Abstract

Objective To investigate the effects of penequinine hydrochloride on receptor for advanced glycation end products (RAGE) expression in rats with lipopolysaccharide (LPS)-induced acute lung injury,its correlation with nuclear factor-kappaB (NF-κB) in the lung tissue,and the effect on tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) expression.Methods 30 male SD rats were randomly divided into three groups:control group,LPS group and penequinine hydrochloride group (n =10 each).The rats in the LPS group and penequinine hydrochloride group were injected intravenously with LPS (5 mg/kg) via tail vein to induce acute lung injury.The rats in penequinine hydrochloride group were injected intraperitoneally with penequinine hydrochloride (1 mg/kg body weight),and those in control group with the same volume of normal saline.All rats were sacrificed at 6 h later.The levels of TNF-α and IL-1 β in left bronchoalveolar lavage fluid (BALF) were determined by using enzyme linked immunosorbent assay (ELISA).The expression of RAGE in BALF and NF-κB p65 in the right lung was detected by using Western blotting.Results As compared with control group,the ALI scores (12.28 ±2.42),and the expression of TNF-α [(167.27 ± 23.61) ng/L],IL-1β [(114.38 ± 15.14) ng/L],RAGE (0.74 ± 0.15) and NF-κB p65 (0.69± 0.12) were significantly increased in LPS group (P < 0.01).As compared with LPS group,the ALI scores (8.93 ± 1.86),and the expression of TNF-α [(118.64 ± 19.43) ng/L],IL-1β [(98.16 ± 12.55) ng/L],RAGE (0.43 ±0.08) and NF-κB p65 (0.49 ±0.10) were significantly reduced in penequinine hydrochloride group (P < 0.05).Conclusion Penequinine hydrochloride has protective effects on LPS-induced acute lung injury in rats through inhibiting the expression of RAGE. Key words: Penequinine hydrochloride; Lipopolysaccharide; Acute lung injury; Receptor for advanced glycation end products; Nuclear factor-κB

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