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Salvianolic Acid A Prevents the Pathological Progression of Hepatic Fibrosis in High-Fat Diet-Fed and Streptozotocin-Induced Diabetic Rats

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机构: [1]Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China [2]Beijing Key Laboratory of Drug Target Identification and Drug Screening Beijing 100050, China [3]Xuanwu Hospital, Capital Medical University, Beijing 100053, China
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关键词: Salvianolic Acid A Type 2 Diabetes Hepatic Fibrosis alpha-SMA TGF-beta 1 Apoptosis

摘要:
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.

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出版当年[2013]版:
大类 | 4 区 医学
小类 | 3 区 全科医学与补充医学 3 区 医学:内科
最新[2025]版:
大类 | 2 区 医学
小类 | 2 区 全科医学与补充医学 2 区 医学:内科
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出版当年[2012]版:
Q1 INTEGRATIVE & COMPLEMENTARY MEDICINE Q1 MEDICINE, GENERAL & INTERNAL
最新[2023]版:
Q1 INTEGRATIVE & COMPLEMENTARY MEDICINE Q1 MEDICINE, GENERAL & INTERNAL

影响因子: 最新[2023版] 最新五年平均 出版当年[2012版] 出版当年五年平均 出版前一年[2011版] 出版后一年[2013版]

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第一作者机构: [1]Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China
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通讯机构: [*1]National Center for Pharmaceutical Screening, Institute of Materia Medica, Chinese Academy of Medical Sciences, 1 Xian Nong Tan Street, Xi Cheng District, Beijing 100050, P. R. China.
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