Srilaxmi Polimetla, Sareddy Gangadhara Reddy, Kavi Kishor Polavarapu Bilhan, Setty Oruganti Hussainaiah, Babu Phanithi Prakash
Department of Genetics, Osmania University, Hyderabad, India.
BMC Pharmacol. 2010 Oct 12;10:13. doi: 10.1186/1471-2210-10-13.
Carbon tetra chloride (CCl4), an industrial solvent, is a hepatotoxic agent and it is the well established animal model for free radical-induced liver injury. The present investigation was carried out to establish the protective effect of natansnin, a novel dibenzoyl glycoside from Salvinia natans against CCl4 induced oxidative stress and cellular degeneration in rat liver.
CCl4 significantly increased the levels of lipid peroxides, oxidized glutathione and decreased the levels of reduced glutathione, SOD and CAT. CCl4 induce marked histopathological changes and increase in the levels of apoptotic proteins. CCl4 treatment significantly increased the levels of apoptotic proteins such as caspases-3, PARP, Bax, Bid and cytochrome C and also increased the levels of inflammatory mediators iNos and Cox-2. Natansnin treatment significantly decreased the levels of CCl4 induced apoptotic proteins and inflammatory mediators. Further natansinin treatment significantly inhibited the CCl4 induced apoptosis which was evident form the reduced TUNEL positive cells.
In conclusion, our study demonstrated the protective effect of natansnin against CCl4 induced oxidative stress and cellular degeneration in rat liver tissue. This protective effect of natansnin can be correlated to its direct antioxidant effect.
四氯化碳(CCl4)是一种工业溶剂,是一种肝毒性剂,是自由基诱导肝损伤的成熟动物模型。本研究旨在确定来自槐叶苹的新型二苯甲酰糖苷——槐叶苹苷对CCl4诱导的大鼠肝脏氧化应激和细胞变性的保护作用。
CCl4显著增加脂质过氧化物、氧化型谷胱甘肽水平,降低还原型谷胱甘肽、超氧化物歧化酶和过氧化氢酶水平。CCl4诱导明显的组织病理学变化并增加凋亡蛋白水平。CCl4处理显著增加凋亡蛋白如半胱天冬酶-3、聚(ADP-核糖)聚合酶、Bax、Bid和细胞色素C的水平,还增加炎症介质诱导型一氧化氮合酶和环氧化酶-2的水平。槐叶苹苷处理显著降低CCl4诱导的凋亡蛋白和炎症介质水平。此外,槐叶苹苷处理显著抑制CCl4诱导的凋亡,这从TUNEL阳性细胞减少可以明显看出。
总之,我们的研究证明了槐叶苹苷对CCl4诱导的大鼠肝组织氧化应激和细胞变性具有保护作用。槐叶苹苷的这种保护作用可能与其直接的抗氧化作用有关。