Student Research Committee, Shahrekord University of Medical Sciences, Shahrekord, Iran.
Clinical Biochemistry Research Center, Shahrekord University of Medical Sciences, Shahrekord, Iran.
Pharmacol Rep. 2017 Aug;69(4):830-835. doi: 10.1016/j.pharep.2017.03.011. Epub 2017 Mar 23.
Fluoxetine-induced liver damage is a cause of chronic liver disease. In the present study the hepatoprotective effects of gallic acid against fluoxetine-induced liver damage were examined.
Forty-eight male rats were divided into six groups as follow: group 1, the control group; group 2, rats receiving fluoxetine (24mg/kg bw daily, po) without treatment; group 3, rats receiving 24mg/kg bw fluoxetine, treated with 50mg/kg bw silymarin and groups 4, 5, and 6 in which gallic acid (50, 100, and 200mg/kg bw, po, respectively) was prescribed after the consumption of fluoxetine. The histopathological changes of hepatic tissues were checked out.
Fluoxetine caused a significant increase in the levels of serum glutamate oxaloacetate transaminase (GOT), serum glutamate pyruvate transaminase (GPT), lipid profiles, urea, fasting blood sugar (FBS), creatinine (Cr), protein carbonyl (PC) content, malondialdehyde (MDA), and liver TNF-α as an inflammatory element. Also, the obtained results of group 2 revealed a significant decline in ferric reducing ability of plasma (FRAP), liver catalase (CAT), superoxide dismutase (SOD), and vitamin C levels. The treatment with gallic acid showed significant ameliorations in abnormalities of fluoxetine-induced liver injury as represented by the improvement of hepatic CAT, SOD activities, vitamin C levels, serum biochemical parameters, and histopathological changes, in addition to the recovery of antioxidant defense system status.
Gallic acid has inhibitory effects on fluoxetine-induced liver damage. The effect of gallic acid is derived from free radical scavenging properties and the anti-inflammatory effect related to TNF-α.
氟西汀引起的肝损伤是慢性肝病的一个原因。本研究考察了没食子酸对氟西汀诱导的肝损伤的保护作用。
将 48 只雄性大鼠分为 6 组：第 1 组，对照组；第 2 组，给予氟西汀（24mg/kg bw 每日，po）未治疗；第 3 组，给予 24mg/kg bw 氟西汀，用 50mg/kg bw 水飞蓟素治疗；第 4、5、6 组分别给予 50、100、200mg/kg bw 没食子酸（po）。检查肝组织的组织病理学变化。
氟西汀导致血清谷氨酸草酰乙酸转氨酶（GOT）、血清谷氨酸丙酮酸转氨酶（GPT）、血脂谱、尿素、空腹血糖（FBS）、肌酐（Cr）、蛋白羰基（PC）含量、丙二醛（MDA）和肝 TNF-α水平显著升高，作为炎症因子。此外，第 2 组的结果表明，血浆铁还原能力（FRAP）、肝过氧化氢酶（CAT）、超氧化物歧化酶（SOD）和维生素 C 水平显著下降。没食子酸治疗显著改善了氟西汀诱导的肝损伤异常，表现为肝 CAT、SOD 活性、维生素 C 水平、血清生化参数和组织病理学变化的改善，以及抗氧化防御系统状态的恢复。
没食子酸对氟西汀诱导的肝损伤有抑制作用。没食子酸的作用来源于清除自由基的特性和与 TNF-α相关的抗炎作用。
