| 引用本文: |
赵雅情, 杨柳, 沈乐乐, 席建元, 蒋宁兰.银屑平丸通过调控JAK1/STAT3信号通路调节巨噬细胞极化对银屑病样小鼠皮损的影响[J].湖南中医药大学学报,2026,46(4):680-687[点击复制] |
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| 银屑平丸通过调控JAK1/STAT3信号通路调节巨噬细胞极化对银屑病样小鼠皮损的影响 |
| 赵雅情,杨柳,沈乐乐,席建元,蒋宁兰 |
| (湖南中医药大学, 湖南 长沙 410208;湖南中医药大学第一附属医院, 湖南 长沙 410007) |
| 摘要: |
| 目的 探讨银屑平丸通过Janus激酶1/信号转导及转录激活因子3(JAK1/STAT3)信号通路对银屑病样小鼠巨噬细胞极化的影响及其机制。方法 采用咪喹莫特诱导建立银屑病样小鼠模型。小鼠随机分为空白组，模型组，阿维A组，银屑平丸低、中、高剂量组及JAK1抑制剂Upadacitinib组，每组8只。观察皮损并计算银屑病面积及严重程度指数（PASI）评分；HE染色观察病理变化；免疫荧光染色检测分化簇（CD）86、CD206表达；Western blot检测JAK1、p-JAK1、STAT3、p-STAT3蛋白表达；ELISA检测血清白细胞介素（IL）-6、肿瘤坏死因子-α(TNF-α)及IL-10水平。结果 与空白组比较，模型组PASI评分升高（P<0.01）；皮肤组织呈典型银屑病样病理改变，如角化过度、角化不全及炎症细胞浸润；皮损中CD86表达升高（P<0.01）；血清IL-6、TNF-α水平升高，IL-10水平降低（P<0.01）;p-JAK1/JAK1、p-STAT3/STAT3比值升高（P<0.01）。与模型组比较，阿维A组、低剂量组、中剂量组、高剂量组及JAK1抑制剂Upadacitinib组PASI评分降低（P<0.05,P<0.01）；皮肤组织角化过度、角化不全及炎症细胞浸润减轻；CD206阳性细胞比例升高（P<0.01）;p-JAK1/JAK1、p-STAT3/STAT3比值，IL-6、TNF-α水平均降低（P<0.01）；阿维A组、中剂量组、高剂量组及JAK1抑制剂Upadacitinib组IL-10水平升高，CD86阳性细胞比例降低（P<0.05,P<0.01）。结论 银屑平丸可能通过抑制JAK1/STAT3信号通路活化，促进巨噬细胞由M1型向M2型极化，从而调节炎症反应，减轻银屑病样皮损。 |
| 关键词: 银屑病|银屑平丸|巨噬细胞极化|JAK1/STAT3通路|炎症水平 |
| DOI：10.3969/j.issn.1674-070X.2026.04.004 |
| 投稿时间：2025-10-06 |
| 基金项目:2024年度湖南省中医药管理局科研课题一般项目(B2024054);湖南中医药大学“一方”研究生创新项目(2023YF07) |
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| Yinxieping Pill alleviates skin lesions in psoriasis-like mice by modulating macrophage polarization through the JAK1/STAT3 signaling pathway |
| ZHAO Yaqing, YANG Liu, SHEN Lele, XI Jianyuan, JIANG Ninglan |
| (Hunan University of Chinese Medicine, Changsha, Hunan 410208, China;The First Hospital of Hunan University of Chinese Medicine, Changsha, Hunan 410007, China) |
| Abstract: |
| Objective To investigate the effects and underlying mechanisms of Yinxieping Pill on macrophage polarization in psoriasis-like mice via the Janus kinase 1/signal transducer and activator of transcription 3(JAK1/STAT3) signaling pathway.Methods A psoriasis-like mouse model was induced using imiquimod. Mice were randomly assigned to seven groups(n =8 each): blank control group, model group, Alitretin group, low-, medium-, and high-dose Yinxieping Pill groups, and JAK1 inhibitor Upadacitinib group. Skin lesions were evaluated, and the psoriasis area and severity index(PASI) scores were calculated.Histopathological changes were assessed by HE staining. Immunofluorescence staining was used to determine CD86 and CD206 expressions. Protein levels of JAK1, p-JAK1, STAT3, and p-STAT3 were measured by Western blot. Serum levels of interleukin IL-6, tumor necrosis factor-α(TNF-α), and IL-10 were quantified using ELISA. Results Compared with the blank control group, the model group exhibited significantly increased PASI scores(P<0.01), typical psoriasis-like histopathological features including hyperkeratosis, parakeratosis, and inflammatory cell infiltration, elevated CD86 expression in skin lesions(P<0.01),increased serum IL-6 and TNF-α levels, decreased IL-10 levels(P<0.01), and elevated p-JAK1/JAK1 and p-STAT3/STAT3 ratios(P<0.01). Compared with the model group, the PASI scores decreased in the Acitretin group, low-dose group, medium-dose group,high-dose group, and JAK1 inhibitor Upadacitinib group(P<0.05, P<0.01); hyperkeratosis, parakeratosis, and inflammatory cell infiltration in skin tissues were alleviated; the proportion of CD206-positive cells increased in all treatment groups(P<0.01), while the ratios of p-JAK1/JAK1 and p-STAT3/STAT3, as well as the levels of IL-6 and TNF-α decreased(P<0.01); the levels of IL-10 increased and the proportion of CD86-positive cells reduced in the Acitretin group, medium-dose group, high-dose group, and JAK1 inhibitor Upadacitinib group(P<0.05, P<0.01). Conclusion Yinxieping Pill may alleviate psoriasis-like skin lesions by inhibiting JAK1/STAT3 signaling pathway activation, promoting macrophage polarization from the pro-inflammatory M1 phenotype to the anti-inflammatory M2 phenotype, thereby regulating the inflammatory response. |
| Key words: psoriasis|Yinxieping Pill|macrophage polarization|JAK1/STAT3 pathway|inflammation levels |
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