Methane-rich saline protects against concanavalin A-induced autoimmune hepatitis in mice through anti-inflammatory and anti-oxidative pathways

He, Rong; Wang, Liping; Zhu, Jiali; Fei, Miaomiao; Bao, Suhong; Meng, Yan; Wang, Yuanyuan; Li, Jinbao; Deng, Xiaoming

doi:10.1016/j.bbrc.2015.12.080

Cited by 37 publications

(20 citation statements)

References 36 publications

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“…Unlike the pro-inflammatory cytokines described above, IL-10 can inhibit inflammation and protect hepatocytes. In support of the findings of this present study, He et al reported that serum IL-10 expression levels were significantly increased in a mouse model of Con A-induced immune liver injury [ 24 ].…”

Section: Discussionsupporting

confidence: 91%

The Effects of Berberine on Concanavalin A-Induced Autoimmune Hepatitis (AIH) in Mice and the Adenosine 5’-Monophosphate (AMP)-Activated Protein Kinase (AMPK) Pathway

Wang

Zhou

et al. 2017

Med Sci Monit

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BackgroundBerberine, a herbal extract, has been reported to protect against inflammatory disorders. The adenosine 5′-monophosphate (AMP)-activated protein kinase (AMPK) signaling pathway can be activated by berberine and inhibited by the synthetic, reversible AMP-competitive inhibitor, Compound C. The aim of this study was to investigate the effects of berberine on concanavalin A (Con A)-induced autoimmune hepatitis (AIH) in mice via the AMPK pathway.Material/MethodsBALB/c mice were treated with berberine, with or without Compound C, followed by treatment with Con A. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were measured. Liver tissue histology was performed to evaluate hepatic injury and AIH. Cytokine levels in serum and hepatic tissue were measured by enzyme-linked immunoassay (ELISA) and used quantitative polymerase chain reaction (qPCR). Levels of phosphorylated acetyl coenzyme-A carboxylase (ACC), representing AMPK activation, were detected by Western blotting.ResultsSerum ALT and AST levels were significantly reduced by berberine (100 and 200 mg/kg/day) in mice with Con A-induced hepatitis. Berberine also reduced Con A-induced hepatocyte swelling, cell death, and infiltration of leukocytes. Serum levels of tumor necrosis factor (TNF)-alpha, interferon (IF)-gamma, interleukin (IL)-2, and IL-1beta were reduced by berberine pre-treatment; levels of serum IL-10, an anti-inflammatory cytokine, was elevated. These protective effects of berberine on Con-A-induced AIH were reversed by treatment with Compound C.ConclusionsIn a murine model of Con A-induced AIH, berberine treatment reduced hepatic injury via activation of the AMPK pathway. Further studies are recommended to determine the potential therapeutic role for berberine in AIH.

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Section: Discussionsupporting

confidence: 91%

The Effects of Berberine on Concanavalin A-Induced Autoimmune Hepatitis (AIH) in Mice and the Adenosine 5’-Monophosphate (AMP)-Activated Protein Kinase (AMPK) Pathway

Wang

Zhou

et al. 2017

Med Sci Monit

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“…[12][13][14][15][16] In addition, many published articles suggest that CH 4 -based treatments have antiapoptotic effects in model experiments. [17][18][19][20][21][22][23] These converging research findings suggest that CH 4 can influence the permeability status of the mucosa, a most critical factor in GI injuries in clinical settings. Consequently, we devised experiments to investigate the kinetics of CH 4 distribution in the blood and small intestine and the effects of exogenous CH 4 which leads to an approximately twofold increase in the intraluminal CH 4 concentration over background levels; we evaluated these effects on the epithelial and endothelial permeability and secondary inflammatory reactions in a standardized rat model of mesenteric IR.…”

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confidence: 97%

Inhalation of methane preserves the epithelial barrier during ischemia and reperfusion in the rat small intestine

Mészáros

Buki

Fazekas

et al. 2017

Surgery

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“…Oxidative stress has been considered as a cornerstone in the pathophysiological process of various hepatic diseases. In Con A-induced liver injury, one of the important characteristics is the imbalance of oxidative stress [36]. He et al showed elevated oxidative products (MDA and 8-hydroxy-2′-deoxyguanosine) and reduced activities of SOD and cata-lase in Con A-treated mice [7].…”

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confidence: 99%

The Role of Serotonin in Concanavalin A-Induced Liver Injury in Mice

Pang

Jin

et al. 2020

Oxidative Medicine and Cellular Longevity

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Serotonin is involved in the pathological processes of several liver diseases via the regulation of inflammatory response and oxidative stress. We aimed to investigate the role of serotonin in Concanavalin A- (Con A-) induced acute liver injury (ALI). ALI was induced in C57B/6 wild-type (WT) mice and tryptophan hydroxylase 1 (TPH1) knockout mice through tail vein injection of Con A (15 mg/kg body weight). Another group of TPH1 knockout ALI mice was supplied with 5-hydroxytryptophan (5-HTP) in advance to recover serotonin. The blood and liver tissues of mice were collected in all groups. Markedly increased serum levels of serotonin were identified after the injection of Con A. Increased serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) and stronger hepatic tissue pathology were detected, suggesting that serotonin could mediate Con A-induced liver damage. Serotonin significantly facilitated the release of serum and intrahepatic inflammatory cytokines, including interleukin-2 (IL-2), interleukin-6 (IL-6), interleukin-17A (IL-17A), interferon-gamma (IFN-γ), and tumor necrosis-alpha (TNF-α), after the administration of Con A. In addition, serotonin significantly increased the intrahepatic levels of oxidative stress markers malonaldehyde (MDA), myeloperoxidase (MPO), and nitric oxide (NO) and decreased antioxidant stress indicator glutathione (GSH) in Con A-treated mice. Additionally, serotonin promoted hepatocyte apoptosis and autophagy based on B-cell lymphoma-2 (Bcl-2), Bcl-2-asociated X protein (Bax), and Beclin-1 levels and TUNEL staining. More importantly, serotonin activated nuclear factor kappa B (NF-κB) and upregulated the hepatic expressions of high mobility group protein B1 (HMGB1), toll-like receptor-4 (TLR4), and downstream molecules in Con A-mediated liver injury. Serotonin 2A receptor was upregulated in liver tissue after Con A injection, and serotonin 2A receptor antagonist Ketanserin protected against Con A-induced hepatitis. These results indicated that serotonin has the potential to aggravate Con A-induced ALI via the promotion of inflammatory response, oxidative stress injury, and hepatocyte apoptosis and the activation of hepatic HMGB1-TLR signaling pathway and serotonin 2A receptor.

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Methane-rich saline protects against concanavalin A-induced autoimmune hepatitis in mice through anti-inflammatory and anti-oxidative pathways

Cited by 37 publications

References 36 publications

The Effects of Berberine on Concanavalin A-Induced Autoimmune Hepatitis (AIH) in Mice and the Adenosine 5’-Monophosphate (AMP)-Activated Protein Kinase (AMPK) Pathway

The Effects of Berberine on Concanavalin A-Induced Autoimmune Hepatitis (AIH) in Mice and the Adenosine 5’-Monophosphate (AMP)-Activated Protein Kinase (AMPK) Pathway

Inhalation of methane preserves the epithelial barrier during ischemia and reperfusion in the rat small intestine

The Role of Serotonin in Concanavalin A-Induced Liver Injury in Mice

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