Ginsenoside Rg1 alleviates lipopolysaccharide-induced neuronal damage by inhibiting NLRP1 inflammasomes in HT22 cells

xlomafota13 shared this article with you from Inoreader Ginsenoside Rg1 alleviates lipopolysaccharide-induced neuronal damage by inhibiting NLRP1 inflammasomes in HT22 cells Via Experimental and therapeutic medicine Exp Ther Med. 2021 Jul;22(1):782. doi: 10.3892/etm.2021.10214. Epub 2021 May 19. ABSTRACT Lipopolysaccharide (LPS) is a toxic component of cell walls of Gram-negative bacteria that are widely present in gastrointestinal tracts. Increasing evidence showed that LPS plays important roles in the pathogeneses of neurodegenerative disorders, such as Alzheimer's disease (AD). NADPH oxidase s2 (NOX2) is a complex membrane protein that contributes to the production of reactive oxygen species (ROS) in several neurological diseases. The NLRP1 inflammasome can be activated in response to an accumulation of ROS in neurons. However, it is still unknown whether LPS exposure can deteriorate neuronal damage by activating NOX2-NLRP1 inflammasomes. Ginsenoside Rg1 (Rg1) has protective effects on neurons, although whether Rg1 alleviates LPS-induced neuronal damage by inhibiting NOX2-NLRP1 inflammasomes remains unclear. In the present study, the effect of concentration gradients and different times of LPS exposure on neuronal damage was investigated in HT22 cells, and further observed the effect of Rg1 treatment on NOX2-NLPR1 inflammasome activation, ROS production and neuronal damage in LPS-treated HT22 cells. The results demonstrated that LPS exposure significantly induced NOX2-NLRP1 inflammasome activation, excessive production of ROS, and neuronal damage in HT22 cells. It was also shown that Rg1 treatment significantly decreased NOX2-NLRP1 inflammasome activation and ROS production and alleviated neuronal damage in LPS-induced HT22 cells. The present data suggested that Rg1 has protective effects on LPS-induced neuronal damage by inhibiting NOX2-NLRP1 inflammasomes in HT22 cells, and Rg1 may be a potential therapeutic approach for delaying neuronal damage in AD. PMID:34055081 | PMC:PMC8145787 | DOI:10.3892/etm.2021.10214 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.