怀牛膝丸通过阻断收费样受体 4/髓系分化主要反应基因 88/核因子卡巴 B 亚基 1 通路,缓解小鼠的炎症性肠病。

Yang Chunyan, Luo Jia, Peng Weijie, Dai Weibo
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引用次数: 0

摘要

目的研究怀牛膝丸(HYP)对炎症性肠病(IBD)的治疗作用及其机制:为了建立 IBD 模型,给小鼠注射右旋糖酐硫酸钠(DSS)。方法:为建立 IBD 模型,给小鼠注射硫酸右旋糖酐钠(DSS),并预先在胃内注射磺胺沙拉嗪(SASP)和 HYP。监测疾病活动指数(DAI)和结肠长度,并对结肠组织进行苏木精-伊红染色。使用酶联免疫吸附试验(ELISA)测定了促炎因子和血管炎症相关蛋白。使用 Western 印迹法或免疫组化分析法检测了结肠组织中闭孔带 1(ZO-1)、闭孔素、类收费受体 4(TLR4)、髓样分化主要反应基因 88(MYD88)和核因子卡巴 B p65 亚基(NF-κB p65)的表达情况:结果:用 HYP 预处理可增加 DSS 处理小鼠的结肠长度、降低 DAI 评分并减轻组织病理学改变。HYP 通过下调白细胞介素 1 beta(IL-1β)、白细胞介素 6(IL-6)、肿瘤坏死因子α(TNF-α)和白细胞介素 17(IL-17)的水平缓解了肠道炎症。此外,HYP 还通过上调 ZO-1、闭塞素和粘蛋白 2 (MUC2) 的水平以及下调内皮素 1 (ET-1) 和促红细胞生成素 (EPO) 的水平来抑制肠道屏障的破坏。网络药理学分析和实验结果表明,HYP 可下调 DSS 处理小鼠结肠组织中 TLR4、MYD88 和 NF-κB p65 的水平:本研究探讨了 HYP 对 IBD 的活体治疗作用及其分子机制。这些发现为 HYP 的临床应用提供了实验基础。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Huaiyu pill alleviates inflammatory bowel disease in mice blocking toll like receptor 4/ myeloid differentiation primary response gene 88/ nuclear factor kappa B subunit 1 pathway.

Objective: To investigate the therapeutic effects of Huaiyu pill (, HYP) on inflammatory bowel disease (IBD) and the underlying mechanisms have not been elucidated.

Methods: To establish the IBD model, mice were administered with dextran sulfate sodium (DSS). Mice were intragastrically pre-treated with sulfasalazine (SASP) and HYP. Disease activity index (DAI) and colon length were monitored, and the colonic tissues were subjected to hematoxylin-eosin staining. Pro-inflammatory factors and vascular inflammation-related proteins were determined using enzyme-linked immunosorbent assay (ELISA). The potential mechanisms of HYP were examined using network pharmacology analysis.The expressions of zona occludens 1 (ZO-1), occludin, toll like receptor 4 (TLR4), myeloid differentiation primary response gene 88 (MYD88), and nuclear factor kappa B p65 subunit (NF-κB p65) in colon tissues were examined using Western blotting or immunohistochemical analyses.

Results: Pre-treatment with HYP enhanced the colon length, decreased DAI scores, and mitigated histopathological alterations in DSS-treated mice. HYP alleviated intestinal inflammation by downregulating the levels of interleukin 1 beta (IL-1β), interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-α) and interleukin 17 (IL-17). Additionally, HYP suppressed the disruption of the gut barrier by upregulating the ZO-1, occludin, and mucin 2 (MUC2) levels and downregulating the endothelin 1 (ET-1) and erythropoietin (EPO) levels. Network pharmacological analysis and experimental results revealed that HYP downregulated the colonic tissue levels of TLR4, MYD88, and NF-κB p65 in DSS-treated mice.

Conclusion: This study investigated the in vivotherapeutic effects of HYP on IBD and the underlying molecular mechanisms. These findings provide an experimental foundation for the clinical application of HYP.

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