Abstract
Aim To explore the treatment effect of mica on 2,4,6-trinitrobenzenesulfonic acid solution- (TNBS-) induced colitis in mice. Materials and Methods Thirty male BALB/C mice were randomly divided into the control group, the TNBS group, and the mica group. Control mice were treated with saline solution. Experimental colitis was induced by TNBS (250 mg/kg/d) in the TNBS group and the mica group. After modeling, the mica group was treated with mica (180 mg/kg/d) for 3 days, while the TNBS group continued the treatment with TNBS. All solutions were injected intrarectally. During treatment, body weight and mice activity were monitored daily. After treatment, the colon tissues of mice were collected; angiotensin II (Ang II), angiotensin-converting enzyme 2 (ACE2), angiotensin 1-7 (Ang (1-7)), IL-17A, and IL-10 expression was analyzed by ELISA and immunohistochemistry. Results Food intake, activity, and body weight gradually decreased in the TNBS group compared to the control group and the mica group (all P < 0.05). Also, black stool adhesion in the anus and thin and bloody stool were observed in the TNBS group, but not in the other two groups. Moreover, the expression of Ang II, ACE2, Ang (1-7), IL-17A, and IL-10 in the TNBS group increased compared to that in the control group. Compared to the TNBS group, ACE2, Ang (1-7), and IL-10 in the mica group increased, while Ang II and IL-17A decreased (all P < 0.05). Conclusion Mica can alleviate TNBS-induced colitis in mice by regulating the inflammation process; it reduces Ang II and IL-17A and increases ACE2, IL-10, and Ang (1-7).
Highlights
Inflammatory bowel disease (IBD) is a chronic nonspecific inflammatory disease that affects the gastrointestinal tract
The results showed that the expression of IL-17A in the TNBS group and the mica group was significantly increased compared to that in the control group (6:93 ± 0:44 vs. 0:65 ± 0:03, 2:63 ± 0:64 vs. 0:65 ± 0:03, P < 0:01)
angiotensin II (Ang II) is a proinflammatory substance, which induces the expression of NF-κB, p38MAPK activation, and generates a variety of inflammatory factors, such as IL-6 and IL-17 [12]
Summary
Inflammatory bowel disease (IBD) is a chronic nonspecific inflammatory disease that affects the gastrointestinal tract. Over the past 20 years, the incidence of IBD in Asian countries, especially China, has shown a rapid increase [1]. In 2018, the standardized incidence of IBD in Daqing, a city in the west of Heilongjiang province, was 177/100,000, while it was only 3.14/100,000 in Zhongshan city, Guangdong [2]. IBD is characterized by chronic inflammation of your digestive tract. And rapid diagnosis of the disease and improvement of intestinal inflammation are critical steps in preventing further progression and improving prognosis. The exact etiology and pathogenesis of IBD remain unclear
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