Effects of capsaicin on oxidative stress in lipopolysaccharide-induced acute lung injury in mice / 中华急诊医学杂志

ABSTRACT

Objective To investigate the effects of transient receptor potential vanilloid 1 activation by capsaicin on the oxidative stress in lipopolysaccharide-induced lung injury in mice in order to elucidate the potential mechanisms.Methods A total of 108 specific pathogen free (SPF) ICR male mice were randomly divided into six groupsnormal control group (n =18),capsaicin control group (CAP control group,n =18),capsazepine control group (CAPZ control group,n =18),acute lung injury group (n =18),capsaicin treatment group (CAP treatment group,n =18) and capsazepine treatment group (CAPZ treatment group,n =18).After modeling,superoxide dismutase (SOD),catalase (CAT) and malondiachehyche (MDA) levels in lung were measured with the method of chromatometry,and the expression of heme oxygenase 1 (HO-1) in lung tissue was assessed with enzyme linked immunosorbent assay (ELISA),while the level of NF-E2-related factor-2 (Nrf2) was determined by western blotting and the expression of Nrf2 mRNA was measured by RTPCR.Pathological changes of lung tissue were observed under light microscope.Results The activities of SOD and CAT in lung tissue at 3,8,16 h were dramatically lower in acute lung injury group than those in normal control group (P ＜ 0.05),while the level of MDA was higher.Compared with acute lung injury group,the lung levels of SOD and CAT at 8 h and 16 h were higher in CAP treatment group (P ＜0.05),while the lung level of MDA was lower (P ＜ 0.05).The levels of SOD and CAT in CAPZ treatment group were decreased at 8 h and 16 h,while the levels of MDA in this group were increased at 3,8,16 h (P ＜0.05).The pulmonary levels of HO-1,Nrf2 and expression of Nrf2 mRNA were significantly higher in acute lung injury group than those in normal control group (P ＜ 0.05).Compared with acute lung injury group,the levels of HO-1,NRF2 and expression of NRF2 mRNA were increased markedly in CAP treatment group (P ＜ 0.05)and were obviously decreased in CAPZ treatment group (P ＜0.05).At 8 h,16 h after modeling,the degree of lung damage was ameliorated in CAP treatment group compared with acute lung injury group under light microscope,while the lung damage was aggravated in CAPZ treatment group.Conclusions The activation of TRPV1 could apparently up-regulate the levels of CAT,SOD,Nrf2,HO-1,and reduce the MDA level in lung tissue of mice with acute lung injury,ultimately protecting the endotoxemia mice from oxidative stress.