Neuroscience and Toxicology Unit, Pharmacology & Toxicology Department, Pharmacy College, Jazan University, Gizan, Saudi Arabia.
Neuroscience and Toxicology Unit, Pharmacology & Toxicology Department, Pharmacy College, Jazan University, Gizan, Saudi Arabia.
Exp Mol Pathol. 2018 Aug;105(1):81-88. doi: 10.1016/j.yexmp.2018.06.001. Epub 2018 Jun 20.
The aim of this research was to investigate the therapeutic potential of Vanillylacetone against carbon tetrachloride (CCl) induced hepatotoxicity in mice through understanding the serum marker, oxidative stress mechanism and cytokine networks. Carbon tetrachloride is highly hepatotoxic used as research based on animal model. The mice were classified into five groups and each had eight mice. Group-I was controlled and the vehicle was given orally. Group-II was toxic and carbon tetrachloride (1.5 ml/kg) twice a week for 15 days was administered by intra-peritoneal injections. Group- III and IV were pre-treated with Vanillylacetone 50 & 100 mg kg body weight given every day p.o. while, Group-V received only Vanillylacetone (100 mg kg body weight) for 15 days orally. The finding indicates that the administration of CCl causes significant elevation of enzyme markers, oxidative stress, inflammatory cytokine and apoptotic markers in Group-II as compared to Group-I. The administration of Vanillylacetone (50 and100 mg kg) significantly suppresses the elevated serum enzymes, oxidative stress (TBARS), an inflammatory cytokine (IL2 and TNFα) and apoptotic markers (Caspase-3 and 9) in Group-III and IV as compared to Group-II. It was also noticed that the higher dose of Vanillylacetone (100 mg) is more effective than lower dose of Vanillylacetone (50 mg). There were no significant changes observed with higher dose of Vanillylacetone (100 mg kg) in Group-V as compared to Group-I. Histopathological analysis also supported the above findings. Overall, this results shows that Vanillylacetone has a good antioxidant and therapeutic properties which can help in preventing the chemically (CCl) induced hepatotoxicity.
本研究旨在通过研究血清标志物、氧化应激机制和细胞因子网络,探讨香草乙酮(Vanillylacetone)对四氯化碳(CCl)诱导的小鼠肝毒性的治疗潜力。四氯化碳作为动物模型研究用具有高度肝毒性。将小鼠分为五组,每组 8 只。第 I 组为对照组,给予口服载体。第 II 组为中毒组,每周两次通过腹腔注射给予 1.5 ml/kg 的四氯化碳,共 15 天。第 III 组和第 IV 组分别用 50 和 100 mg/kg 体重的香草乙酮预处理,每天口服,而第 V 组仅在 15 天内口服 100 mg/kg 体重的香草乙酮。结果表明,与第 I 组相比,CCl 的给药导致第 II 组酶标志物、氧化应激、炎症细胞因子和凋亡标志物显著升高。与第 II 组相比,香草乙酮(50 和 100 mg/kg)的给药显著抑制了第 III 组和第 IV 组中升高的血清酶、氧化应激(TBARS)、炎症细胞因子(IL2 和 TNFα)和凋亡标志物(Caspase-3 和 9)。还注意到,较高剂量的香草乙酮(100 mg)比较低剂量的香草乙酮(50 mg)更有效。与第 I 组相比,第 V 组给予较高剂量的香草乙酮(100 mg/kg)没有观察到明显变化。组织病理学分析也支持了上述发现。总体而言,这些结果表明,香草乙酮具有良好的抗氧化和治疗特性,可帮助预防化学物质(CCl)引起的肝毒性。