Induction of heme oxygenase-1 protects against nutritional fibrosing steatohepatitis in mice

Wang, Rong Qi; Yang, Nan; Wu, Wen Juan; Kong, Ling Bo; Han, Fang; Zhao, Su Xian; Kong, Li; Yu, Jun

doi:10.1186/1476-511x-10-31

Cited by 33 publications

(35 citation statements)

References 38 publications

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“…Induction of HO-1 expression contributes to protection against liver damage in various liver diseases (36,37). We found that up-regulation of HO-1 could alleviate liver damage in BDL rats, which is in accordance with the findings of Barikbin et al In their study, induction of HO-1 interfered with chronic inflammation and prevented progression of liver fibrosis in Mdr2 knockout mice (36).…”

Section: Ho-1 Increased Occludin and Inhibited Phospho-nf-jb P65 Protsupporting

confidence: 90%

The Protective Effect of Heme Oxygenase-1 against Intestinal Barrier Dysfunction in Cholestatic Liver Injury Is Associated with NF-κB Inhibition

Zhang

Liu

et al. 2017

Mol Med

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Heme oxygenase-1 (HO-1) is reported to protect against liver injury, but little is known about its effect on the intestinal barrier in cholestatic liver injury. In this study, we investigated the effects of HO-1 and its enzymatic by-product on intestinal barrier dysfunction in bile duct ligation (BDL) rats and explored the possible mechanism. The HO-1 inducer cobalt protoporphyrin (CoPP) and carbon monoxide-releasing molecule-2 (CORM-2) were used; the expression levels of tight junction (TJ) proteins, intestinal inflammation and NF-κB p65 were measured. For an in vitro experiment, stable Caco-2 cell lines were constructed, one overexpressed the HO-1 gene and another with that gene knocked down, and the specific NF-κB inhibitor JSH-23 was used. CoPP and CORM-2 treatment alleviated liver and intestinal mucosa injury in BDL rats; improved ZO-1, claudin-1 and PCNA expression; and reduced cell apoptosis and intestinal interleukin-6 (IL-6) expression. In vitro studies confirmed that HO-1, ZO-1 and occludin were overexpressed in HO-1-transfected Caco-2 cells, while decreased in the short hairpin HO (sh-HO-1) group. JSH-23 significantly increased occludin expression in both the HO-1 overexpression and sh-HO-1 groups, compared with their respective controls. HO-1 overexpression also inhibited the nuclear translocation of NF-κB p65 after lipopolysaccharide (LPS) treatment. Additionally, phospho-p65 expression in sh-HO-1 cells was significantly increased compared with that of the HO-1 overexpression group. In conclusion, HO-1 and CORM-2 improved intestinal epithelial barrier function in BDL-induced cholestatic liver injury mainly by restoring TJ, reducing cell apoptosis and intestinal inflammation. HO-1 exerts a protective effect, which is partially correlated with the regulation of NF-κB.

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Section: Ho-1 Increased Occludin and Inhibited Phospho-nf-jb P65 Protsupporting

confidence: 90%

The Protective Effect of Heme Oxygenase-1 against Intestinal Barrier Dysfunction in Cholestatic Liver Injury Is Associated with NF-κB Inhibition

Zhang

Liu

et al. 2017

Mol Med

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“…HO-1, the rate-limiting enzyme in heme catabolism, has been reported to have potential antioxidant properties (Farombi and Surh, 2006). Previous studies have demonstrated the protective role of HO-1 in ameliorating MCD diet induced NASH (Wang et al, 2011;Nan et al, 2010). In addition, it was found that treatment with baicalein restored the activities of SOD and catalase, another two antioxidant enzymes, in livers of MCD fed rats.…”

Section: Discussionmentioning

confidence: 96%

Treatment with baicalein attenuates methionine−choline deficient diet-induced non-alcoholic steatohepatitis in rats

Xin

Zhang

et al. 2014

European Journal of Pharmacology

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“…Lee et al, 139 Wang et al, 140 Velayudham et al Uchinami et al, 142 Buryova et al, 143 Popov et al, 144 Schrading et al, 145 Díaz-Gil et al, 146 Kossakowska et al 147 …”

Section: Metalloproteinases In the Development Of Liver Fibrosismentioning

confidence: 99%

Metalloproteinases in liver fibrosis: current insights

Zbodakova¹,

Chalupský²,

Turečková³

et al. 2017

MNM

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Liver fibrosis is defined by excessive deposition of extracellular matrix. The fibrotic conditions result from the imbalance between synthesis and deposition of fibrous tissues and decomposition of these matrix proteins. This process can be reversed as a regular part of the healing process after hepatic damage or can become chronic. When the protein matrix synthesis predominates and the decomposition is suppressed, fibrosis will progress into irreversible cirrhosis or steatosis. Among the molecular players involved in fibrotic liver diseases, metalloproteinases of matrix metalloproteinase (MMP) and a disintegrin and metalloproteinase (ADAM) families are critical in the development of liver fibrosis and its resolution. Previously, MMPs were recognized as extracellular matrix degrading enzymes. Currently, they are also known as mediators in a variety of processes related to immunity and tissue repair. In this article, we have reviewed the models of liver fibrosis and findings on MMPs and ADAMs in hepatic fibrosis conditions.

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Induction of heme oxygenase-1 protects against nutritional fibrosing steatohepatitis in mice

Cited by 33 publications

References 38 publications

The Protective Effect of Heme Oxygenase-1 against Intestinal Barrier Dysfunction in Cholestatic Liver Injury Is Associated with NF-κB Inhibition

The Protective Effect of Heme Oxygenase-1 against Intestinal Barrier Dysfunction in Cholestatic Liver Injury Is Associated with NF-κB Inhibition

Treatment with baicalein attenuates methionine−choline deficient diet-induced non-alcoholic steatohepatitis in rats

Metalloproteinases in liver fibrosis: current insights

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