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首页> 外文期刊>Life sciences >Evaluation of the therapeutic effects of mycophenolate mofetil targeting Nrf-2 and NLRP3 inflammasome in acetic acid induced ulcerative colitis in rats
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Evaluation of the therapeutic effects of mycophenolate mofetil targeting Nrf-2 and NLRP3 inflammasome in acetic acid induced ulcerative colitis in rats

机译：评价霉酚酸酯MOFETIL靶向NRF-2和NLRP3氨基氨基中的醋酸诱导溃疡性结肠炎的治疗效果

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Ulcerative colitis (UC) is a chronic inflammatory bowel disease that increases the risk of colorectal cancer. UC is highly associated with the disturbance of the immune system leading to oxidative stress and chronic inflammation of intestine. Therefore, the current study was conducted to investigate the potential anti-oxidant and antiinflammatory effects of MMF against acetic acid-induced UC that might be associated with the regulation of Nrf-2 and NLRP3 inflammasome signaling. UC was induced in Sprague-Dawley rats by intracolonic instillation of acetic acid. Forty-eight hours post UC induction, MMF (50 mg/kg/day, orally) was given for 8 consecutive days. Then, colon tissues and blood samples were collected. Results showed that MMF significantly attenuated the acetic acid-induced functional, biochemical, and inflammatory injuries in colon. MMF significantly decreased oxidative stress as indicated by the decreased malondialdehyde concentration and the increased total antioxidant capacity, glutathione, catalase, and superoxide dismutase concentrations in colon tissues. MMF also significantly increased Nrf-2 and decreased NLRP3 inflammasome expressions. Moreover, MMF decreased expression of interferongamma and increased expression of interferon-alpha. MMF also significantly decreased expression of proinflammatory cytokines, interleukin IL-1 beta and IL-18. These results suggest that MMF has antioxidant and anti-inflammatory effects against acetic acid-induced UC through the upregulation of Nrf-2, and INF-alpha expression in addition to the suppression of NLRP3 inflammasome and subsequent release of IL1 beta, IL-18 and INF-gamma.
机译：溃疡性结肠炎（UC）是一种慢性炎症性肠病，可增加结直肠癌的风险。UC与导致氧化应激和肠道慢性炎症的免疫系统紊乱高度相关。因此，本研究旨在研究MMF对醋酸诱导的UC的潜在抗氧化和抗炎作用，其可能与Nrf-2和NLRP3炎症体信号的调节有关。在Sprague-Dawley大鼠中通过结肠内滴注乙酸诱导UC。UC诱导后48小时，连续8天给予MMF（50 mg/kg/天，口服）。然后，收集结肠组织和血液样本。结果表明，MMF能显著减轻醋酸诱导的结肠功能、生化和炎症损伤。MMF显著降低氧化应激，表现为结肠组织中丙二醛浓度降低，总抗氧化能力、谷胱甘肽、过氧化氢酶和超氧化物歧化酶浓度增加。MMF还显著增加Nrf-2，降低NLRP3炎症体表达。此外，MMF降低干扰素γ的表达，增加干扰素α的表达。MMF还显著降低促炎细胞因子、白细胞介素-1β和白细胞介素-18的表达。这些结果表明，MMF通过上调Nrf-2和INF-α表达，以及抑制NLRP3炎性体和随后释放IL1β、IL-18和INF-γ，对醋酸诱导的UC具有抗氧化和抗炎作用。

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