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Background Its widely accepted thatTumor Necrosis Factor-α (TNF-α) plays an important role in the pathogenesis of emphysema.This study aimed at investigating the protective effects of anti-TNF-α antibody,infliximab onemphysema induced by passive smoking in rats and the mechanisms involved in its effect.Methods Thirty-nine rats were randomly divided into a normal control group,an emphysema group,and an infliximab-intervention group.Rat models of emphysema were established by exposure to cigarette smoking daily for 74 days.After 1 month,infliximab-intervention group was interfered with intliximab subcutaneous injection.The levels of TNF-α,IL-8 and VEGF in BALF were measured with ELISA.Lung tissure section stained by hematoxylin and eosin (HE) was observed,mean linear intercept (MLI) and mean alveolar numbers (MAN)measured.Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling(TUNEL)methods were carded out to examine the percentage of positive cells and distribution of apoptotic cells.Results The levels of TNF-α and IL-8 in BALF were higher in emphysema group than in the normal control and infliximab-intervention group.MLI was higher in emphysema rats than that in the normal control and infliximab-intervention group while MAN was decreased on the contrary.The concentrations of VEGF in BALF of emphysema group were significantly decreased as compared with normal control group.The number of TUNEL positive cells in alveolar septa was significantly increased in emphysema group as compared with normal control group and infliximab-intervention group.Conclusions Infliximab has protective effects on smoking-induced emphysema by reducing inflammatory cytokine levels,improving pathological changes and attenuating alveolar septa cell apoptosis.