Galangin Protects against Symptoms of Dextran Sodium Sulfate-Induced Acute Colitis by Activating Autophagy and Modulating the Gut Microbiota

Han, Xuan; Ou, Aiqun; Hao, Shengyu; Shi, Jiajun; Jin, Xi

doi:10.3390/nu12020347

Cited by 39 publications

(19 citation statements)

References 43 publications

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“…Studies demonstrated that autophagy contributed to the maintaining and restoration of gut microbiota homeostasis in DSS-induced UC models. Those studies indicate that enhancing the level of autophagy may probably serve as a potential regulator of gut microbiota ( Ng, 2015 ; Xuan et al, 2020 ; Zha et al, 2020 ). In addition, it was lately demonstrated by Zhang et al (2020b) that specific knocking out intestinal Metrnl in epithelial cells produced a detrimental effect UC severity via the reduction of autophagy in epithelial cells in DSS-induced colitis models.…”

Section: Part I: Autophagy In Ibdmentioning

confidence: 99%

“…So far, several therapies are available in the alleviation of IBD taking advantage of autophagy-mediated modulation of intestinal microbiota ( Sun, 2016 ; Bakke and Sun, 2018 ; Kokten et al, 2018 ; Xuan et al, 2020 ). It has been reported that vitamin D promoted intestinal autophagy, thus alleviating IBD ( Sun, 2016 ).…”

Section: Part Ii: Application Of Autophagy Regulators In the Treatmenmentioning

confidence: 99%

“…In addition, Kokten et al (2018) demonstrated that the inhibition of triggering receptor expressed on myeloid cells-1 (TREM-1) contributed to the restoration of impaired autophagy activity, thus positively regulating the intestinal microbiota in colitis mice. Xuan et al (2020) uncovered that Galangin, a natural flavonoid, could fight against DSS-induced colitis through the promotion of autophagy-mediated regulation of gut microbiota. The modulation of inflammatory reaction and myeloperoxidase activities was shown to be involved in this process.…”

Section: Part Ii: Application Of Autophagy Regulators In the Treatmenmentioning

confidence: 99%

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The Role of Autophagy in Inflammatory Bowel Disease

et al. 2021

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Inflammatory bowel disease (IBD) is an idiopathic intestinal inflammatory disease, including ulcerative colitis (UC) and Crohn’s disease (CD). The abnormality of inflammatory and immune responses in the intestine contributes to the pathogenesis and progression of IBD. Autophagy is a vital catabolic process in cells. Recent studies report that autophagy is highly involved in various kinds of diseases, especially inflammation-related diseases, such as IBD. In this review, the biological characteristics of autophagy and its role in IBD will be described and discussed based on recent literature. In addition, several therapies for IBD through modulating the inflammasome and intestinal microbiota taking advantage of autophagy regulation will be introduced. We aim to bring new insight in the exploration of mechanisms for IBD and development of novel therapeutic strategies against IBD.

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Section: Part I: Autophagy In Ibdmentioning

confidence: 99%

Section: Part Ii: Application Of Autophagy Regulators In the Treatmenmentioning

confidence: 99%

Section: Part Ii: Application Of Autophagy Regulators In the Treatmenmentioning

confidence: 99%

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The Role of Autophagy in Inflammatory Bowel Disease

et al. 2021

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“…Like the AHR-deficient mice, animals fed purified, phytochemical-free diets exhibit enhanced susceptibility to severe colitis [ 113 , 114 , 115 ]. Furthermore, there are numerous reports that phytochemicals—including berberine [ 116 ], curcumin [ 117 ], galangin [ 118 ], resveratrol [ 119 ], and rutin [ 120 ]—can prevent microbial dysbiosis and stimulate colonization of the gut by beneficial anaerobic bacteria (reviewed by [ 121 , 122 ]). 13C, which is commonly used to activate the AHR and stimulates IL-22 expression, can also promote colonization by beneficial bacteria, both when administered in the diet [ 113 ] and injected intraperitoneally [ 123 ].…”

Section: The Mechanism(s) By Which Ficz Il-22 and Butyrate Promotmentioning

confidence: 99%

How the AHR Became Important in Intestinal Homeostasis—A Diurnal FICZ/AHR/CYP1A1 Feedback Controls Both Immunity and Immunopathology

Rannug

2020

IJMS

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Ever since the 1970s, when profound immunosuppression caused by exogenous dioxin-like compounds was first observed, the involvement of the aryl hydrocarbon receptor (AHR) in immunomodulation has been the focus of considerable research interest. Today it is established that activation of this receptor by its high-affinity endogenous ligand, 6-formylindolo[3,2-b]carbazole (FICZ), plays important physiological roles in maintaining epithelial barriers. In the gut lumen, the small amounts of FICZ that are produced from L-tryptophan by microbes are normally degraded rapidly by the inducible cytochrome P4501A1 (CYP1A1) enzyme. This review describes how when the metabolic clearance of FICZ is attenuated by inhibition of CYP1A1, this compound passes through the intestinal epithelium to immune cells in the lamina propria. FICZ, the level of which is thus modulated by this autoregulatory loop involving FICZ itself, the AHR and CYP1A1, plays a central role in maintaining gut homeostasis by potently up-regulating the expression of interleukin 22 (IL-22) by group 3 innate lymphoid cells (ILC3s). IL-22 stimulates various epithelial cells to produce antimicrobial peptides and mucus, thereby both strengthening the epithelial barrier against pathogenic microbes and promoting colonization by beneficial bacteria. Dietary phytochemicals stimulate this process by inhibiting CYP1A1 and causing changes in the composition of the intestinal microbiota. The activity of CYP1A1 can be increased by other microbial products, including the short-chain fatty acids, thereby accelerating clearance of FICZ. In particular, butyrate enhances both the level of the AHR and CYP1A1 activity by stimulating histone acetylation, a process involved in the daily cycle of the FICZ/AHR/CYP1A1 feedback loop. It is now of key interest to examine the potential involvement of FICZ, a major physiological activator of the AHR, in inflammatory disorders and autoimmunity.

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“…The gut microbiota plays a crucial role in mediating the pharmacological activities of various natural products. Many flavonoids have been reported to exhibit their beneficial effects by modulating the gut microbiota [ 7 – 10 ]. In this study, we used a cocktail of antibiotics to disrupt the gut microbiota and observed the alteration of hepatoprotective effects of SCU on CCl 4 -induced chronic liver injury.…”

Section: Discussionmentioning

confidence: 99%

Scutellarein Aggravated Carbon Tetrachloride-Induced Chronic Liver Injury in Gut Microbiota-Dysbiosis Mice

Miao

Lai

Zhao

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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Scutellarein (SCU) is an herbal flavonoid, showing hepatoprotective potentials. The study was aimed to investigate whether the hepatoprotective effect of SCU is dependent on the integrity of gut microbiota. Mice received repeated intraperitoneal injections of CCl4, followed with or without SCU treatment (15, 30, and 60 mg/kg). Gut microbial community of mice was disrupted by administrating a cocktail of antibiotics (ampicillin, neomycin sulfate, metronidazole, and vancomycin) in drinking water. The results showed SCU plus antibiotics aggravated CCl4-induced chronic liver injury, as demonstrated by liver function analysis, histological analysis, and TUNEL assay. SCU activated CYP2E1 expression and worsened CYP2E1-mediated lipid peroxidation and oxidative stress as coadministered with antibiotics. Moreover, when gut microbiota was disrupted by antibiotics, SCU activated IκBα/NF-κB pathway and promoted the release of subsequent proinflammatory cytokines including interleukin-6 (IL-6), interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α). Remarkably, the 16 S rRNA sequencing demonstrated that SCU greatly decreased the relative abundance of Bifidobacterium and Lactobacillus and increased the relative abundance of Enterococcus in gut microbiota-dysbiosis mice. Spearman correlation analysis showed that Lactobacillus was positively correlated with SOD and negatively correlated with AST. Collectively, the hepatoprotective effect of SCU is reversed under antibiotics intervention, which may partly involve the activation of CYP2E1 and IκBα/NF-κB pathway and diminishment of Lactobacillus.

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Galangin Protects against Symptoms of Dextran Sodium Sulfate-Induced Acute Colitis by Activating Autophagy and Modulating the Gut Microbiota

Cited by 39 publications

References 43 publications

The Role of Autophagy in Inflammatory Bowel Disease

The Role of Autophagy in Inflammatory Bowel Disease

How the AHR Became Important in Intestinal Homeostasis—A Diurnal FICZ/AHR/CYP1A1 Feedback Controls Both Immunity and Immunopathology

Scutellarein Aggravated Carbon Tetrachloride-Induced Chronic Liver Injury in Gut Microbiota-Dysbiosis Mice

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