Helicid Reverses Lipopolysaccharide‐Induced Inflammation and Promotes GDNF Levels in C6 Glioma Cells through Modulation of Prepronociceptin

Helicid suppresses inflammatory factors and protects nerve cells in the hippocampus of rats with depression, but the mechanisms underlying its protective effects are unclear at present. In this investigation, we conducted gene silencing, Helicid intervention and rescue experiments to explore the pro...

Full description

Saved in:
Bibliographic Details
Published in:Chemistry & biodiversity 2020-07, Vol.17 (7), p.e2000063-n/a
Main Authors: Zhang, Yuanxiang, Luan, Di, Liu, Yanhao, Li, Hongjin, Dong, Jian, Zhang, Xiaotong, Yuan, Lili, Zhong, Zhengling, Jiang, Lan, Li, Xuyi, Ye, Mingquan, Tong, Jiucui
Format: Article
Language:English
Subjects:
Acidic oxides
AKT protein
Cell lines
Enzyme-linked immunosorbent assay
Flow cytometry
GDNF
Gene silencing
Glial cell line-derived neurotrophic factor
Glial fibrillary acidic protein
Glioma
Glioma cells
Helicid
Immunofluorescence
Inflammation
inflammatory
Lipopolysaccharides
Neuronal-glial interactions
Oxidative stress
prepronociceptin (PNOC)
Signal transduction
Signaling
Western blotting
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Helicid suppresses inflammatory factors and protects nerve cells in the hippocampus of rats with depression, but the mechanisms underlying its protective effects are unclear at present. In this investigation, we conducted gene silencing, Helicid intervention and rescue experiments to explore the protective actions of PNOC, the prepronociceptin gene known to regulate inflammatory processes, and Helicid on a C6 cell model of inflammation induced by LPS. Collective data from Western blots, ELISA, immunofluorescence and flow cytometry experiments showed that PNOC silencing or administration of Helicid led to reduced inflammatory factor levels, oxidative stress and expression of glial fibrillary acidic protein (GFAP), along with increased glial cell lines‐derived neurotrophic factor (GDNF) expression. Furthermore, expression of p‐Akt in the Akt signaling pathway was increased. Interestingly, overexpression of PNOC in the Helicid treatment group partially reversed the Helicid‐induced changes in the above biochemical indexes. Our collective results provide strong evidence of Helicid‐mediated regulation of the Akt signaling pathway through PNOC to improve cell inflammation and oxidative stress.
ISSN:1612-1872
1612-1880
DOI:10.1002/cbdv.202000063