Journal
AMERICAN JOURNAL OF CHINESE MEDICINE
Volume 42, Issue 5, Pages 1183-1198Publisher
WORLD SCIENTIFIC PUBL CO PTE LTD
DOI: 10.1142/S0192415X14500748
Keywords
Salvianolic Acid A; Type 2 Diabetes; Hepatic Fibrosis; alpha-SMA; TGF-beta 1; Apoptosis
Funding
- Key Project for Drug Innovation [2009ZX09102-123, 2009ZX09302-003]
- Ministry of Science and Technology of China, National Natural Science Foundation of China [2008DFA31710, 81102492]
Ask authors/readers for more resources
Type 2 diabetes patients have an increased risk of developing hepatic fibrosis. Salvianolic acid A (SalA) has been reported to be a strong polyphenolic anti-oxidant and free radical scavenger. The aim of the present study was to evaluate the effect of SalA on the pathological progression of hepatic fibrosis in high-fat diet (HFD)-fed and streptozotocin (STZ)-induced diabetic rats and to clarify the underlying mechanisms. Type 2 diabetic animal model with hepatic fibrosis was developed by a high-sucrose, HFD and low-dose STZ injection (i: p:). Diabetic rats were randomly divided into SalA group (0.3 mg/kg/day) and diabetic control groups fed with a HFD. After administration for four months, SalA reversed the hyperlipidemia and reduced hepatic triglyceride (TG). Hematoxylin-Eosin (HE) and Picro acid-Sirius red staining results indicated that SalA significantly alleviated the lesions of hepatic steatosis and fibrosis, with the reduction of type I and III collagens. The expression of alpha-smooth-muscle-actin (alpha-SMA) and transforming growth factor beta 1 (TGF-beta 1) in the liver were markedly down-regulated by SalA treatment. TUNEL staining showed that SalA reduced apoptosis in hepatocytes. In addition, SalA improved hepatic mitochondrial respiratory function in diabetic rats. Taken together, these findings demonstrated that SalA could prevent the pathological progression of hepatic fibrosis in HFD-fed and STZ-induced diabetic rats. The underlying mechanisms may be involved in reducing oxidative stress, suppressing alpha-SMA and TGF-beta 1 expression, as well as exerting anti-apoptotic and mitochondria-protective effects.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available