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Protective effects of Toll-like receptor 4 inhibitor on myocardial injury and lung injury in sepsis rat model
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作者 rong-bing he Zhao-Fen Lin 《Journal of Hainan Medical University》 2017年第14期1-4,共4页
Objective:To study the protective effects of Toll-like receptor 4 (TLR4) inhibitor on myocardial injury and lung injury in sepsis rat model.Methods:A total of 18 adult male SD rats were selected as experimental animal... Objective:To study the protective effects of Toll-like receptor 4 (TLR4) inhibitor on myocardial injury and lung injury in sepsis rat model.Methods:A total of 18 adult male SD rats were selected as experimental animals and randomly divided into control group, model group and intervention group, with 6 in each group. The sepsis models were established by cecal ligation and given intragastric administration of TLR4 inhibitor C34. Twenty four hours after model establishment, the levels of myocardial injury molecules and lung injury molecules in serum as well as the expression of inflammatory cytokines, the levels of oxidative stress molecules and the expression of apoptosis molecules in myocardial tissue and lung tissue were determined.Results: KL-6, cTnI and CK-MB levels in serum, NF-kB, TNF-α, IL-1β, Bax, Caspase-3 and Caspase-9 mRNA expression as well as MDA and OH- levels in myocardial tissue and lung tissue of model group were significantly higher than those of control group while SOD levels in myocardial tissue and lung tissue were significantly lower than those of control group;KL-6, cTnI and CK-MB levels in serum, NF-kB, TNF-α, IL-1β, Bax, Caspase-3 and Caspase-9 mRNA expression as well as MDA and OH-levels in myocardial tissue and lung tissue of intervention group were significantly lower than those of model group while SOD levels in myocardial tissue and lung tissue were significantly higher than those of model group.Conclusions: Toll-like receptor 4 inhibitor has protective effect on myocardial injury and lung injury in model rats with sepsis. 展开更多
关键词 SEPSIS TOLL-LIKE receptor 4 INFLAMMATORY response OXIDATIVE stress Apoptosis
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