Effects of rhein on intestinal epithelial tight junction in IgA nephropathy

Peng, Sheng-Nan; Zeng, Huihong; Fu, Aixiang; Chen, Xiaowen; Zhu, Qing

doi:10.3748/wjg.v19.i26.4137

Cited by 30 publications

(18 citation statements)

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“…In the sham group, occludin staining was found at the apical part of the lateral membranes of the polar epithelial cells and was distributed continuously (Fig. 2C), which is consistent with pervious reports [10]. As expected, the tight junctions were well preserved in PHx and G-PHx groups and were significantly disrupted in SHx.…”

Section: 2supporting

confidence: 91%

“…According to previous reports, delayed TLR4 activation would likely lead to delayed clearance of LPS and prolonged endotoxemia after extended hepatectomy [32,33], although an earlier response is beneficial for prognosis [33]. The activation of LPS-TLR4 and/or nuclear factor-kappaB signaling pathway [10] would upregulate SOCS3. The expression of SOCS3 accompanies the severity of inflammation and has a protective role in LPS-induced acute injury [14,15].…”

Section: Discussionmentioning

confidence: 89%

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Selective bowel decontamination improves the survival of 90% hepatectomy in rats

Ren

Zhang

et al. 2015

Journal of Surgical Research

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Section: 2supporting

confidence: 91%

Section: Discussionmentioning

confidence: 89%

Selective bowel decontamination improves the survival of 90% hepatectomy in rats

Ren

Zhang

et al. 2015

Journal of Surgical Research

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“…The mechanism underlying the protective activity of rhein may be associated with the generation of nitric oxide, ion secretions and chemotaxis, and with the apoptosis of human-derived Caco-2 colorectal cancer cells (11). Notably, rhein has been shown to successfully repair damaged intestinal tight junctions and protect the intestinal barrier, by enhancing the expression of zona occludens-1 and occludin (12). Furthermore, rhein significantly increased the expression of interleukin (IL)-10, and decreased the expression of tumor necrosis factor (TNF)-α (13).…”

Section: Introductionmentioning

confidence: 99%

Rhein inhibits lipopolysaccharide-induced intestinal injury during sepsis by blocking the toll-like receptor 4 nuclear factor-κB pathway

Zhang

Jiao

et al. 2015

Molecular Medicine Reports

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Abstract. Sepsis is one of the leading causes of mortality in severe systemic inflammatory syndrome. The endotoxin-induced inflammatory response has been linked to the development of sepsis. Rhein is a lipophilic anthraquinone isolated from Rheum rhabarbarum (rhubarb), which has a protective effect on intestinal damage in vivo. However, the underlying mechanism responsible for the protective effects of rhein remains to be elucidated. In the present study, mice were exposed to 20 mg/kg lipopolysaccharide (LPS), prior to being treated with either 100 mg/kg rhein or 0.3 mg/kg toll-like receptor 4 (TLR4) signaling inhibitor TAK-242. In the rhein-treated mice, the colon length (cm) was extended and colon injury was attenuated. In addition, treatment with rhein significantly decreased the expression levels of the LPS-induced inflammatory cytokines interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor-α, in both the plasma and colon tissue. However, mice treated with TAK-242 exhibited increased expression levels of IL-10, as determined by ELISA and western blot analysis. In addition, immunohistochemistry and western blot analyses demonstrated that treatment with rhein was able to reduce TLR4 expression and inhibit nuclear factor-κB (NF-κB) phosphorylation in colon tissue. Furthermore, LPS induction was blocked by TAK-242. These results demonstrate that the observed rhein-attenuated inflammatory response during sepsis may be achieved via the TLR4 NF-κB signaling pathway. In conclusion, the results of the present study provide a novel insight into the protective effects of rhein on LPS-induced intestinal inflammation, and demonstrate that rhein may act as a beneficial therapeutic agent in the treatment of sepsis-induced intestinal damage.

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“…In epithelial cells, TJs are the most apical intercellular junctions, and function as selective barriers to macromolecules and prevent the diffusion of macromolecules or bacterial translocation. In recent years, there have been a number of research studies pertaining to compounds that enhance the intestinal tight junction (e.g., adalimumab, berberine, curcumin, rhein, butyrate, soybean agglutinin, and flavonoids) (30)(31)(32)(33)(34)(35)(36). Nevertheless, polysaccharides that protect the intestinal epithelium tight junctions were not identified.…”

Section: Discussionmentioning

confidence: 96%

The Squid Ink Polysaccharides Protect Tight Junctions and Adherens Junctions from Chemotherapeutic Injury in the Small Intestinal Epithelium of Mice

Zuo

Cao

et al. 2015

Nutrition and Cancer

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Gastrointestinal mucositis and infection by chemotherapy treatment are associated with alterations in the functioning of the intestinal barrier, due to the potential damage induced by anticancer drugs on the epithelial tight junctions and adheren junction. We aimed to study the protective effect of dietary polysaccharides on chemotherapy-induced injury in the epithelial cells. In the current study, using mice that were intraperitoneally injected with 50 mg/kg cyclophosphamide for 2 days, we reveal that polysaccharides from the ink of Ommastrephes bartrami (OBP) enhanced the mRNA and protein expression levels of Occludin, zonulae occluden (ZO)-1, and E-cadherin. Immunohistochemistry staining of ZO-1 and E-cadherin confirmed the increase in the mRNA and protein levels. OBP also remarkably enhanced the mRNA expression of other tight junction proteins, ZO-2, ZO-3, claudin-2, and cingulin. Our results may have important implications in host defense, especially the immunopotentiation function of OBP on the cyclophosphamide-induced epithelial cell injury, as well as intestinal disorders involving inflammation and infection.

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Effects of rhein on intestinal epithelial tight junction in IgA nephropathy

Abstract: Rhein can enhance the expression of ZO-1 and occludin, repair damaged tight junctions, and protect the intestinal barrier.

Cited by 30 publications

References 0 publications

Selective bowel decontamination improves the survival of 90% hepatectomy in rats

Selective bowel decontamination improves the survival of 90% hepatectomy in rats

Rhein inhibits lipopolysaccharide-induced intestinal injury during sepsis by blocking the toll-like receptor 4 nuclear factor-κB pathway

The Squid Ink Polysaccharides Protect Tight Junctions and Adherens Junctions from Chemotherapeutic Injury in the Small Intestinal Epithelium of Mice

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