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[Dracorhodin perchlorate inhibit high glucose-induced connective tissue growth factor formation in human mesangial
Yonghui Wang1, Quansheng Wang, Jianguo Liu
1Department of Integrated Chinese Medicine and Western Medicine, Union Hospital, Tongfi Medical College, Huazhong Science and Technology University, Wuhan 430022, China.
Objective:
To study the effect of dracorhodin perchlorate on high glucose-induced connective tissue growth factor (CTGF) expression in human mesangial cells (HMC), and its mechanism of prevention and treatment on renal fibrosis in diabetic nephropathy (DN).
Method:
The HMC were divided into low glucose group (LG group, 5.5 mmol x L(-1) D-glucose), high glucose group (HG Group 25 mmol x L(-1) D-glucose), each group was located with dracorhodin perchlorate (7. 5 micromol x L(-1)) as comparison, and was examined at 24, 48 h. The expression of CTGF mRNA was assessed by semi quantatiue RT-PCR, and the expression of CTGF protein was assessed by Western blot.
Result:
Compared to HG group, the expression of CTGF mRNA and protein were reduced in LG group after stimulating 24, 48 hours (P < 0.01). Compared to HG group, the expression of CTGF mRNA and protein were reduced in HG group by added with dracorhodin perchlorate after stimulating 24, 48 hours (P < 0.01).
Conclusion:
Dracorhodin perchlorate can inhibit high glucose-induced connective tissue growth factor expression in human mesangial cells, and this may be its mechanism of prevention and treatment on renal fibrosis in diabetic nephropathy (DN).
Insights
Dracorhodin perchlorate effectively reduces high glucose-induced connective tissue growth factor (CTGF) expression in human mesangial cells. This finding suggests a potential therapeutic mechanism for preventing diabetic nephropathy renal fibrosis.
Area of Science:
- Biochemistry
- Cell Biology
- Pharmacology
Context:
- Diabetic nephropathy (DN) is a major complication of diabetes characterized by renal fibrosis.
- High glucose levels induce connective tissue growth factor (CTGF) expression in human mesangial cells (HMC), contributing to fibrosis.
- Understanding the molecular mechanisms underlying DN is crucial for developing effective treatments.
Purpose:
- To investigate the inhibitory effect of dracorhodin perchlorate on high glucose-induced CTGF expression in HMC.
- To explore the potential of dracorhodin perchlorate as a therapeutic agent for DN by examining its impact on CTGF.
- To elucidate the mechanism by which dracorhodin perchlorate may prevent or treat renal fibrosis in DN.
Summary:
- Human mesangial cells were exposed to low glucose (LG) or high glucose (HG) conditions, with or without dracorhodin perchlorate.
- CTGF mRNA and protein expression were measured using RT-PCR and Western blot at 24 and 48 hours.
- Dracorhodin perchlorate significantly reduced CTGF expression in HG-treated HMC compared to the HG group without treatment.
Impact:
- Dracorhodin perchlorate demonstrates potential as a therapeutic agent for diabetic nephropathy.
- Inhibition of CTGF expression by dracorhodin perchlorate offers a novel strategy for managing renal fibrosis.
- This study provides a molecular basis for the use of dracorhodin perchlorate in DN treatment.