Abstract

Objective. To investigate the effects of Dendrobium officinale polysaccharides (DOPS) on the expression of inflammatory factors IL-1β and TNF-α and the MKP-1/MAPK signal pathway. Methods. PTZ-induced epileptic rat models were established. The rats were randomly divided into four groups: the control group, the DOPS group, the model group, and the DOPS intervention group. RT-PCR was used to measure the mRNA expression of IL-1β and TNF-α in the hippocampi of all groups; western blot was used to measure the protein expression of IL-1β and TNF-α and phosphorylation of ERK1/2, JNK, p38, and MKP-1 in the hippocampi of all groups at weeks 1, 2, 3, and 4 after modeling. Results. At weeks 1, 2, 3, and 4 after modeling, there were no significant differences between the control group and the DOPS group in the mRNA and protein expression of IL-1β and TNF-α and phosphorylation of ERK1/2, JNK, p38, and MKP-1 (all P>0.05); the mRNA and protein expression of IL-1β and TNF-α and phosphorylation of ERK1/2, JNK, and p38 were significantly increased, while the phosphorylation of MKP-1 was decreased in the model group compared with the control group. The mRNA and protein expression of IL-1β and TNF-α and phosphorylation of ERK1/2, JNK, and p38 were significantly decreased, while the phosphorylation of MKP-1 was increased in the DOPS intervention group compared with the model group. Conclusion. DOPS can reduce PTZ-induced brain inflammation and seizures of epileptic rats by inhibiting IL-1β, TNF-α, and MAPK signal pathways.

Highlights

  • Epilepsy is one of the most common chronic brain diseases characterized by frequent recurrent seizures [1], as well as emotional and cognitive dysfunction [2]

  • It is reported that the expression of mRNA and the protein level of various proinflammatory cytokines in epileptics and rat models were increased, such as tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β) [4, 5]

  • IL-1β single nucleotide polymorphism was associated with temporal lobe epilepsy [7], and downregulation of the IL-1β signal delayed the onset of seizures, preventing the generalization of epilepsy, and elevated the threshold for post-discharge induction [8]

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Summary

Introduction

Epilepsy is one of the most common chronic brain diseases characterized by frequent recurrent seizures [1], as well as emotional and cognitive dysfunction [2]. IL-1β single nucleotide polymorphism was associated with temporal lobe epilepsy [7], and downregulation of the IL-1β signal delayed the onset of seizures, preventing the generalization of epilepsy, and elevated the threshold for post-discharge induction [8]. These studies indicated that inflammatory factors played a key role in the development of epilepsy. This study will investigate the effects of DOPS on brain inflammation in SD epileptic rats and its mechanism

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