AMPK/PGC-1α signal pathway coordinates HBO-induced oxidative stress response

Abstract

Objective To investigate the adaptive response of the organism to oxidative stress induced by HBO, through observation of the effects of HBO on mitochondrial DNA (Mt-DNA) copy number and the expression of anti-oxidative protein and possible mechanism involved. Methods Twenty-eight C57BL/6 mice were randomly divided into 5 groups: the control group (with atmospheric pressure air exposure), the HBO group (with 0.2 MPa exposure for 1, 5, 14 and 28 days) (or the 1-d HBO group, the 5-d HBO group, the 14-d HBO group and the 28-d HBO group. Following exposure, the animals were immediately executed and hepatic tissues were collected. When total protein and DNA in the liver tissue were harvested, Mt-DNA copy number was determined by RT-PCR. The expression levels of superoxide dismutase 2 (SOD2), mitochondrial transcription factor A (TFAM), uncoupling protein 2 (UCP2) and AMPK/PGC-1α signaling pathway proteins were detected by Western blotting. Results Compared with that of the control group (1.00±0.19), the Mt-DNA copy numbers in the 1-d HBO group(0.61±0.18), the 5-d HBO group(0.58±0.01), the 14-d HBO group (0.74±0.07) and the 28-d HBO group (0.71±0.07) were significantly reduced (P<0.05), while the expression levels of SOD2, TFAM, UCP2 and AMPK/PGC-1α were all obviously increased. Statistical significance could be noted, when comparisons were made between the groups(P<0.05 or P<0.01). Conclusion The coordination of HBO-induced oxidative stress response through access of the enhancement of anti-oxidative capacity and decrease of Mt-DNA copy number via activating AMPK/PGC-1α signaling pathway might be the mechanism involved in HBO-induced oxidative stress response in mice. Key words: AMPK/PGC-1α signaling pathway; Hyperbaric oxygen; Oxidative stress; Mouse; Hepatocyte; Mitochondria