PDF(Pubmed)
Abstract：
The aim of this study was to investigate the effect of hesperidin on the liver and kidney dysfunctions induced by nickel. The mice were divided into six groups: nickel treatment with 80 mg/kg, 160 mg/kg, 320 mg/kg hesperidin groups, 0.5% CMC-Na group, nickel group, and blank control group. Histopathological techniques, biochemistry, immunohistochemistry, and the TUNEL method were used to study the changes in structure, functions, oxidative injuries, and apoptosis of the liver and kidney. The results showed that hesperidin could alleviate the weight loss and histological injuries of the liver and kidney induced by nickel, and increase the levels of lactate dehydrogenase (LDH), alanine aminotransferase (GPT), glutamic oxaloacetic transaminase (GOT) in liver and blood urea nitrogen (BUN), creatinine (Cr) and N-acetylglucosidase (NAG) in kidney. In addition, hesperidin could increase the activities of superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), and glutathione peroxidase (GSH-Px) in the liver and kidney, decrease the content of malondialdehyde (MDA) and inhibit cell apoptosis. It is suggested that hesperidin could help inhibit the toxic effect of nickel on the liver and kidney.
摘要：
本研究旨在探讨橙皮苷对镍所致肝肾功能损害的影响。将小鼠分为六组：以80mg/kg的镍处理，160mg/kg,320mg/kg橙皮苷组，0.5%CMC-Na基团，镍组，和空白对照组。组织病理学技术，生物化学,免疫组织化学，TUNEL方法用于研究结构的变化，功能,氧化损伤，以及肝脏和肾脏的细胞凋亡。结果表明，橙皮苷可以减轻镍引起的体重下降和肝、肾组织损伤，并增加乳酸脱氢酶（LDH）的水平，丙氨酸氨基转移酶（GPT），谷氨酸草酰乙酸转氨酶（GOT）在肝脏和血液尿素氮（BUN），肾脏中的肌酐（Cr）和N-乙酰葡萄糖苷酶（NAG）。此外,橙皮苷能提高超氧化物歧化酶(SOD)的活性,过氧化氢酶(CAT),谷胱甘肽(GSH),和谷胱甘肽过氧化物酶（GSH-Px）在肝脏和肾脏，降低丙二醛(MDA)含量,抑制细胞凋亡。提示橙皮苷有助于抑制镍对肝脏和肾脏的毒性作用。
