Cell & Molecular Research Center, Faculty of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Department of Anatomical Sciences, Faculty of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Chem Biol Interact. 2014 Sep 5;220:214-21. doi: 10.1016/j.cbi.2014.07.001. Epub 2014 Jul 10.
Many recent studies demonstrate that most nanoparticles (NPs) have an adverse or toxic action on liver. The aim of this study was to investigate the hepatoprotective effect of glycyrrhizic acid (GA) against hepatic injury induced by titanium dioxide nanoparticles (NTiO2) in rats. Thirty-two Wistar rats were randomly divided into 4 groups. NTiO2-intoxicated rats received 300 mg/kg of NTiO2 for 14 days by gavage method. Protection group pretreated with GA for 7 days before NTiO2 administration. Alanine aminotransferase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP) were detected as biomarkers in the blood to indicate hepatic injury. Product of lipid peroxidation (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GPx) were evaluated for oxidative stress in hepatic injury. Light microscopy for histopathological studies and TUNEL assay was also done. Administration of NTiO2 induced a significant elevation in plasma AST, ALT and ALP. In the liver, NTiO2 increased oxidative stress through the increase in lipid peroxidation and decrease in SOD and GPx enzymes. Histopathological studies showed that treatment with NTiO2 caused liver damage including centrilobular necrosis, which was accompanied by congestion and accumulation of inflammatory cells. Apoptotic index was also significantly increased in this group. Pretreatment of GA significantly decreased ALT, AST and ALP, attenuated the histopathology of hepatic injury, decreased apoptotic index, ameliorated oxidative stress in hepatic tissue, and increased the activities of SOD and GPx. These findings indicate that GA effectively protects against NTiO2-induced hepatotoxicity. GA has a potent protective effect against the NPs induced hepatotoxicity and might be clinically useful.
许多最近的研究表明，大多数纳米粒子（NPs）对肝脏有不良或毒性作用。本研究旨在探讨甘草酸（GA）对二氧化钛纳米粒子（NTiO2）诱导的大鼠肝损伤的保护作用。32 只 Wistar 大鼠随机分为 4 组。NTiO2 中毒组通过灌胃法给予 300mg/kg 的 NTiO2 14 天。保护组在给予 NTiO2 前用 GA 预处理 7 天。丙氨酸氨基转移酶（ALT）、天冬氨酸氨基转移酶（AST）和碱性磷酸酶（ALP）作为血液中的生物标志物，用于指示肝损伤。检测脂质过氧化产物（MDA）、超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GPx）以评估肝损伤中的氧化应激。还进行了光镜组织病理学研究和 TUNEL 测定。给予 NTiO2 可显著提高血浆 AST、ALT 和 ALP。在肝脏中，NTiO2 通过增加脂质过氧化和减少 SOD 和 GPx 酶来增加氧化应激。组织病理学研究表明，NTiO2 处理导致肝损伤，包括中央小叶坏死，伴有充血和炎症细胞积聚。该组的凋亡指数也显著增加。GA 预处理可显著降低 ALT、AST 和 ALP，减轻肝损伤的组织病理学变化，降低凋亡指数，改善肝组织氧化应激，并增加 SOD 和 GPx 的活性。这些发现表明，GA 可有效对抗 NTiO2 诱导的肝毒性。GA 对 NPs 诱导的肝毒性具有有效保护作用，可能具有临床应用价值。
