Abstract
Objective Evaluate the role of melatonin on atmospheric fine particulate matter (PM2.5) exposed rat pulmonary inflammatory response and the influence of oxidative stress and its mechanism. Methods 48 SD rats clean level only stochastic (random number method) is divided into four groups: blank control group, NS control group, PM2.5 group and melatonin (MT) group, each group 12, injections into the lungs through the trachea PM2.5 suspension PM2.5 infected lung tissue of rats model was constructed, and through lavage solution, using HE staining and lung tissue enzyme linked immunosorbent assay (ELISA) method and protein imprinting method respectively to detect changes in lung tissue pathology, TNF-α, IL-6, IL-1, MPO, SOD, MDA and the NF-κB p65 protein expression. Results ①Compared with blank control group and NS control group, a significant lung tissue injury in rats PM2.5 group change, MT group rats lung tissue injury was significantly reduce PM2.5 group; ②PM2.5 group of rat lung tissue TNF-α, IL-6, IL-1 expression appears significantly increased (P<0.05), MT group more PM2.5 group TNF-α, IL-6, IL-1 expression decreased obviously (P<0.05); ③PM2.5 group of rat lung tissue SOD expression compared with blank control group and NS control group significantly decreased (P<0.05), while MPO and MDA increased significantly (P<0.05), while compared with PM2.5 group, MT group of rat lung tissue SOD expression appears to increase, MPO and MDA decreased (P<0.05); ④p65 protein expression in PM2.5 group was obviously raised (P<0.05), while MT group more PM2.5 group p65 protein expression decreased obviously (P<0.05). Conclusions PM2.5 can pass mediated inflammatory reaction of lung tissue and oxidative stress leads to lung tissue damage, and related to the activation of the NF-κB, MT can significantly inhibit PM2.5 caused by the NF-κB activation, reducing inflammatory reaction and oxidative stress, improve PM2.5 exposure of lung injury in rats. Key words: PM2.5; Melatonin; Lung tissue; Inflammation; Oxidative stress
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