Berberrubine attenuates mucosal lesions and inflammation in dextran sodium sulfate-induced colitis in mice

Yu, Xiu-Ting; Xu, Yifei; Huang, Yanfeng; Qu, Chang; Xu, Lie-Qiang; Su, Zi‐Ren; Zeng, Hong‐Yan; Zheng, Lin; Yi, Tiegang; Li, Hui-Lin; Chen, Jianping; Zhang, Xiaojun

doi:10.1371/journal.pone.0194069

Cited by 58 publications

(41 citation statements)

References 55 publications

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“…Instead, idebenone significantly improved the body weight, DAI and histopathology. Our results support the previously reported involvement of oxidative stress in the pathogenesis of disease [15] and justify the use of antioxidants to alleviate structural tissue damage [19,27,46,47].…”

Section: Discussionsupporting

confidence: 92%

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Idebenone Protects against Acute Murine Colitis via Antioxidant and Anti-Inflammatory Mechanisms

Shastri

Shinde

Sohal

et al. 2020

IJMS

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Oxidative stress is a key player of the inflammatory cascade responsible for the initiation of ulcerative colitis (UC). Although the short chain quinone idebenone is considered a potent antioxidant and a mitochondrial electron donor, emerging evidence suggests that idebenone also displays anti-inflammatory activity. This study evaluated the impact of idebenone in the widely used dextran sodium sulphate (DSS)-induced mouse model of acute colitis. Acute colitis was induced in C57BL/6J mice via continuous exposure to 2.5% DSS over 7 days. Idebenone was co-administered orally at a dose of 200 mg/kg body weight. Idebenone significantly prevented body weight loss and improved the disease activity index (DAI), colon length, and histopathological score. Consistent with its reported antioxidant function, idebenone significantly reduced the colonic levels of malondialdehyde (MDA) and nitric oxide (NO), and increased the expression of the redox factor NAD(P)H (nicotinamide adenine dinucleotide phosphate) dehydrogenase quinone-1 (NQO-1) in DSS-exposed mice. Immunohistochemistry revealed a significantly increased expression of tight junction proteins, which protect and maintain paracellular intestinal permeability. In support of an anti-inflammatory activity, idebenone significantly attenuated the elevated levels of pro-inflammatory cytokines in colon tissue. These results suggest that idebenone could represent a promising therapeutic strategy to interfere with disease pathology in UC by simultaneously inducing antioxidative and anti-inflammatory pathways.

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Section: Discussionsupporting

confidence: 92%

“…It is well known that the anti-inflammatory cytokine IL-10 is elevated in colitis patients [47,[82][83][84][85][86]] and our study mirrored this effect upon DSS exposure. Elevated levels of IL-10 could be interpreted as a compensatory mechanism to counteract the substantial inflammation in the colon.…”

Section: Discussionsupporting

confidence: 84%

Idebenone Protects against Acute Murine Colitis via Antioxidant and Anti-Inflammatory Mechanisms

Shastri

Shinde

Sohal

et al. 2020

IJMS

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“…Herbal medicine from plants has been used in healing various diseases owing to its long history in clinical practice as well as therapeutic effects [10,11]. Recently, the protection effects of Xuanfudaizhetang has been proved in rats with RE via increasing the pH value of the esophagus and reducing inflammation stimulation [7].…”

Section: Introductionmentioning

confidence: 99%

Geraniin ameliorate experimental acute reflux esophagitis via NF-κB regulated anti-inflammatory activities in rats

Nam

Park

et al. 2019

Appl Biol Chem

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Repeated reflux of gastric acid and stomach contents into the esophagus leads to esophagus damage, including inflammation, ulcer, and hemorrhage in the epithelium. In this study, we aimed to demonstrate the ameliorating effects of geraniin, a phytochemical in the geraniums, on esophagus damage in an acute reflux esophagitis (RE) rat model. The inflammatory effects of geraniinwas measured by nitric oxide (NO) production and pro-inflammatory protein levels in lipopolysaccharide (LPS)-induced RAW 264.7 cells. To evaluate the protective effects of geraniin on damaged esophagus tissue in RE rats, the rats were divided into the following groups: normal control; RE-induced control; RE rats pretreated with geraniin 15 and 30 mg/kg body weight; and RE rats pretreated with ranitidine 30 mg/ kg body weight as a positive control. The lesion area of esophagus was determined by the Image J program, and histological changes were examined by hematoxylin and eosin staining of rat esophageal tissue. The expression of proinflammatory proteins, cytokines, and tight junction proteins involved in esophagus damages was determined using western blotting of esophageal tissue. Geraniin revealed that anti-inflammatory effects against LPS-induced cells by significantly decreasing NO production and iNOS proteins level. Additionally, the results showed that improvement effects of geraniin on esophagus damages in RE induced rats. The expression of inflammatory proteins involved in nuclear factor NF-kB signaling pathways significantly decreased and tight junction protein (claudin-4 and claudin-5) was increased in esophageal tissue. We found the potential of geraniin as source of replacement therapy products source for inflammatory and reflux esophagitis disease.

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“…Gut barrier typically consists of colonocyte plasma membrane tight junctions, secreted mucus, and mucosal immune cells [ 13 ]. It is reported that the destruction of the tight junctions is one possible mechanism for the breached gut barrier in DSS-treated mice [ 11 ] and a variety of phytochemicals, such as naringenin from citrus fruits and berberrubine from berberis, are reported to upregulate tight junction proteins in DSS-treated mice [ 29 , 30 ]. To investigate whether protection by RB and CB against increased gut permeability is through effects on tight junctions, mRNA expression of genes involved in the production of tight junction proteins, as well as protein expression of two tight junction proteins was determined.…”

Section: Discussionmentioning

confidence: 99%

Lightly Cooked Broccoli Is as Effective as Raw Broccoli in Mitigating Dextran Sulfate Sodium-Induced Colitis in Mice

et al. 2018

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Dietary broccoli is anti-inflammatory. Past studies have typically investigated raw broccoli, even though most consumers prefer cooked broccoli, where the plant myrosinase is inactivated by heat, resulting in failure of formation of the anti-inflammatory bioactive compound sulforaphane (SF). This study compareed efficacy of lightly cooked broccoli (CB) containing greatly diminished myrosinase activity, with raw broccoli (RB), in mitigating colitis in dextran sulfate sodium (DSS)-treated mice. Male C57BL/6 mice were fed for two weeks on a 10% RB, 10% CB or control diet, all based on the AIN-93M diet. Half (n = 9) of each group received drinking water, half received 2.5% DSS in water for one week, starting from Day 7 of the diet. Even with far less plant myrosinase activity, CB was essentially as effective as RB in lessening damage by DSS, evidenced by decreased disease activity index, attenuated colon length shrinkage, less endotoxin (lipopolysaccharide) leakage into blood, and less severe colon lesions as assessed by histopathology. mRNA expression of pro-inflammatory cytokines indicated that broccoli anti-inflammatory action may be through inhibition of the IL-6 trans-signaling pathway, as evidenced by reversal of the DSS-increased expression of IL-6, CCR2 and vascular cell adhesion molecule 1 (VCAM-1).

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Berberrubine attenuates mucosal lesions and inflammation in dextran sodium sulfate-induced colitis in mice

Cited by 58 publications

References 55 publications

Idebenone Protects against Acute Murine Colitis via Antioxidant and Anti-Inflammatory Mechanisms

Idebenone Protects against Acute Murine Colitis via Antioxidant and Anti-Inflammatory Mechanisms

Geraniin ameliorate experimental acute reflux esophagitis via NF-κB regulated anti-inflammatory activities in rats

Lightly Cooked Broccoli Is as Effective as Raw Broccoli in Mitigating Dextran Sulfate Sodium-Induced Colitis in Mice

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