Abstract: PO0949
Shen-Qi-Yan-Shen Formula Attenuates Diabetic Renal Lipid Deposition by Down-Regulating Proteoglycan Expression
Session Information
- Diabetic Kidney Disease: New Pathways and Therapies
October 22, 2020 | Location: On-Demand
Abstract Time: 10:00 AM - 12:00 PM
Category: Diabetic Kidney Disease
- 601 Diabetic Kidney Disease: Basic
Authors
- Li, Ying, Chongqing Traditional Chinese Medicine Hospital, Chongqing, China
- Xiong, Weijian, Chongqing Traditional Chinese Medicine Hospital, Chongqing, China
Background
Renal lipid deposition is a crucial factor in the pathophysiology of diabetic nephropathy (DN). Proteoglycan (PG) is an important component of the extracellular matrix. Shen-Qi-Yan-Shen Formula (SQYSF) is a clinical empirical formula in treating DN. In this study, db/db mice are used to explore the potential mechanism of SQYSF by down-regulating PG expression.
Methods
We divide the mice into db/m normal control group, db/db model group, SQYSF treated group, captopril treated group, and SQYSF + captopril treated group. The groups of mice are given continuous administration of saline, SQYSF, captopril or SQYSF + captopril for 12 weeks, respectively.
Results
We have revealed that treating db/db mice with SQYSF protects them against renal injury. Our finding is supported by lower blood urea nitrogen and serum creatinine and less urinary albumin in the treated mice compared with the saline-treated db/db controls . Mice treated with SQYSF have significantly reduced protein levels of fasting blood glucose (FBG), HbA1c, TG, LDL-c and HDL-c . SQYSF markedly down-regulates protein expression of proteoglycan (PG), apoB and LDL- receptor in the db/db mice. In addition, captopril exhibits a partial inhibitory effect on PG and other proteins, which can be enhanced by SQYSF .
Conclusion
SQYSF may protect db/db mice by relieving lipid deposition through the down-regulation of PG. These encouraging results corroborate SQYSF’s potential of becoming a novel therapeutic strategy for diabetic nephropathy.
Funding
- Government Support - Non-U.S.