Abstract: SA-PO492
Effects of Triptolide on Macrophage Function and Phenotype by Modulating Autophagy
Session Information
- Diabetic Kidney Disease: Basic - III
November 09, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Diabetic Kidney Disease
- 601 Diabetic Kidney Disease: Basic
Authors
- Jiang, Yuteng, Institute of Nephrology, Zhong Da Hospital, Southeast University, School of Medicine, Nanjing, JIANGSU , China
- Zhao, Yu, Institute of Nephrology, Zhong Da Hospital, Southeast University, School of Medicine, Nanjing, JIANGSU , China
- Zhu, Xiaodong, Institute of Nephrology, Zhong Da Hospital, Southeast University, School of Medicine, Nanjing, JIANGSU , China
- Wu, Beibei, Institute of Nephrology, Zhong Da Hospital, Southeast University, School of Medicine, Nanjing, JIANGSU , China
- Liu, Yuqiu, Institute of Nephrology, Zhong Da Hospital, Southeast University, School of Medicine, Nanjing, JIANGSU , China
- Liu, Bi-Cheng, Institute of Nephrology, Zhong Da Hospital, Southeast University, School of Medicine, Nanjing, JIANGSU , China
- Zhang, Xiaoliang, Institute of Nephrology, Zhong Da Hospital, Southeast University, School of Medicine, Nanjing, JIANGSU , China
Group or Team Name
- Institute of Nephrology, Zhong Da Hospital, Southeast University, School of Medicine
Background
Macrophage infiltration process including capacity of adhesion migration and phenotype transformation are key points in diabetic nephropathy (DN). Triptolide (TP), a classic Chinese immunosuppressor, can alleviate macrophage infiltration effectively in renal inflammatory diseases. However, the relationships between autophagy and Triptolide are unknown. This study aims to investigate whether Triptolide affects macrophage function and phenotype through modulating autophagy.
Methods
RAW264.7 cells were divided into normal (NC) and high glucose treatment groups (HG). Triptolide (10.0ng/mL) was added to respective groups after 24 hours of cell incubated. Western blot and immunofluorescence staining were used to detect the expression of M1 macrophage marker (iNOS, TNF-α), M2 macrophage markers (MR, Arg-1) and autophagy markers (LC3, Beclin-1 and p62). The capacity of macrophage adhesion and migration with and without Triptolide treatment were assessed.
Results
Our study showed that macrophage autophagy was inhibited by HG, which results revealed a decrease expression of LC3 and Beclin-1, but increase expression of P62. Subsequently, the numbers of macrophage adhesion and migration were increased (P<0.05). HG induces M1 activation (with increase expression of iNOS and TNF-α) and inhibits M2 transformation (with increase expression of MR and Arg-1)(P<0.05). However, TP recovers macrophage autophagy level that inhibited by HG (with increase expression of LC3 and Beclin-1, whereas a reduction expression of P62), which lead to inhibition of macrophage adhesion and migration under HG (P<0.05). In addition, TP inhibits M1 macrophage transformation (with decrease expression of iNOS and TNF-α) while induces M2 macrophage activation (with increase expression of MR and Arg-1) (P<0.05).
Conclusion
HG induces classical activation of M1 macrophages and promotes macrophage adhesion and migration, which is associated with decreased autophagy level. TP promotes M2 macrophage transformation under HG through reducing expression of inflammatory factors may affect macrophage adhesion and migration, which is related to the recovery of autophagy.
Funding
- Government Support - Non-U.S.