Picroside II Diminishes Oxidative Stress Induced By Cerebral Ischemic Injury In Rats

Abstract

Stoke is a major health problem and there is no effective treatment of the disease. Therefore, finding novel chemicals that can be used to treat stroke has been an intensive research area. Picroside II seems to be a promising compound, yet its utilization in particular, the dosage and time window of its application after stroke has not been optimized. In this study, we wanted to address this problem using Malondialdehyde (MDA) and superoxide dismutase (SOD) as two parameters. MDA, a lipid peroxidation product formed by reactions between free radicals and polyunsaturated fatty acids, can be measured to reflect the magnitude of oxidative stress [1]. The aldehyde of MDA can occur crosslinking reaction with the amino groups of phosphatidylserine in neuronal membrane phospholipids [2]. The lipid peroxidation of biomembrane and its lipid peroxide products can also implicate the protein in the membrane to result in oxidative damage and apoptosis[3,4]. The content of MDA can reflect the levels of the free radicals and lipid peroxidation in tissue [5,6]. When the level of oxygen free radicals (OFR) elevates, SOD can react with superoxide anion with the generation of hydrogen peroxide. And hydrogen peroxide (H2O2) can turn into water under the effect of catalase and glutathione peroxidase to remove the OFR to protect cells from damage. Therefore, the level of SOD activity can reflect the ability of the body in clearing OFR [7,8]. Cell culture experiments confirmed that picroside II can reduce H2O2-induced injury in PC12 cells and improve cell survival [9,10,11]. Animal experiments showed that picroside II, an active ingredient of traditional Chinese medicine, can also inhibit the expression of inflammatory factors and apoptosis in cerebral ischemic penumbra, thus improve the neurobehavioral functions in rats [12,13,14]. Our group dealt the rats with different doses of picroside II at different ischemic time, and the result showed that the optimized therapeutic dose and time window of picroside II in cerebral ischemia reperfusion injury was ischemia 1.5 h with 20mg/kg body weight by intraperitoneal injection [15]. This study was designed to detect the MDA levels and SOD activity in blood and brain tissue to further explore the anti-oxidation effect and the optimal therapeutic dose and time window of picroside II in cerebral ischemic injury. Abstract