Protective effect of Fructus corni polysaccharide on hippocampal tissues and its relevant mechanism in epileptic rats induced by lithium chloride‑pilocarpine

Sun,Xiaomin; Kong,Lingting; Zhou,Li

doi:10.3892/etm.2018.6142

Protective effect of Fructus corni polysaccharide on hippocampal tissues and its relevant mechanism in epileptic rats induced by lithium chloride‑pilocarpine

Authors:
- Xiaomin Sun
- Lingting Kong
- Li Zhou
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Affiliations: Department of Neurology, Weifang People's Hospital, Weifang, Shandong 261041, P.R. China, Department of Pharmacy, People's Hospital of Gaotang County, Liaocheng, Shandong 252800, P.R. China
Published online on: May 10, 2018 https://doi.org/10.3892/etm.2018.6142
Pages: 445-451

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Abstract

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.

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