[Role of PPARα in the oxidative damage of rat liver cells BRL-3A induced by perfluorooctanoic acid].

Objective: To investigate the role of PPARα in oxidative damage of BRL-3A cells induced by perfluorooctanoic acid( PFOA) by inhibiting and activating gene expression.

Methods: In vitro culture of rat liver BRL-3A cells were divided into blank control group, PFOA experimental control group, PPARα inhibition group( GW6471), PPARα agonist group( WY14643), PPARα inhibitor pretreatment PFOA group( GW6471 + PFOA), PPARα agonist pretreatment PFOA group( WY14643 + PFOA). Fluorescence immunocytochemistry was used to detect the expression of PPARα. The expression of PPARα and its downstream target gene was detected by q PCR. The expression of related protein was detected by Western blot.

Results: The expression of PPARα in rat liver BRL-3A cells was successfully inhibited and stimulated by inhibitors and agonists( P < 0. 05). Compared with the blank control group and the PFOA experimental control group, there was a significant decrease in the content of ROS in the WY14643 + PFOA group compared with the blank control group and the PFOA experimental control group( P < 0. 05). The expression of PPARα and its downstream gene Cyp4a1 in GW6471 + PFOA group was higher than that in PPARα inhibitor group( P < 0. 05), but it was significantly lower than that in PFOA experimental control group( P < 0. 05). The expression of related genes in WY14643 + PFOA group was significantly lower than that in PPARα agonist group( P < 0. 05). The protein expression of PPARα in GW6471 + PFOA group was up-regulated compared with the inhibitor group, there was no difference compared with the blank control group. The protein expression of PPARα in WY14643 + PFOA group was not significantly different from that in agonist group, but it was significantly higher than that in PFOA experimental control group( P < 0. 05).

Conclusion: PFOA exposure can activate the expression of PPARα, remove ROS, PPARα played a protective role in PFOA-induced rat liver cell oxidative damage.