| 杨柳,席建元,赵雅情,沈乐乐,蒋宁兰.基于JAK1/STAT3通路探讨银屑平丸含药血清对RAW264.7巨噬细胞M1/M2极化的影响[J].中医药信息,2026,43(6):8-14 |
| 基于JAK1/STAT3通路探讨银屑平丸含药血清对RAW264.7巨噬细胞M1/M2极化的影响 |
| Exploration on Effects of Yinxieping Pill Drug - Containing Serum on M1/M2 Polarization of RAW264.7 Macrophages Based on the JAK1/STAT3 Pathway |
| 投稿时间:2025-12-05 录用日期:2026-01-28 |
| DOI:10.19656/j.cnki.1002-2406.20260602 |
| 中文关键词: 银屑平丸 银屑病 RAW264.7 巨噬细胞极化 JAK/STAT3通路 |
| 英文关键词: Yinxieping Pill Psoriasis RAW264.7 Macrophage polarization JAK/STAT3 pathway |
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| 中文摘要: |
| 目的 基于JAK1/STAT3信号通路探究银屑平丸对脂多糖(LPS)诱导的RAW264.7细胞模型M1/M2极化的影响及其调控机制。方法 SD大鼠分别灌胃银屑平丸和阿维A溶液,制备相对应含药血清,建立LPS诱导的RAW264.7细胞炎性模型,设置空白组、模型组(100 ng/mL LPS)、银屑平丸组(20%银屑平丸含药血清 + 100 ng/mL LPS)、阿维A组(20%阿维A含药血清 + 100 ng/mL LPS)、抑制剂组(100 ng/mL LPS + 10 ng/mL ABT494)、银屑平丸 + 抑制剂组(20%银屑平丸含药血清 + 100 ng/mL LPS + 10 ng/mL ABT494),按照相应药物给予干预。CCK8法检测银屑平丸含药血清对LPS诱导前后RAW264.7细胞活力的影响;ELISA法检测上清液中白细胞介素(IL)-6、IL-10、肿瘤坏死因子(TNF)-α的含量;Western blot检测JAK1、磷酸化JAK1(p-JAK1)、STAT3及磷酸化STAT3(p-STAT3)的蛋白表达水平;流式细胞术检测巨噬细胞亚型标志物的表达情况。结果 银屑平丸含药血清对原始RAW264.7细胞无明显毒性作用但能显著抑制经LPS诱导后RAW264.7细胞的增殖,且呈浓度依赖趋势(P < 0.05);与空白组比较,模型组IL-6、TNF-α水平、CD86分子表达、p-JAK1、p-STAT3蛋白表达显著上升(P < 0.05),IL-10水平、CD206分子表达显著下降(P < 0.05);与模型组比较,银屑平丸组、阿维A组、抑制剂组、银屑平丸 + 抑制剂组的IL-6、TNF-α水平、CD86分子表达、p-JAK1、p-STAT3蛋白表达显著下降(P < 0.05),IL-10水平、CD206分子表达显著上升(P < 0.05);与抑制剂组比较,银屑平丸 + 抑制剂组的IL-6、TNF-α水平、CD86分子表达、p-JAK1、p-STAT3蛋白表达显著下降(P < 0.05),IL-10水平、CD206分子表达显著上升(P < 0.05)。结论 银屑平丸含药血清通过抑制JAK1/STAT3信号通路,抑制巨噬细胞M1型极化及促进巨噬细胞M2型极化,调节巨噬细胞M1/M2的平衡。 |
| 英文摘要: |
| Objective To explore the effect of Yinxieping Pill on M1/M2 polarization in lipopolysaccharide (LPS)-induced RAW264.7 cell model and its regulatory mechanism based on JAK1/STAT3 signaling pathway.Methods The corresponding drug-containing serum was prepared by intragastric administration of Yinxieping Pill and Acitretin solution in SD rats. The inflammatory model of RAW264.7 cells induced by LPS was established, and the rats were divided into blank group, model group (with 100 ng/mL LPS), Yinxieping Pill group (with 20% Yinxieping Pill drug-containing serum + 100 ng/mL LPS), Acitretin group (with 20% Acitretin drug-containing serum + 100 ng/mL LPS), inhibitor group (with 100 ng/mL LPS + 10 ng/mL ABT494) and Yinxieping Pill + inhibitor group (with 20% Yinxieping Pill drug-containing serum + 100 ng/mL LPS + 10 ng/mL ABT494). Each group received the intervention according to their respective drug regimens. CCK8 method was used to detect the effect of Yinxieping Pill drug-containing serum on the viability of RAW264.7 cells before and after LPS induction. The secretion levels of interleukin (IL)-6, IL-10 and tumor necrosis factor (TNF)-α in the supernatant were detected by ELISA. The protein expressions of JAK1, phosphorylated JAK1 (p-JAK1), STAT3 and phosphorylated STAT3 (p-STAT3) were detected by Western Blot. Flow cytometry was used to detect the expression of macrophage subtype markers.Results The Yinxieping Pill-containing serum had no obvious toxic effect on primitive RAW264.7 cells, but could significantly inhibit the proliferation of RAW264.7 cells induced by LPS, which showed a concentration-dependent trend (P < 0.05). Compared with the blank group, the levels of IL-6, TNF-α, CD86 molecule expression, p-JAK1 and p-STAT3 protein expression in the model group increased significantly (P < 0.05), while the levels of IL-10 and CD206 molecule expression decreased significantly (P < 0.05). Compared with the model group, the levels of IL-6, TNF-α, CD86 molecule expression, p-JAK1 and p-STAT3 protein expression in Yinxieping Pill group, Acitretin group, inhibitor group and Yinxieping Pill + inhibitor group decreased significantly (P < 0.05), while the levels of IL-10 and CD86 molecule expression increased significantly (P < 0.05). Compared with the inhibitor group, the levels of IL-6, TNF-α, CD206 molecule expression, p-JAK1 and p-STAT3 protein expression in Yinxieping Pill + inhibitor group decreased significantly (P < 0.05), while the levels of IL-10 and CD206 molecule expression increased significantly (P < 0.05).Conclusion The Yinxieping Pill drug-containing serum can inhibit M1-type polarization of macrophages, promote M2-type polarization of macrophages and regulate the balance of macrophage M1/M2 by inhibiting JAK1/STAT3 signaling pathway. |
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