Compound sophorae decoction enhances intestinal barrier function of dextran sodium sulfate induced colitis via regulating notch signaling pathway in mice

Wu, Hui; Chen, Qian-Yun; Wang, Wenzhu; Chu, Si; Liu, Xingxing; Liu, Yujin; Tan, Chen; Zhu, Feng; Deng, Shuangjiao; Dong, Yalan; Takata, Yasuyuki; Gao, Fei; He, Hongqing; Leng, Xue-Yuan; Fan, Heng

doi:10.1016/j.biopha.2020.110937

Cited by 71 publications

(29 citation statements)

References 40 publications

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“…Ⅰ To investigate the protective effect of MGQD against UC, 60 mice were stochastically divided into six groups (n = 10/group): a control group, DSS group, low-dose MGQD group (GL), medium-dose MGQD group (GM), high-dose MGQD group (GH), and 5-ASA group. Except for the normal group, all other five groups received 3% (w/v) DSS diluted in drinking water to induce acute experimental UC for 7 days ( Wu et al, 2021 ). At the same time, each treatment group was given the corresponding dose of drugs once per day orally for seven consecutive days, namely, GL (5 g/kg), GM (10 g/kg), GH (20 g/kg) and 5-ASA (100 mg/kg) ( Jing et al, 2019 ).…”

Section: Methodsmentioning

confidence: 99%

Modified Gegen Qinlian Decoction Regulates Treg/Th17 Balance to Ameliorate DSS-Induced Acute Experimental Colitis in Mice by Altering the Gut Microbiota

Wang

Zhang

et al. 2021

Front. Pharmacol.

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Inflammatory bowel disease (IBD) is characterized by chronic pathology associated with extensive intestinal microbial dysregulation and intestinal inflammation. Thus, efforts are underway to manipulate the gut microbiome to improve inflammatory pathology. Gegen Qinlian decoction (GQD), a traditional Chinese medicine prescription, has been widely utilized for treating diarrhea and ulcerative colitis (UC) for thousands of years. However, the underlying mechanism of its efficacy and whether its protective effect against colitis is mediated by the gut microbiota are poorly understood. In the present study, our data demonstrated that modified GQD (MGQD) administration significantly improved the pathological phenotypes and colonic inflammation challenged by DSS in mice, which were specifically manifested as reduced loss of body weight, shortening of colon length, DAI score, histological score and suppressed inflammatory response. 16S rRNA sequencing and targeted metabonomics analysis showed that MQGD altered the diversity and community landscape of the intestinal microbiota and the metabolic profiles. In particular, MQGD significantly boosted the abundance of the intestinal microbiota producing short-chain fatty acids (SCFAs), which are causally associated with promoting the development of Treg cells and suppressing the differentiation of pro-inflammatory Th17 cells. More importantly, transferring fecal microbiota from MGQD-treated or healthy controls exhibited equivalent alleviative effects on colitis mice. However, this protective effect could not be replicated in experiments of mice with depleted intestinal microbes through broad-spectrum antibiotic cocktails (ABX), further supporting the importance of SCFA-producing gut microbiota in the beneficial role of MGQD. In general, MGQD therapy has the potential to remodel the intestinal microbiome and reestablish immune homeostasis to ameliorate DSS-induced colitis.

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Section: Methodsmentioning

confidence: 99%

Modified Gegen Qinlian Decoction Regulates Treg/Th17 Balance to Ameliorate DSS-Induced Acute Experimental Colitis in Mice by Altering the Gut Microbiota

Wang

Zhang

et al. 2021

Front. Pharmacol.

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“…5 F and G).TJ proteins are the major connecting protein between intestinal epithelial cells, represented by claudins, occludin, junctional adhesion molecules, and scaffold protein zonulaoccludins. They are chiefly responsible for regulating paracellular transport and also the main structural component of the formation of barrier function of epithelial cells [ 39 , 63 ]. In our current study, LUT@TPGS-PBTE NPs maintained the intestinal integrity by reducing the loss of claudin-1, occludin and ZO-1, and the tissue injury, diarrhea and bloody stools were significantly relieved.…”

Section: Discussionmentioning

confidence: 99%

ROS-responsive nanoparticles for oral delivery of luteolin and targeted therapy of ulcerative colitis by regulating pathological microenvironment

Tan

Fan

Ding

et al. 2022

Materials Today Bio

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“…More M1 macrophages and fewer M2 macrophages were founded in peripheral blood of UC patients [31]. In DSS-induced experimental colitis, M1/M2 macrophage polarisation imbalance was observed in the spleen and mesenteric lymph nodes [32]. Macrophages expressed Tim-1 [33] and TLR4 upon activation, M1 macrophages expressed iNOS [34], and M2 macrophages expressed CD206 and CD163 [35].…”

Section: Discussionmentioning

confidence: 99%

Ginsenoside Rg1 Ameliorated Colitis by Regulating the Homeostasis of M1/M2 Macrophage Polarization and Intestinal Flora

Long

Liu

Kang

et al. 2021

Preprint

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Background: Aberrant M1/M2 macrophage polarization and intestinal flora disruption are involved in the pathological processes associated with ulcerative colitis (UC). Ginsenoside Rg1 has good immunomodulatory and anti-inflammatory effects and is effective in treating UC of humans and animals. However, it is unclear how ginsenoside Rg1 regulate the homeostasis of M1/M2 macrophage polarization and intestinal flora.Methods: BALB/c mice were randomly divided into 4 groups: Control, DSS, DSS+Rg1, DSS+Y27632 groups. In this study, experiment colitis was induced in BALB/c mice using sodium dextran sulfate (DSS). Mice of DSS+Rg1, DSS+Y27632 groups were treated respectively with ginsenoside Rg1 and Rock inhibitor Y27632 for 14 consecutive days. On day 21, all mice were sacrificed. Histopathological analysis of the colon tissues was performed by Hematoxylin Eosin sinning. Cytokines (IL-6, IL-33, CCL-2, TNF-α, IL-4 and IL-10) were detected by Elisa. Flow cytometry was used to analyse macrophage activation and M1/M2 macrophage polarisation. Western blotting were applied to detect the levels of Macrophage polarization-associated protein (Arg-1, MIF-1, PIM-1, TLR2) and Nogo-B/RhoA signaling molecules (Rock1, RhoA and Nogo-B). The fecal microbial populations were analyzed using 16S gene sequencing. Results: After ginsenoside Rg1 and Y27632 treatment, the changes of body weight, colon length, colonic weight index and colonic mucosal injury of colitis mice were effectively improved, accompanied by less ulcer formation and inflammatory cell infiltration, lower levels of pro-inflammatory cytokines (IL-6, IL-33, CCL-2, TNF-α) and higher anti-inflammatory cytokines (IL-4 and IL-10). Importantly, the percentage of CD11b+F4/80+, CD11b+F4/80+Tim-1+, CD11b+F4/80+TLR4+, and CD11b+F4/80+iNOS+ cells and the expression levels of MIF-1 and PIM-1 proteins were down-regulated significantly after ginsenoside Rg1 and Y27632 treatment, and CD11b+F4/80+CD206+ and CD11b+F4/80+CD163+ cells and Arg-1 up-regulated significantly. Intestinal flora composition were effectively improved after administration of ginsenoside Rg1. The Nogo-B/RchoA signaling pathway were obviously inhibited after ginsenoside Rg1 and Y27632 treatment, and the levels of Rock1, RhoA and Nogo-B proteins were significantly reduced. Conclusions: Ginsenoside Rg1 has the protective effect on UC by inhibiting macrophage activation, restoring the balance of M1/M2 macrophage polarization, and improving intestinal flora composition, associated with inhibition of the Nogo-B/RhoA signaling pathway.

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Compound sophorae decoction enhances intestinal barrier function of dextran sodium sulfate induced colitis via regulating notch signaling pathway in mice

Cited by 71 publications

References 40 publications

Modified Gegen Qinlian Decoction Regulates Treg/Th17 Balance to Ameliorate DSS-Induced Acute Experimental Colitis in Mice by Altering the Gut Microbiota

Modified Gegen Qinlian Decoction Regulates Treg/Th17 Balance to Ameliorate DSS-Induced Acute Experimental Colitis in Mice by Altering the Gut Microbiota

ROS-responsive nanoparticles for oral delivery of luteolin and targeted therapy of ulcerative colitis by regulating pathological microenvironment

Ginsenoside Rg1 Ameliorated Colitis by Regulating the Homeostasis of M1/M2 Macrophage Polarization and Intestinal Flora

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