Kinase

MAPK/ERK pathway

NF-κB

Lipopolysaccharide

Endocrinology

Neuroinflammation

p38 mitogen-activated protein kinases

Signal transduction

Nitric oxide

Biochemistry

Phosphorylation

Microglia

Hippocampus

Inflammation

Internal medicine

Pharmacology

Nitric oxide synthase

Medicine

Chemistry

Tumor necrosis factor alpha

IκBα

Brain Research

Microglial activation plays a pivotal role in the pathogenesis of neurodegenerative diseases by producing various pro-inflammatory cytokines and nitric oxide (NO). In the paper, the anti-inflammatory effect of ginsenoside Rg1 was investigated in mice intracerebroventricular injected of lipopolysaccharide (LPS). NO and tumor necrosis factor (TNF)-α production in both cerebral cortex and hippocampus decreased at dose-dependent manner by oral administration with Rg1. And the expression of ionized calcium binding adaptor molecule 1 (Iba-1) increased in both cerebral cortex and hippocampus in LPS-injected group compared to that in control group. However, Rg1 inhibited microglial activation by suppressing Iba-1 expression. In addition, the expression of inducible nitric oxide synthase (iNOS) was inhibited by Rg1. Moreover, Rg1 suppressed the phosphorylation level of IκB, nuclear translocation of p65 subunit of NFκB, and phosphorylation level of p38, ERK1/2, JNK mitogen-activated protein kinase (MAPK) induced by LPS. Concluding, Rg1 inhibited the inflammation mediated by LPS by suppressing NFκB and MAPK pathway, which provided the explanation for its therapeutic effect on neurodegenerative diseases.

Inhibitory effect of ginsenoside Rg1 on lipopolysaccharide-induced microglial activation in mice