,while the OD450 value decreased(P<0.05).Compared with the LPS group,the levels of IL-1β,TNF-α and apoptosis rate in AR42J cells in the L/M/H-shikonin group decreased,while the OD450 value increased,and which in the H-shikonin group decreased or increased more(P<0.05).Compared with the control group,the SOCS1 protein level in AR42J cells in the LPS group decreased,while the p-JAK2 and p-STAT3 protein level increased(P<0.05).Compared with the LPS group,the SOCS1 protein level in AR42J cells in the H-shikonin group increased,while the p-JAK2 and p-STAT3 proteins decreased(P<0.05);the SOCS1 protein level in AR42J cells in the si-SOCS1group decreased,while the p-JAK2 and p-STAT3 protein level increased(P<0.05).Compared with the H-shikonin group,the SOCS1 protein level in AR42J cells in the H-shikonin+si-SOCS1 group decreased,while the p-JAK2 and p-STAT3 protein level increased(P<0.05).Conclusions:Shikonin can inhibit the inflammatory response and apoptosis of AR42J cells induced by LPS,and enhance cell viability,which may be achieved by regulating the SOCS1/JAK2/STAT3 signaling pathway.
作者
韩洁
孟晨
郭楠楠
HAN Jie;MENG Chen;GUO Nannan(Department of Critical Medicine,Shijiazhuang Ping′an Hospital,Shijiazhuang Hebei 050000,China;Department of Neurosurgery,Shijiazhuang Ping′an Hospital,Shijiazhuang Hebei 050000,China;Intensive Care Unit,Shijiazhuang Ping′an Hospital,Shijiazhuang Hebei 050000,China)
出处
《蚌埠医科大学学报》
2025年第11期1517-1522,共6页
Journal of Bengbu Medical University
