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Zhiyong Cai,Jindi Liu,Hongliang Bian,Jinlan Cai,Gendi Zhu 대한약학회 2016 Archives of Pharmacal Research Vol.39 No.4
The aim of the present study was to assess theeffects and mechanisms of Schisandrin B (SchB) onlipopolysaccharide (LPS)-induced acute lung injury (ALI). ALI was induced in mice by intratracheal instillation ofLPS (1 mg/kg), and SchB (25, 50, and 75 mg/kg) wasinjected 1 h before LPS challenge by gavage. After 12 h,bronchoalveolar lavage fluid (BALF) samples and lungtissues were collected. Histological studies demonstratedthat SchB attenuated LPS-induced interstitial edema,hemorrhage, and infiltration of neutrophils in the lung tissue. SchB pretreatment at doses of 25, 50, and 75 mg/kgwas shown to reduce LPS-induced lung wet-to-dry weightratio and lung myeloperoxidase activity. In addition, pretreatmentwith SchB lowered the number of inflammatorycells and pro-inflammatory cytokines including tumornecrosis factor-a, interleukin-1b, and interleukin-6 inBALF. The mRNA and protein expression levels of nuclearfactor kappa B (NF-jB) signaling-related molecules activatedby P2X7 were investigated to determine the molecularmechanism of SchB. The findings presented heresuggest that the protective mechanism of SchB may beattributed partly to the decreased production of pro-inflammatorycytokines through the inhibition of P2X7/NFjBactivation.