紫草素调节SOCS1/JAK2/STAT3信号通路对脂多糖诱导的胰腺腺泡细胞炎症反应和凋亡的影响

韩洁; 孟晨; 郭楠楠

doi:10.13898/j.cnki.issn.2097-5252.2025.11.004

紫草素调节SOCS1/JAK2/STAT3信号通路对脂多糖诱导的胰腺腺泡细胞炎症反应和凋亡的影响

Impacts of shikonin on lipopolysaccharide-induced inflammation and apoptosis of pancreatic acinar cells by regulating SOCS1/JAK2/STAT3 signaling pathway

摘要

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。

Abstract:
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 factor α (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.

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