Abstract
For the development of Lupus nephritis, environmental factors are reasoned to be one of the risk factors. In recent years, the role of bisphenol A (BPA) in kidney injury has attracted wide attention. In this study, we explored the nephrotoxicity and its possible mechanism of BPA exposure to lupus-prone MRL/lpr mice. Orally exposure of BPA increased serum anti-dsDNA level and urinary protein, and aggravated renal pathological injury in MRL/lpr mice. BPA increased the expression of NF-κB protein and activated the inflammatory response in both MRL/lpr and C57 mice. Unlike C57 mice, BPA exposure partially activated autophagy associated proteins, but the autophagy signaling pathway lacked the regulation of Becline1 and LC3-associated phagocytosis deficiency, and decreased Nrf2 protein expression in renal tissue of MRL/lpr mice. Therefore, exacerbating lupus nephritis induced by BPA exposure was associated with the activation of inflammation, abnormal autophagy and decreased antioxidant ability.