Abstract:
Objective: To explore the relationship between apoptosis and trauma-hemorrhagic shock-induced lung injury and whether pentylenetetrazol hydrochloride (PHC) can attenuate trauma/hemorrhagic shock-induced acute lung injury by inhibiting the FAS/FASL signaling pathway.
Methods A hemorrhagic shock model due to blunt chest trauma was made. Arterial blood gas analysis, lung dry-to-wet ratio were performed. TNF-α and IL-1β content in serum, bronchoalveolar lavage fluid, and lung tissues, as well as the expression of FAS and FASL in the homogenate of lung tissues were detected using ELISA, HE staining, Tunel staining, immunohistochemistry, and Western blotting.
Results The lung dry-to-wet ratio in PHC pretreatment and post-treatment groups was significantly higher than that in the model group (P < 0.01) and lower than that in the sham-operated group (P < 0.01), and the ratio in the post-treatment group was higher than that in the PHC pretreatment group (P < 0.01). The serum levels of TNF-α and IL-1β, bronchoalveolar lavage TNF-α levels, the amount of FAS, FASL, and TNF-α in lung tissue, the amount of apoptosis by Tunel staining, and the degree of lung injury, and. the expression of FAS and FASL detected by Western blotting were significantly lower than those of the model group (P < 0.01) and higher than those of the sham-operated group; and those measures of the PHC pretreatment were lower than those of the PHC post-treatment group,
Conclusions : FAS/FASL expression is significantly upregulated after trauma/hemorrhagic shock. PHC may attenuate trauma/hemorrhagic shock-induced acute lung injury by inhibiting the expression of the FAS/FASL signaling pathway and attenuating apoptosis.