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KMID : 0613820130230111342
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Journal of Life Science
2013 Volume.23 No. 11 p.1342 ~ p.1350
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Protection of Primary Cultured Mouse Hepatocytes from Chemical Hypoxia-induced Injury by Hydrogen Sulfide
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Lee Min-Young
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Abstract
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We examined the effect of hydrogen sulfide (H₂S) in chemical hypoxia-induced injury in mouse hepatocytes. Cell viability was significantly decreased by cobalt chloride (CoCl₂), a well-known hypoxia mimetic agent in a time- and dose- dependent manner. Sodium hydrosulfide (NaHS, a donor of H₂S) pretreatment before exposure to CoCl₂ significantly attenuated the CoCl₂-induced decrease of cell viability. CoCl₂ treatment resulted in an increase of intracellular ROS generation, which is inhibited by NaHS or N-acetyl-cysteine (NAC, a ROS scavenger), and p38 MAPK phosphorylation, which is also blocked by NaHS or NAC. The CoCl₂-induced increase of the Bax/Bcl-2 ratio was attenuated by NaHS, NAC, and SB 203580 (p38 MAPK inhibitor). The CoCl₂-induced decrease of cell viability was also attenuated by NaHS, NAC, and SB 203580 pretreatment. Additionally, NaHS inhibited the CoCl₂-induced COX-2. Similar to the effect of NaHS, NAC blocked CoCl₂-induced COX-2 expression. Furthermore, NS-398 (a selective COX-2 inhibitor) attenuated not only the CoCl₂-induced increase of the Bax/Bcl-2 ratio, it also decreased cell viability. Taken together, H₂S protects primary cultured mouse hepatocytes against CoCl₂-induced cell injury through inhibition of the ROS-activated p38 MAPK cascade and the COX-2 pathway.
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KEYWORD
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Hydrogen sulfide, cobalt chloride, chemical hypoxia, mouse hepatocytes
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