Effect of deep-sea fish oil on PM2.5-induced inflammatory and oxidative stress damage of cardiovascular system in rats

Objective To explore the effect of deep-sea fish oil on inflammatory and oxidativestress damage of cardiovascular system caused by particulate matter ≤ 2.5 μm in aerodynamic diameter(PM2.5).Methods Male Sprague-Dawley rats were divided into low-, medium-, and high-dose deep-sea fish oil groups, deep-sea fish oil control group, solvent group(corn oil)and PM2.5 exposure group.The PM2.5 was sampled from ambient air in an urban area of Shanghai city.The rats in deep-sea fish oil groups were administered with deep-sea fish oil by gavage for 28 days and then exposed to PM2.5(8.0 mg/kg)with intratracheal instillation once the other day for 3 times.The rats in PM2.5 exposure group were bred normally for 28 days and then exposed to PM2.5 by intratracheal instillation.The rats in deep-sea fish oil and solvent control groups were administered with deep-sea fish or corn oil for 35 days, respectively.Serum interleukin 1-beta(IL-1β), interleukin 6(IL-6), tumor necrosis factor alpha(TNF-α), high sensitive C-reaction protein(hs-CRP), malondialdehyde(MDA), total superoxide dismutase(T-SOD), glutathione(GSH), and glutathione peroxidase(GSH-Px)of the rats were detected after the completion of the treatments.Results Compared with the solvent group, the contents of IL-1β(1 155.98±100.28 ng/ml), IL-6(24.94±2.06 ng/ml), TNF-α(821.45±14.26 ng/ml), hs-CRP(3.10±0.28 mg/L), and MDA(15.88±1.41 nmol/ml)increased and the contents of GSH(4.62±0.37 μmol/L), GSH-Px(289.28±30.65 U/ml), and T-SOD(239.26±4.97 U/ml)decreased in the rats of PM2.5 exposure group.Compared with the PM2.5 exposure group, the contents of IL-6(16.67±0.23 ng/mL), TNF-α(73.01±3.80 ng/mL), hs-CRP(1.36±0.22 mg/L), and MDA(11.82±0.79 nmol/mL) were decreased and GSH(24.05±3.83 μmol/L), GSH-Px(531.33±40.39 U/mL), and T-SOD(273.36±3.92 U/mL)increased in a dose-response manner in the rats of high-dose deep-sea fish oil treatment group.Conclusion Deep-sea fish oil has obvious antagonistic effect on the inflammatory reaction and oxidative stress damage caused by atmospheric PM2.5 in rats.