Carbon monoxide alleviates ethanol-induced oxidative damage and inflammatory stress through activating p38 MAPK pathway
Toxicology and Applied Pharmacology, ISSN: 0041-008X, Vol: 273, Issue: 1, Page: 53-58
2013
- 29Citations
- 33Captures
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Metrics Details
- Citations29
- Citation Indexes29
- 29
- CrossRef24
- Captures33
- Readers33
- 33
Article Description
Stress-inducible protein heme oxygenase-1(HO-1) is well-appreciative to counteract oxidative damage and inflammatory stress involving the pathogenesis of alcoholic liver diseases (ALD). The potential role and signaling pathways of HO-1 metabolite carbon monoxide (CO), however, still remained unclear. To explore the precise mechanisms, ethanol-dosed adult male Balb/c mice (5.0 g/kg.bw.) or ethanol-incubated primary rat hepatocytes (100 mmol/L) were pretreated by tricarbonyldichlororuthenium (II) dimmer (CORM-2, 8 mg/kg for mice or 20 μmol/L for hepatocytes), as well as other pharmacological reagents. Our data showed that CO released from HO-1 induction by quercetin prevented ethanol-derived oxidative injury, which was abolished by CO scavenger hemoglobin. The protection was mimicked by CORM-2 with the attenuation of GSH depletion, SOD inactivation, MDA overproduction, and the leakage of AST, ALT or LDH in serum and culture medium induced by ethanol. Moreover, CORM-2 injection or incubation stimulated p38 phosphorylation and suppressed abnormal Tnfa and IL-6, accompanying the alleviation of redox imbalance induced by ethanol and aggravated by inflammatory factors. The protective role of CORM-2 was abolished by SB203580 (p38 inhibitor) but not by PD98059 (ERK inhibitor) or SP600125 (JNK inhibitor). Thus, HO-1 released CO prevented ethanol-elicited hepatic oxidative damage and inflammatory stress through activating p38 MAPK pathway, suggesting a potential therapeutic role of gaseous signal molecule on ALD induced by naturally occurring phytochemicals.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0041008X13003694; http://dx.doi.org/10.1016/j.taap.2013.08.019; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84884721349&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/23994557; https://linkinghub.elsevier.com/retrieve/pii/S0041008X13003694; https://dx.doi.org/10.1016/j.taap.2013.08.019
Elsevier BV
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