Objective To assess the effects of NOX2 (nicotinamide adenine dinucleotide phosphate oxidase) inhibitor gp91 ds-tat on lung injury of rats caused by gas explosion.
Methods A total of 90 SD male rats were randomly divided into control group, gas explosion lung injury model group, and NOX2 inhibitor gp91 ds-tat group(n=30/group). The rats in the model group and gp91 ds-tat group were placed in the alleyway 240 m away from the point of detonation. After the explosion, the rats of the gp91 ds-tat group were immediately given once intraperitoneal injection of gp91 ds-tat (1 mg/kg). Then the rats were anaesthetized with blood taken from the abdominal aorta at 24 h, 72 h and 7 d (10 rats in each group) and then executed, respectively. ATP, α -KGDH, ICDHm and PFK were detected in frozen lung tissues. The expression levels of NOX2, CAT protein and mRNA as well as the expression of mitochondrial function -related protein genes were also detected with western blotting and real-time quantitative PCR in rat lung tissues.
Results Lung bleeding and collapse were observed in the model group, and the expression of CAT, AMPK, TFAM decreased (P < 0.05), but the expression of NOX2 increased significantly(P < 0.05). Compared with the model group, levels of α-KGDH, ICDHm, PFK and ATP in gp91 ds-tat treatment group increased (P < 0.05), the relative mRNA expression of CAT and TFAM increased(P < 0.05), and the expression of NOX2 decreased(P < 0.05).
Conclusions Gp91 ds-tat could reduce the lung injury degree in gas explosion injury by regulating the disorder of energy metabolism and oxidative stress status in the lung, and its effect may be related to the inhibition of NOX2 expression.
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