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无梗海桑对三硝基苯磺酸诱导大鼠实验性结肠炎的影响。

Effects of Rhizophora mangle on Experimental Colitis Induced by TNBS in Rats.

机构信息

Departamento de Farmacologia, Faculdade de Ciências Médicas, Universidade Estadual de Campinas (UNICAMP), 13083-970 Campinas, SP, Brazil.

出版信息

Evid Based Complement Alternat Med. 2012;2012:753971. doi: 10.1155/2012/753971. Epub 2012 Sep 27.

DOI:10.1155/2012/753971
PMID:23056142
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3465987/
Abstract

Male Unib-WH rats were pretreated for two weeks with butanolic (BuOH) and ethyl acetate (EtOAc) fractions. Colitis was induced by rectal administration of TNBS, the treatment continued, and animals were sacrificed on day 7 after the TNBS administration. Phytochemical studies were performed in order to provide the characterization of the tannins present in the bark of R. mangle. Results showed that EtOAc fraction increased the levels of IL-10 (∗∗P < 0.01) and diminished the levels of TNF-α (∗∗∗P < 0.001) and IL-6 (∗∗P < 0.01). BuOH fraction reduced the MPO activity (∗∗P < 0.01) and levels of TBARS (∗∗∗P < 0.001); it also increased COX-1 expression, diminished the levels of TNF-α (∗∗∗P < 0.001), and increased the levels of IL-12 (∗∗∗P < 0.001). Besides, both treatments augmented the levels of GSH (∗P < 0.05), the activity of GSH-Px (∗∗P < 0.01 for BuOH fraction and ∗∗∗P < 0.001 for EtOAc fraction), and CAT (∗∗P < 0.01). In conclusion, both treatments ameliorated the injury induced by TNBS through different mechanisms, probably by their chemical composition which directed its activity into an antioxidant or anti-inflammatory response, leading to an immune modulation.

摘要

雄性 Unib-WH 大鼠用正丁醇(BuOH)和乙酸乙酯(EtOAc)部分预处理两周。通过直肠给予 TNBS 诱导结肠炎,继续治疗,并在 TNBS 给药后第 7 天处死动物。进行了植物化学研究,以提供存在于罗望子树皮中的单宁的特征。结果表明,EtOAc 部分增加了 IL-10 的水平(∗∗P < 0.01),并降低了 TNF-α(∗∗∗P < 0.001)和 IL-6(∗∗P < 0.01)的水平。BuOH 部分降低了 MPO 活性(∗∗P < 0.01)和 TBARS 水平(∗∗∗P < 0.001);它还增加了 COX-1 的表达,降低了 TNF-α(∗∗∗P < 0.001)的水平,并增加了 IL-12(∗∗∗P < 0.001)的水平。此外,两种治疗方法都增加了 GSH(∗P < 0.05)的水平,GSH-Px(BuOH 部分为∗∗P < 0.01,EtOAc 部分为∗∗∗P < 0.001)和 CAT(∗∗P < 0.01)的活性。总之,两种治疗方法都通过不同的机制改善了 TNBS 诱导的损伤,可能是由于其化学成分使其活性转向抗氧化或抗炎反应,从而导致免疫调节。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ee8/3465987/17d90c646793/ECAM2012-753971.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ee8/3465987/9325e897fed4/ECAM2012-753971.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ee8/3465987/be977c7dd780/ECAM2012-753971.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ee8/3465987/f6a40d938035/ECAM2012-753971.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ee8/3465987/bb546af5377c/ECAM2012-753971.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ee8/3465987/17d90c646793/ECAM2012-753971.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ee8/3465987/9325e897fed4/ECAM2012-753971.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ee8/3465987/be977c7dd780/ECAM2012-753971.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ee8/3465987/f6a40d938035/ECAM2012-753971.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ee8/3465987/bb546af5377c/ECAM2012-753971.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ee8/3465987/17d90c646793/ECAM2012-753971.005.jpg

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