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植酸可改善 1,2-二甲基肼诱导的大鼠结直肠肿瘤模型的肠道黏膜屏障损伤,并降低促炎细胞因子的血清水平。

Phytic acid improves intestinal mucosal barrier damage and reduces serum levels of proinflammatory cytokines in a 1,2-dimethylhydrazine-induced rat colorectal cancer model.

机构信息

1School of Public Health,Qingdao University,Qingdao 266021,Shandong,People's Republic of China.

2School of Nursing,Qingdao University,Qingdao 266021,Shandong,People's Republic of China.

出版信息

Br J Nutr. 2018 Jul;120(2):121-130. doi: 10.1017/S0007114518001290.

Abstract

Phytic acid (PA) has been demonstrated to have a potent anticarcinogenic activity against colorectal cancer (CRC). Defects of the intestinal mucosal barrier and inflammation processes are involved in the development and progression of CRC. In the present study, we evaluated the effect of PA on the intestinal mucosal barrier and proinflammatory cytokines. After a 1-week acclimatisation period, sixty Wistar male rats were divided into the following five groups, with twelve rats per group: the control group (CG), model group (MG), low-PA-dose group (0·25 g/kg per d), middle-PA-dose group (0·5 g/kg per d), and high-PA-dose group (1 g/kg per d). 1,2-Dimethylhydrazine (DMH) at a dosage of 30 mg/kg of body weight was injected weekly to induce CRC for 18 weeks. We examined the expression of genes related to the intestinal mucosal barrier in the model. The results demonstrated that tumour incidence was decreased following PA treatment. The mRNA and protein expression of mucin 2 (MUC2), trefoil factor 3 (TFF3) and E-cadherin in the MG were significantly lower than those in the CG (P<0·05). The mRNA and protein expression of claudin-1 in the MG were significantly higher than those in the CG (P<0·05). PA elevated the mRNA and protein expression of MUC2, TFF3 and E-cadherin, and diminished the mRNA and protein expression of claudin-1. Furthermore, PA decreased serum levels of proinflammatory cytokines, which included TNF-α, IL-1β and IL-6. In conclusion, this study suggests that PA has favourable effects on the intestinal mucosal barrier and may reduce serum proinflammatory cytokine levels.

摘要

植酸(PA)已被证明具有很强的抗癌活性,可抑制结直肠癌(CRC)。肠黏膜屏障缺陷和炎症过程参与了 CRC 的发展和进展。在本研究中,我们评估了 PA 对肠黏膜屏障和促炎细胞因子的影响。经过一周的适应期后,将 60 只 Wistar 雄性大鼠分为以下五组,每组 12 只:对照组(CG)、模型组(MG)、低 PA 剂量组(0.25 g/kg/d)、中 PA 剂量组(0.5 g/kg/d)和高 PA 剂量组(1 g/kg/d)。每周用 30 mg/kg 体重的 1,2-二甲基肼(DMH)注射诱导 CRC 18 周。我们检测了模型中与肠黏膜屏障相关的基因表达。结果表明,PA 治疗可降低肿瘤发生率。MG 中黏蛋白 2(MUC2)、三叶因子 3(TFF3)和 E-钙黏蛋白的 mRNA 和蛋白表达明显低于 CG(P<0.05)。MG 中 Claudin-1 的 mRNA 和蛋白表达明显高于 CG(P<0.05)。PA 上调 MUC2、TFF3 和 E-钙黏蛋白的 mRNA 和蛋白表达,下调 Claudin-1 的 mRNA 和蛋白表达。此外,PA 降低了 TNF-α、IL-1β 和 IL-6 等促炎细胞因子的血清水平。综上所述,本研究表明 PA 对肠黏膜屏障具有有益作用,可能降低血清促炎细胞因子水平。

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