Protective Effect of Procyanidin B2 against CCl4-Induced Acute Liver Injury in Mice

Molecules

Bing-Ya Yang²  Xiang-Yu Zhang²  Sheng-Wen Guan²  Zi-Chun Hua¹ 

[1] State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing 210023, Jiangsu, China;

关键词: procyanidin B2;    acute liver injury;    oxidative stress;    inflammatory response;    apoptosis;   

DOI  :  10.3390/molecules200712250

来源: mdpi

【 摘 要 】

Procyanidin B2 has demonstrated several health benefits and medical properties. However, its protective effects against CCl₄-induced hepatotoxicity have not been clarified. The present study aimed to investigate the hepatoprotective effects of procyanidin B2 in CCl₄-treated mice. Our data showed that procyanidin B2 significantly decreased the CCl₄-induced elevation of serum alanine aminotransferase activities, as well as improved hepatic histopathological abnormalities. Procyanidin B2 also significantly decreased the content of MDA but enhanced the activities of antioxidant enzymes SOD, CAT and GSH-Px. Further research demonstrated that procyanidin B2 decreased the expression of TNF-α, IL-1β, cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS), as well as inhibited the translocation of nuclear factor-kappa B (NF-κB) p65 from the cytosol to the nuclear fraction in mouse liver. Moreover, CCl₄-induced apoptosis in mouse liver was measured by (terminal-deoxynucleotidyl transferase mediated nick end labeling) TUNEL assay and the cleaved caspase-3. Meanwhile, the expression of apoptosis-related proteins Bax and Bcl-xL was analyzed by Western blot. Results showed that procyanidin B2 significantly inhibited CCl₄-induced hepatocyte apoptosis, markedly suppressed the upregulation of Bax expression and restored the downregulation of Bcl-xL expression. Overall, the findings indicated that procyanidin B2 exhibited a protective effect on CCl₄-induced hepatic injury by elevating the antioxidative defense potential and consequently suppressing the inflammatory response and apoptosis of liver tissues.

【 授权许可】

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