Aim of the study: Podocytes injury mediated by complement complex C5b-9 is the main feature of membranous nephropathy (MN). Little work has been done to prove that ginsenoside-Rg1 could inhibit this process. Our study aims to investigate the efficacy of ginsenoside-Rg1 in protecting the podocyte from complement mediated injury.
Materials and methods: We chose sublethal C5b-9 induced podocyte injury as the model of MN in vitro. Ginsenoside-Rg1 was given as an intervention. Morphological changes were observed by electron microscope and fluorescence microscope. The production of reactive oxygen species (ROS) was detected by flow cytometry. The expression of the mitogen activated protein kinase (MAPK) including JNK, ERK and P38 was detected by western-blot technique.
Results: Ginsenoside-Rg1 could protect foot processes of podocytes, suppress the damage of F-actin, decrease the production of ROS, and inhibit the activation of P38 kinase pathway.
Conclusion: These results suggest that ginsenoside-Rg1 could protect podocyte from sMAC-induced injury partly because of its antioxidant property and inhibit the activation of P38 kinase pathway. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
[1]Sichuan Univ, Dept Nephrol, W China Hosp, Chengdu 610041, Sichuan, Peoples R China.
[2]Sichuan Univ, State Key Lab Biotherapy, Chengdu 610041, Sichuan, Peoples R China.
[3]Luzhou Med Coll, Dept Nephrol, Affiliated Hosp, Luzhou City, Peoples R China.
[4]Nanchong Cent Hosp, N Sichuan Med Coll, Clin Med Inst 2, Dept Nephrol, Nanchong City, Peoples R China.
[5]Shanghai Tradit Chinese Med Univ, Longhua Hosp, Dept Nephrol, Shanghai, Peoples R China.
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