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

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

Abstract:

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.

原花青素B2已经证明了一些健康益处和医疗特性。然而,其对ccl4诱导的肝毒性的保护作用尚不清楚。本研究旨在探讨原花青素B2对ccl4处理小鼠的肝保护作用。我们的数据显示,原花青素B2显著降低了ccl4诱导的血清丙氨酸转氨酶活性升高,并改善了肝脏组织病理学异常。原花青素B2显著降低MDA含量,提高SOD、CAT和GSH-Px活性。进一步的研究表明,原花青素B2可降低小鼠肝脏TNF-α、IL-1β、COX-2和诱导型一氧化氮合酶(iNOS)的表达,并抑制NF-κB p65从胞质向核部分的转移。采用(末端脱氧核苷酸转移酶介导的划痕末端标记)TUNEL法和cleaved caspase-3检测ccl4诱导的小鼠肝脏凋亡。Western blot检测凋亡相关蛋白Bax、Bcl-xL的表达。结果显示,原花青素B2显著抑制ccl4诱导的肝细胞凋亡,显著抑制Bax表达上调,恢复Bcl-xL表达下调。综上所述,原花青素B2对ccl4诱导的肝损伤具有保护作用,通过提高抗氧化防御能力,从而抑制肝组织的炎症反应和凋亡。

 

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https://xueshu.baidu.com/usercenter/paper/show?paperid=0b8d8740d7398624d64274c05b299ba3&site=xueshu_se

2021年7月22日 14:20
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