Ginsenoside-Rg1 protects podocytes from complement mediated injury.

Abstract

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.

• Authors: Ming-Hua Zhang, Jun-Ming Fan, Xi-Sheng Xie, Yue-Yi Deng, Yi-Pin Chen, Rong Zhen, Jing Li, Yuan Cheng, Ji Wen
• Journal: Journal of ethnopharmacology (J Ethnopharmacol) Vol. 137 Issue 1 Pg. 99-107 (Sep 01 2011) ISSN: 1872-7573 [Electronic] Ireland
• PMID: 21600971 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.

Chemical References

• Actins
• Antioxidants
• Complement Membrane Attack Complex
• Ginsenosides
• Reactive Oxygen Species
• Extracellular Signal-Regulated MAP Kinases
• JNK Mitogen-Activated Protein Kinases
• p38 Mitogen-Activated Protein Kinases
• ginsenoside Rg1

Topics

• Actins (metabolism)
• Animals
• Antioxidants (pharmacology)
• Blotting, Western
• Cell Line, Transformed
• Complement Activation
• Complement Membrane Attack Complex (metabolism)
• Cytoprotection
• Dose-Response Relationship, Drug
• Enzyme Activation
• Extracellular Signal-Regulated MAP Kinases (metabolism)
• Flow Cytometry
• Ginsenosides (pharmacology)
• JNK Mitogen-Activated Protein Kinases (metabolism)
• Mice
• Microscopy, Electron, Scanning
• Microscopy, Fluorescence
• Podocytes (drug effects, immunology, metabolism, pathology)
• Reactive Oxygen Species (metabolism)
• Time Factors
• p38 Mitogen-Activated Protein Kinases (metabolism)