Abstract:

Objective To estimate the influences of N-acetyl cysteine （NAC） on a chemical hypoxia-mimetic agent CoCl2 induced-injury to, and expressions of inflammatory factors by, an immortal human skin kera-tinocyte line HaCaT. Methods HaCaT cells were treated with CoCl2 of 2000 μmol/L for 4 hours to set up a chemical hypoxia-induced cell model of skin injury. NAC of various concentrations （1000, 2000, 3000 μmol/L） was used to pretreat HaCaT cells for 2 hours prior to the establishment of cell model. After these treatments, cell viability was detected by cell counting kit 8 （CCK-8）, the levels of interleukin 6 and 8 （IL-6 and -8） and tumor necrosis factor α （TNF-α） in culture supernatant by ELISA kits, mitochondrial membrane potential （MMP） by rhodamine 123 （Rh123） staining and photofluorography, intracellular reduced glutathione （GSH） content by glutathione detection kit. Results An obvious decline was observed in HaCaT cell viability after pretreatment with various concentrations of NAC for 2 hours. The treatment with CoCl2 of 2000 μmol/L for 4 hours induced an elevation in the supernatant levels of IL-6, IL-8 and TNF-α and a decrease in GSH content and MMP, while the pretreatment with NAC for 2 hours retarded the CoCl2 -induced increase in IL-6 and IL-8 levels as well as decrease in GSH content and MMP. Conclusion The reactive oxygen species （ROS） scavenger NAC can protect against CoCl2 -induced injury to and inflammatory reaction in HaCaT cells, which may be associated with a decrement in oxidative stress.