; Food Processing Department, ISET, BP 377, 9100 Sidi Bouzid, Tunisia.
Eur J Pharmacol. 2011 Oct 1;668(1-2):133-9. doi: 10.1016/j.ejphar.2011.07.001. Epub 2011 Jul 13.
The antioxidant and anti-inflammatory effects of vanillin are considered as important forces in the protection against liver injury and fibrosis. This study investigated the protective effects of vanillin against carbon tetrachoride (CCl(4))-induced hepatotoxicity in rat. Pretreatment with vanillin prior the administration of CCl(4) significantly prevented the decrease of protein synthesis and the increase in plasma alanine (ALT) and aspartate (AST) aminotransferases. Furthermore, it inhibited hepatic lipid peroxidation (MDA) and protein carbonyl (PCO) formation and attenuated the (CCl(4))-mediated depletion of antioxidant enzyme catalase and superoxide dismutase (SOD) activities and glutathione level (GSH) in the liver. In addition, vanillin markedly attenuated the expression levels of pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6) and prevented CCl(4)-induced hepatic cell alteration and necrosis, as indicated by liver histopathology. These findings suggest that the antioxidant and anti-inflammatory effects of vanillin against CCl(4)-induced acute liver injury may involve its ability to block CCl(4)-generated free radicals.
香草醛的抗氧化和抗炎作用被认为是防止肝损伤和纤维化的重要因素。本研究探讨了香草醛对大鼠四氯化碳（CCl(4)）诱导肝毒性的保护作用。在给予 CCl(4)之前用香草醛预处理可显著防止蛋白质合成的减少和血浆丙氨酸（ALT）和天冬氨酸（AST）转氨酶的增加。此外，它抑制肝脂质过氧化（MDA）和蛋白质羰基（PCO）的形成，并减弱（CCl(4)）介导的肝过氧化氢酶和超氧化物歧化酶（SOD）活性以及谷胱甘肽水平（GSH）的耗竭。此外，香草醛还显著降低了促炎细胞因子如肿瘤坏死因子-α（TNF-α）、白细胞介素-1β（IL-1β）和白细胞介素-6（IL-6）的表达水平，并防止 CCl(4)诱导的肝细胞改变和坏死，如肝组织病理学所示。这些发现表明，香草醛对 CCl(4)诱导的急性肝损伤的抗氧化和抗炎作用可能与其阻断 CCl(4)生成的自由基的能力有关。
