Title:Anti-Inflammatory Effect of Ginsenoside Rg1 on LPS-Induced Septic
Encephalopathy and Associated Mechanism
Volume: 19
Issue: 1
Author(s): Yuan Chen, Miaomiao Chi, Xinyu Qiao, Jiabing Wang*Yong Jin*
Affiliation:
- Department of Neurosurgery, Municipal Hospital Affiliated to Taizhou University, Taizhou 318000, China
- Department of Neurosurgery, Municipal Hospital Affiliated to Taizhou University, Taizhou 318000, China
Keywords:
Sepsis, encephalopathy, anti-inflammatory, ginsenoside Rg1, NF-κB, MAPK.
Abstract:
Background: Sepsis frequently occurs in patients after infection and is highly associated
with death. Septic encephalopathy is characterized by dysfunction of the central nervous system, of
which the root cause is a systemic inflammatory response. Sepsis-associated encephalopathy is a
severe disease that frequently occurs in children, resulting in high morbidity and mortality.
Objectives: In the present study, we aimed to investigate the neuroprotective mechanism of ginsenoside
Rg1 in response to septic encephalopathy.
Methods: Effects of ginsenoside Rg1 on septic encephalopathy were determined by cell viability,
cytotoxicity, ROS responses, apoptosis assays, and histological examination of the brain. Inflammatory
activities were evaluated by expression levels of IL-1β, IL-6, IL-10, TNF-α, and MCP-1 using
qPCR and ELISA. Activities of signaling pathways in inflammation were estimated by the production
of p-Erk1/2/Erk1/2, p-JNK/JNK, p-p38/p38, p-p65/p65, and p-IkBα/IkBα using western blot.
Results: LPS simulation resulted in a significant increase in cytotoxicity, ROS responses, and apoptosis
and a significant decrease in cell viability in CTX TNA2 cells, as well as brain damage in rats.
Moreover, the production of IL-1β, IL-6, IL-10, TNF-α, and MCP-1 was reported to be significantly
stimulated in CTX TNA2 cells and the brain, confirming the establishment of in vitro and in vivo
models of septic encephalopathy. The damage and inflammatory responses induced by LPS were
significantly decreased by treatment with Rg1. Western blot analyses indicated that Rg1 significantly
decreased the production of p-Erk1/2/Erk1/2, p-JNK/JNK, p-p38/p38, p-p65/p65, and p-
IkBα/IkBα in LPS-induced CTX TNA2 cells and brain.
Conclusion: These findings suggested that Rg1 inhibited the activation of NF-κB and MAPK signaling
pathways, which activate the production of proinflammatory cytokines and chemokines. The
findings of this study suggested that ginsenoside Rg1 is a candidate treatment for septic encephalopathy.
