Objective: To evaluate the myocardial protective effect of Gualou Xiebai Banxia decoction (瓜蒌薤白半夏汤GXBD) and explore the mechanisms of inhibition of NF-kappa B activation and blockade of inflammatory responses i...Objective: To evaluate the myocardial protective effect of Gualou Xiebai Banxia decoction (瓜蒌薤白半夏汤GXBD) and explore the mechanisms of inhibition of NF-kappa B activation and blockade of inflammatory responses induced by ischemia-reperfusion in rats. Methods: Twenty-four Sprague Dawley (SD) rats were randomly divided into three groups. Rats in the treatment group received GXBD (13 g crude drug/kg) for three weeks, while rats in the model control and normal control groups received equal volumes of distilled water. On the 22nd day, rats in the ischemia-reperfusion (I/R) control and GXBD-treated groups underwent 30 min occlusion of the left anterior descending (LAD) coronary artery, followed by 120 min reperfusion. Electrocardiogram was recorded, and the activities of cardiac enzymes, cytokines, and NF-кB were assessed after I/R. Results: Compared with the I/R control group, GXBD treatment restored the activity of the specific myocardial-injury marker creatine kinase (CK) and lactate dehydrogenase (LDH), and inhibited the inflammatory response involving the nuclear factor-кB (NF-кB) pathway, including down-regulation of interleukin (IL)-1β and IL-6, and up-regulation of IL-10 gene expression. Conclusion: GXBD strongly reduced myocardial impairment in our I/R model, including inhibition of NF-кB activation and inflammatory cytokine responses.展开更多
基金supported by the National Natural Science Foundation of China (30701066 and 30973696 Science) for financial support
文摘Objective: To evaluate the myocardial protective effect of Gualou Xiebai Banxia decoction (瓜蒌薤白半夏汤GXBD) and explore the mechanisms of inhibition of NF-kappa B activation and blockade of inflammatory responses induced by ischemia-reperfusion in rats. Methods: Twenty-four Sprague Dawley (SD) rats were randomly divided into three groups. Rats in the treatment group received GXBD (13 g crude drug/kg) for three weeks, while rats in the model control and normal control groups received equal volumes of distilled water. On the 22nd day, rats in the ischemia-reperfusion (I/R) control and GXBD-treated groups underwent 30 min occlusion of the left anterior descending (LAD) coronary artery, followed by 120 min reperfusion. Electrocardiogram was recorded, and the activities of cardiac enzymes, cytokines, and NF-кB were assessed after I/R. Results: Compared with the I/R control group, GXBD treatment restored the activity of the specific myocardial-injury marker creatine kinase (CK) and lactate dehydrogenase (LDH), and inhibited the inflammatory response involving the nuclear factor-кB (NF-кB) pathway, including down-regulation of interleukin (IL)-1β and IL-6, and up-regulation of IL-10 gene expression. Conclusion: GXBD strongly reduced myocardial impairment in our I/R model, including inhibition of NF-кB activation and inflammatory cytokine responses.
