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首页> 外文期刊>Experimental and therapeutic medicine >Protective effect of Fructus corni polysaccharide on hippocampal tissues and its relevant mechanism in epileptic rats induced by lithium chloride-pilocarpine
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Protective effect of Fructus corni polysaccharide on hippocampal tissues and its relevant mechanism in epileptic rats induced by lithium chloride-pilocarpine

机译:果酱多糖对氯化锂 - 毛甘油酸锂诱导的癫痫大鼠海马组织及其相关机制的保护作用及其相关机制

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The aim of the present study was to investigate the potential effect of Fructus corni polysaccharide (PFC) on the hippocampus tissues in epileptic rats induced by lithium chloride-pilocarpine, and to explore the underlying mechanism. The epileptic rat models were established using lithium chloride-pilocarpine treatment. According to the dosage of PFC, the rat models were divided into three groups: The low-dose (100 mg/kg/day), middle-dose (200 mg/kg/day) and high-dose (300 mg/kg/day) groups. The intervention for rat models lasted for 24 days. Subsequently, the production levels of reactive oxygen species (ROS) and malondialdehyde (MDA), the activity of superoxide dismutase (SOD), the mitochondrial membrane potential and the expressions of mitogen-activated protein kinase [P-38, Janus kinase (JNK) and extracellular signal-regulated kinase 1/2], cytochrome-C and caspase-3 in hippocampal tissues were detected. In addition, the structure of the CA-1 region of the hippocampus was also observed. Compared with the control group, the production levels of ROS were increased and the mitochondrial membrane potential was decreased in the hippocampus tissues of rats in the model group. In addition, in the model group, it was observed that MDA content was increased, SOD activity was decreased, and the expressions of phosphorylated (p)-p38, p-JNK, cytochrome-c and caspase-3 were increased, compared with the control group. Furthermore, those abnormal variations of the indicators were reversed by the intervention of PFC. These findings suggest that PFC can ameliorate the secondary damage to the hippocampi of epileptic rats, and that the anti-oxidation and -apoptosis effects of PFC may be associated with the mechanism that provides a protective effect for hippocampal tissues.
机译:本研究的目的是探讨Fructus Corni多糖(PFC)对氯化锂 - 氟碳碱诱导的癫痫大鼠海马组织的潜在影响,并探讨下面的机制。使用氯化锂 - 汲取燃烧剂处理建立癫痫大鼠模型。根据PFC的剂量,将大鼠模型分为三组:低剂量(100mg / kg /天),中剂量(200mg / kg /天)和高剂量(300mg / kg /日)群体。大鼠模型的干预持续了24天。随后,反应性氧物质(ROS)和丙二醛(MDA)的生产水平,超氧化物歧化酶(SOD)的活性,线粒体膜电位和丝裂剂活化蛋白激酶的表达[P-38,Janus激酶(JNK)和细胞外信号调节激酶1/2],海马组织中的细胞色素-C和Caspase-3。此外,还观察到海马的Ca-1区的结构。与对照组相比,ROS的生产水平增加,模型组大鼠的海马组织中的线粒体膜电位降低。此外,在模型组中,观察到MDA含量增加,SOD活性降低,与磷酸化(P)-P38,P-JNK,细胞色素-C和Caspase-3的表达增加,相比控制组。此外,通过PFC的干预,指标的那些异常变化是逆转的。这些发现表明,PFC可以改善癫痫大鼠海马的二次损害,并且PFC的抗氧化和凋亡作用可能与为海马组织提供保护作用的机制有关。

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