International journal of molecular medicine
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Oxidative stress and neuroinflammation are important in the pathogenesis of ageing and age‑related neurodegenerative diseases, including Alzheimer's disease. NADPH oxidase 2 (NOX2) is a major source of reactive oxygen species (ROS) in the brain. The nucleotide‑binding oligomerisation domain (NOD)‑like receptor protein 1 (NLRP1) inflammasome is responsible for the formation of pro‑inflammatory molecules in neurons. ⋯ Rg1 decreased ROS production, reducing the expression of NOX2 and the NLRP1 inflammasome in H2O2‑treated hippocampal neurons. Furthermore, Rg1 and tempol treatment significantly decreased neuronal apoptosis and the expression of β‑galactosidase, and alleviated the neuronal senescence and damage induced by H2O2. The present study indicates that Rg1 may reduce NOX2‑mediated ROS generation, inhibit NLRP1 inflammasome activation, and inhibit neuronal senescence and damage.