Protection of Primary Cultured Mouse Hepatocytes from Chemical Hypoxia- induced Injury by Hydrogen Sulfide

서지정보

· 발행기관 : 한국생명과학회
· 수록지 정보 : 생명과학회지 / 23권 / 11호 / 1342 ~ 1350페이지
· 저자명 : 이민영

초록

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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