Padma Viswanadha Vijaya, Baskaran Rathinasamy, Divya Subramani, Priya Lohanathan Bharathi, Saranya Sithuraj
Translational Research Laboratory, Department of Biotechnology, School of Biotechnology and Genetic Engineering, Bharathiar University, Coimbatore, Tamil Nadu, India.
DRDO BU Center for Life Science, Bharathiar University, Coimbatore, Tamil Nadu, India.
Integr Med Res. 2016 Mar;5(1):48-55. doi: 10.1016/j.imr.2015.12.005. Epub 2016 Jan 8.
Cadmium (Cd), a nonessential heavy metal, is a major environmental and public health concern. Oxidative stress plays an important role in Cd-induced kidney dysfunction. , a medicinal plant rich in phytochemicals, possesses antioxidant activity. The objective of the present study was to assess the protective effect of -stem methanolic extract (TCE) on Cd-induced nephrotoxicity in Wistar rats.
Male Wistar rats were administered ∼5 mg/kg body weight Cd orally and 100 mg/kg body weight TCE for 28 days. At the end of Cd and TCE treatment, biochemical assays were performed in serum and tissue homogenate.
Cd-induced oxidative stress in the kidney resulted in increased levels of lipid peroxidation and protein carbonyl content with a significant decrease in cellular antioxidants, such as reduced GSH, SOD, CAT, GPX, and GST. Cd-induced nephrotoxicity was further confirmed by marked changes in the histology of the kidney and increased levels of kidney markers. Additionally, Cd-treated rats showed alterations in membrane-bound ATPase activity and decreased levels of tissue glycoproteins. Cotreatment with TCE considerably reduced the biochemical alterations in serum and renal tissue induced by Cd, and also restored ATPase activity and glycoproteins to near normal levels.
Our results suggested that TCE with its antioxidant effect offered cytoprotection against Cd-induced toxicity in kidneys by restoring the altered cellular antioxidants and renal markers. TCE treatment for 28 days reversed ATPase activity and tissue glycoprotein levels. These results revealed the protective effect of TCE on Cd-induced toxicity in kidneys and oxidative stress.
镉(Cd)是一种非必需重金属,是主要的环境和公共卫生问题。氧化应激在镉诱导的肾功能障碍中起重要作用。[植物名称]是一种富含植物化学物质的药用植物,具有抗氧化活性。本研究的目的是评估[植物名称]茎甲醇提取物(TCE)对Wistar大鼠镉诱导的肾毒性的保护作用。
雄性Wistar大鼠口服约5 mg/kg体重的镉和100 mg/kg体重的TCE,持续28天。在镉和TCE治疗结束时,对血清和组织匀浆进行生化测定。
镉诱导的肾脏氧化应激导致脂质过氧化水平和蛋白质羰基含量增加,细胞抗氧化剂如还原型谷胱甘肽、超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶和谷胱甘肽S-转移酶显著减少。肾脏组织学的明显变化和肾脏标志物水平的升高进一步证实了镉诱导的肾毒性。此外,镉处理的大鼠显示膜结合ATP酶活性改变,组织糖蛋白水平降低。与TCE联合治疗可显著降低镉诱导的血清和肾组织生化改变,并使ATP酶活性和糖蛋白恢复到接近正常水平。
我们的结果表明,TCE具有抗氧化作用,通过恢复改变的细胞抗氧化剂和肾脏标志物,对镉诱导的肾脏毒性提供细胞保护。TCE治疗28天可逆转ATP酶活性和组织糖蛋白水平。这些结果揭示了TCE对镉诱导的肾脏毒性和氧化应激的保护作用。
需注意,原文中部分植物名称未给出具体内容,我用[植物名称]进行了替代。