Acute alcohol intoxication is a central nervous system disease that accounts for a large number of hospital admissions. In the present study, we have explored the role of GINS complex subunit 2 (GINS2) in acute alcohol intoxication and alcohol-induced brain injury. We began by determining that GINS2 mRNA expression was significantly increased in the serum of patients with alcohol abuse. We then found that GINS2 is increased in mouse brains after alcohol consumption. To explore the role of GINS2 in alcohol-induced microglia function, we knocked down GINS2 in mouse microglia and then treated the cells with alcohol. Knockdown of GINS2 significantly increased alcohol-induced ROS production and the oxidative stress marker malondialdehyde. To explore if GINS2 is involved in alcohol-induced microglia apoptosis, we examined cell viability in GINS2 knockdown cells by TUNEL staining and caspase activity assays. Consistently, results showed that alcohol-induced cell apoptosis was promoted by knockdown of GINS2. Finally, we assessed expression levels of inflammatory factors in GINS2 knockdown microglial cells as well as the effects of GINS2 knockdown on NF-κB signalling. Inflammatory factors were stimulated by alcohol and further promoted by GINS2 knockdown, and GINS2 knockdown promoted alcohol-induced NF-κB activity in microglia.
Keywords: GINS2; NF-κB signalling; alcohol; brain injury; microglia.