Xiaojuan Guo1,2, Jingyuan Zhang1, Min Liu1, Guo Chen Zhao1. 1. a Department of Kidney, School of Clinical Medicine, Nanjing University of Traditional Chinese Medicine, Nanjing, China. 2. b Department of Kidney, Nanjing boda kidney hospital affiliated to Nan Jing University Chinese Medicine, Nanjing, China.
Abstract
Background/Aim: Ginsenoside Rg1 exerts a beneficial effect in many kidney diseases. But little work has been done to confirm whether ginsenoside Rg1 could also exert a protective effect on anti-glomerular basement membrane (anti-GBM) glomerular nephritis (GN). We aimed to explore the role of ginsenoside Rg1 in attenuating anti-GBM GN in vitro and in vivo and investigate the mechanism under its action. Methods: Interleukin-1β (IL-1β) treated podocytes were used as a cell model. A total of 20 mice were used to build the Anti-GBM GN mice model. Real-time PCR analysis (RT-PCR), Western blot analysis and ELISA assay were conducted to detect related indicators in this study. The statistical analysis was performed using GraphPad Prism software 6.0. Results: Ginsenoside Rg1 attenuates IL-1β-induced inflammation and apoptosis in podocytes. NRF2 expression can be inhibited by IL-1β, whereas reversed by ginsenoside Rg1. NRF2 inhibitor ML385 can significantly reverse the effects of ginsenoside Rg1 on inflammation and apoptosis induced by IL-1β, and block the inhibitory effect of ginsenoside Rg1 on IL-1β activated MAPK pathway. In addition, ginsenoside Rg1 could improve anti-GBM GN injury in vivo. Conclusion: Ginsenoside Rg1 inhibits the anti-GBM GN damage through regulating NRF2 pathway in vitro and in vivo. Our findings provide new insight and mechanism of ginsenoside Rg1 to prevent anti-GBM GN.
Background/Aim: GinsenosideRg1 exerts a beneficial effect in many kidney diseases. But little work has been done to confirm whether ginsenosideRg1 could also exert a protective effect on anti-glomerular basement membrane (anti-GBM) glomerular nephritis (GN). We aimed to explore the role of ginsenosideRg1 in attenuating anti-GBM GN in vitro and in vivo and investigate the mechanism under its action. Methods: Interleukin-1β (IL-1β) treated podocytes were used as a cell model. A total of 20 mice were used to build the Anti-GBM GN mice model. Real-time PCR analysis (RT-PCR), Western blot analysis and ELISA assay were conducted to detect related indicators in this study. The statistical analysis was performed using GraphPad Prism software 6.0. Results:GinsenosideRg1 attenuates IL-1β-induced inflammation and apoptosis in podocytes. NRF2 expression can be inhibited by IL-1β, whereas reversed by ginsenosideRg1. NRF2 inhibitor ML385 can significantly reverse the effects of ginsenosideRg1 on inflammation and apoptosis induced by IL-1β, and block the inhibitory effect of ginsenosideRg1 on IL-1β activated MAPK pathway. In addition, ginsenosideRg1 could improve anti-GBM GN injury in vivo. Conclusion:GinsenosideRg1 inhibits the anti-GBM GN damage through regulating NRF2 pathway in vitro and in vivo. Our findings provide new insight and mechanism of ginsenosideRg1 to prevent anti-GBM GN.