Biological and Pharmaceutical Bulletin
Online ISSN : 1347-5215
Print ISSN : 0918-6158
ISSN-L : 0918-6158
Regular Articles
LncRNA Snhg5 Attenuates Status Epilepticus Induced Inflammation through Regulating NF-κΒ Signaling Pathway
Ming WangYangmei XieYiye ShaoYinghui Chen
Author information
JOURNAL FREE ACCESS FULL-TEXT HTML

2022 Volume 45 Issue 1 Pages 86-93

Details
Abstract

Status epilepticus (SE) induced inflammation plays an important role in the pathogenesis of SE. Long non-coding RNA small nucleolar RNA host gene 5 (lncRNA Snhg5) has been reported in various inflammatory diseases. However, the mechanism of Snhg5 regulated inflammation in SE remains unclear. Therefore, this study aimed to clarify the role and mechanism of Snhg5 in SE-induced inflammation in vitro and vivo. In vitro, lipopolysaccharide (LPS)-induced inflammation in microglia was used to mimic the inflammation after SE. In vivo, SE model was induced by lithium chloride and pilocarpine. The level of Snhg5, p65, p-p65, p-inhibitor of kappaB (IκB)α, IκBα and inflammatory factors (tumor necrosis factor (TNF)-α, interleukin (IL)-1β) were measured via quantitative real-time PCR or Western blot. The Nissl stain and immunohistochemical stain were performed to observe hippocampal damage and microglia proliferation. The results showed Snhg5 was up-regulated in the rat and microglia. Knockdown of Snhg5 inhibited LPS-induced inflammation and relative expression of p-65/p65, p-IκBα/IκBα. Moreover, down-regulation of Snhg5 attenuated SE-induced inflammation and reduced the number of microglia in hippocampus. These findings indicated that Snhg5 modulates the inflammation via nuclear factor-kappaB (NF-κB) signaling pathway in SE rats.

Fullsize Image
Content from these authors
© 2022 The Pharmaceutical Society of Japan
Previous article Next article
feedback
Top