化合物 Ento-PB 对恶唑酮诱发的大鼠溃疡性结肠炎的改善作用

Acta cirurgica brasileira Pub Date : 2024-09-02 eCollection Date: 2024-01-01 DOI:10.1590/acb395524
Zhi Fan, Jinhu Chen, Jia Wei, ZhiBin Yang, Huai Xiao, Heng Liu
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引用次数: 0

摘要

目的:研究中药复方恩替PB对恶唑酮(OXZ)诱导的大鼠溃疡性结肠炎(UC)的影响:方法:用Ento-PB治疗OXZ诱导的溃疡性结肠炎大鼠。方法:用恩托-PB治疗OXZ诱导的UC大鼠,采用多种方法评估大鼠结肠的损伤情况,包括疾病活动指数(DAI)、结肠长度、结肠重量/长度比、结肠粘膜损伤指数和组织学评分。大鼠血清中白细胞介素-4 (IL-4)、白细胞介素-10 (IL-10)、白细胞介素-13 (IL-13)、表皮生长因子 (EGF)、诱导型一氧化氮合酶和总一氧化氮合酶 (tNOS) 的水平,以及大鼠结肠组织中肿瘤坏死因子-α (TNF-α) 和髓过氧化物酶 (MPO) 的水平,均采用酶联免疫吸附测定法和传统试剂盒进行了测定:结果:恩托-PB治疗后,OXZ诱导的UC大鼠的DAI评分和大肠病变评分明显降低。Ento-PB 可防止大鼠结肠缩短,降低结肠重量与长度之比,改善结肠组织病变。同时,恩替PB能明显抑制促炎细胞因子TNF-α、IL-13和MPO以及tNOS和iNOS的活性,同时上调抗炎细胞因子IL-4和IL-10的表达。此外,用恩托巴西枸杞治疗的 UC 大鼠体内 EGF 的表达水平明显升高,这表明恩托巴西枸杞可促进受损肠上皮组织的修复:结论:恩托-PB通过调节炎症因子的表达水平和促进结肠组织的修复,在OXZ诱导的UC大鼠中显示出显著的抗UC活性。这项研究为进一步开发恩替PB提供了科学依据。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Improvement effect of compound Ento-PB on oxazolone-induced ulcerative colitis in rats.

Purpose: To investigate the impact of the Chinese medicine compound Ento-PB on oxazolone (OXZ)-induced ulcerative colitis (UC) in rats.

Methods: UC rats induced by OXZ were treated with Ento-PB. The damage to the colon was assessed using several measures, including the disease activity index (DAI), colon length, colon weight/length ratio, colonic mucosal damage index, and histological score. The levels of interleukin-4 (IL-4), interleukin-10 (IL-10), interleukin-13 (IL-13), epidermal growth factor (EGF), inducible nitric oxide synthase, and total nitric oxide synthase (tNOS) in rat serum, as well as the levels of tumor necrosis factor-α (TNF-α) and myeloperoxidase (MPO) in rat colon tissue, were determined using enzyme-linked immunosorbent assay and conventional kits.

Results: After being treated with Ento-PB, the DAI score and macroscopic lesion score of OXZ-induced UC rats were significantly reduced. Ento-PB prevented the shortening of rat colons, reduced the ratio of colon weight to length, and improved colon tissue lesions. Meanwhile, Ento-PB could significantly inhibit the activities of proinflammatory cytokines TNF-α, IL-13, and MPO, as well as tNOS and iNOS, while upregulating the expression of anti-inflammatory cytokines IL-4 and IL-10. Moreover, a significant increase in the expression level of EGF was observed in UC rats treated with Ento-PB, indicating that Ento-PB could enhance the repair of damaged intestinal epithelial tissue.

Conclusions: Ento-PB demonstrates significant anti-UC activities in OXZ-induced UC rats by regulating the expression levels of inflammatory factors and promoting the repair of colon tissue. This study provides scientific evidence to support the further development of Ento-PB.

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