Qian Tian; Xiaowei Gong; Zheng Duan & Yadong Yuan

Peroxisome proliferator activated receptor γ co-activator 1α (PGC-1α) plays an important role in antioxidative stress. The aim of this study is to investigate the role of PGC-1α in the oxidative damage of BEAS-2B cells exposed to PM2.5 and hypoxia simultaneously and in the anti-oxidative effect of N-acetyl-L-cysteine (NAC). The PGC-1α mRNA level in human bronchial epithelial BEAS-2B cells exposed to PM2.5, hypoxia and PM2.5 combined with hypoxia were evaluated. The cells were treated for 12 h in the presence or absence of PM2.5 combined with hypoxia and in the presence or absence of NAC. The cell viability after intervention with NAC was assessed. PGC-1α was knocked down by siRNA to investigate the protective mechanism of NAC. The expression levels of PGC-1α and PPARγ were determined at both the mRNA and protein levels. The expression of NF-κBp65, malondialdehyde (MDA) and superoxide dismutase (SOD) were detected at the protein level. PM2.5 combined with hypoxia reduced the expression of PGC-1α and PPAR-γ (P<0.01), increased the protein levels of NF- κBp65 (P<0.01) and MDA(P<0.05), and decreased the SOD activity (P<0.05) compared to the normal control group, and NAC ameliorated the damage(P < 0.05). PGC-1α siRNA blocked the protective effect of NAC. PM2.5 combined with hypoxia can cause oxidative damage to BEAS- 2B cells, and PGC-1α may play an important role in the anti-oxidative effect of NAC. The results of this study suggest for the first time that PGC-1α might play an important role in regulation of oxidative damage induced by PM2l.5 and hypoxia simultaneously in human bronchial epithelial cells, which provides potential ideas for the treatment of PM2.5-induced respiratory diseases.

KEY WORDS: PM2.5; Hypoxia; Peroxisome proliferator-activated receptor gamma coactivator-1 alpha; N-acetyl-L-cysteine; Oxidative damage.

TIAN, Q.; GONG, X.; DUAN, Z. & YUAN, Y. Peroxisome proliferator-activated receptor gamma coactivator-1 alpha play a role in PM2.5 and hypoxia-induced simultaneously oxidative damage in human bronchial epithelial cells. Int. J. Morphol., 42(6):1653-1662, 2024.