目的:本研究旨在确定Swertiamarin(ST)对尼古丁诱导的SD大鼠肝毒性的保护作用。
方法:使用完全随机方法将48只成年雄性SD大鼠分为6组。作为一种控制,I组给予口服(PO)生理盐水。65天,第二组中的动物,III,IV,V和VI腹膜内(IP)接受2.5mg/kg/天的尼古丁,口服100mg/kg/天的ST(PO),口服200mg/kg/天ST(PO),2.5毫克/千克/天的尼古丁(IP)+100毫克/千克/天的ST(PO),和2.5mg/kg/天的尼古丁(IP)+200mg/kg/天的ST(PO)。在第66天处死动物,取出肝组织并用于组织病理学分析以及生化测试(氧化应激参数和肝功能酶)。
结果:与对照动物相比,第二组动物的天冬氨酸转氨酶(AST)显著升高,丙氨酸氨基转移酶(ALT),尿素,和肌酐水平(P<0.001)。此外,与对照动物相比,这些动物表现出增强的肝脏氧化应激,表现为显著较高的丙二醛(MDA)水平(P<0.001)和较低水平的过氧化氢酶(CAT),谷胱甘肽(GSH),谷胱甘肽过氧化物酶(GSH-Px)和超氧化物歧化酶(SOD)(P<0.001)。Further,与对照大鼠相比,尼古丁治疗大鼠的肝脏中观察到更多的组织学异常,包括显著的空泡化,不良的组织结构,侏儒核的生长,和扩张的正弦。与尼古丁治疗的大鼠相反,观察到ST和尼古丁的共同给药可以预防尼古丁引起的异常(V组和VI组)。
结论:目前的研究结果表明,尼古丁可以严重损害肝脏组织,Swertiamarin可以防止尼古丁对大鼠肝脏的有害影响。未来的研究有必要深入研究Swertiamarin对尼古丁诱导的肝毒性的保护作用背后的机制。
OBJECTIVE: The current investigation was aimed to determine the hepatoprotective benefits of Swertiamarin (ST) administration against nicotine-induced hepatotoxicity in SD rats.
METHODS: A total of 48 adult male SD rats were allocated into six groups using a fully randomised approach. As a control, group I was given oral (PO) normal saline. For 65 days, the animals in groups II, III, IV, V and VI received 2.5mg/kg/day of nicotine intraperitoneally (IP), 100mg/kg/day of ST orally (PO), 200mg/kg/day of ST orally (PO), 2.5mg/kg/day of nicotine (IP)+100mg/kg/day of ST (PO), and 2.5mg/kg/day of nicotine (IP)+200mg/kg/day of ST (PO), respectively. Animals were killed on 66thday, liver tissue was removed and used for histopathological analysis as well as biochemical testing (oxidative stress parameters and liver function enzymes).
RESULTS: When compared to control animals, the animals in group II showed a substantial rise in their aspartate aminotransferase (AST), alanine aminotransferase (ALT), urea, and creatinine levels (P˂0.001). Furthermore, compared to control animals, these animals displayed enhanced hepatic oxidative stress as indicated by significantly higher Malondialdehyde (MDA) levels (P˂0.001) and lower levels of Catalase (CAT), Glutathione (GSH), Glutathione peroxidase (GSH-Px) and Superoxide dismutase (SOD) (P˂0.001). Further, more histological anomalies were seen in the liver of nicotine-treated rats compared to control rats, including significant vacuolization, poor tissue architecture, the growth of pycnotic nuclei, and dilated sinusoids. Contrary to nicotine-treated rats, the co-administration of ST and nicotine was observed to prevent the abnormalities caused by nicotine (groups V and VI).
CONCLUSIONS: The results of the current study show that nicotine can seriously harm liver tissue and that swertiamarin can prevent the harmful effects of nicotine on rat liver. Future research is necessary to delve deeply into the mechanisms behind swertiamarin protective impact against nicotine-induced hepatotoxicity.