参芪定悸汤调控p38MAPK表达抑制慢性心力衰竭大鼠心肌的氧化损伤

目的：探究参芪定悸汤对慢性心力衰竭（CHF）大鼠血清N 端B型脑钠肽前体（NT-proBNP）水平、心 功能和p38MAPK信号通路的影响。方法：健康SD 雄性大鼠，随机分对照组，模型组，参芪定悸汤低、高剂 量组。ELISA 法检测NT-proBNP、心肌肌钙蛋白I（cTnI）水平，HX-300S 动物呼吸机记录左心室舒张期末压 （LVEDP）、左心室收缩压（LVSP）水平，免疫印迹检测p38 丝裂原活化蛋白激酶（p38MAPK）、p-p38MAPK 水 平，黄嘌呤氧化酶法检测超氧化物歧化酶（SOD）活性，硫代巴比妥酸法检测丙二醛（MDA）含量，TUNEL 检测 心肌细胞凋亡。结果：与对照组相比，模型组LVSP、SOD 水平降低，NT-proBNP、cTnI、LVEDP、p38MAPK、 p-p38MAPK、MDA 升高。与模型组相比， 参芪定悸汤低剂量组LVSP、SOD 水平升高，NT-proBNP、cTnI、 LVEDP、p38MAPK、p-p38MAPK、MDA 降低。与参芪定悸汤低剂量组相比，参芪定悸汤高剂量组LVSP、SOD 水平升高，NT-proBNP、cTnI、LVEDP、p38MAPK、p-p38MAPK、MDA 降低。正常心肌细胞核显色为蓝色， 凋亡小体显色为绿色。可见对照组大鼠存在大量的存活心肌细胞，无明显的心肌细胞凋亡；模型组大鼠正常心肌 细胞明显减少，存在大量凋亡小体；参芪定悸汤低剂量组与高剂量组较模型组细胞凋亡有所减少。结论：参芪定 悸汤可改善CHF 大鼠心功能，从而达到对CHF 大鼠的治疗效果，其作用机制可能与调控NT-proBNP、p38MAPK 的表达有关。

Shenqi Dingji decoction inhibits oxide injury of myocardium by regulating p38MAPK expression in rats with chronic heart failure

Objective To investigate the effects of Shenqi Dingji decoction on serum N-terminal pro-B type natriuretic peptide（NT-probNP） level， cardiac function and p38MAPK signaling pathway in rats with chronic heart failure（ CHF）. Methods Healthy SD male rats were randomly divided into a control group， a model group， a low and high dose Shenqi Dingji decoction group. The NT-proBNP and cardiac troponin I（ cTnI） were detected by ELISA. The left ventricular systolic pressure was recorded by the HX-300S ventilators. Left ventricular enddiastolic pressur（e LVEDP）， left ventricular systolic pressure（ LVSP）， and the levels of p38MAPK and p-p38MAPK were detected by Western blotting. The activity of superoxide dismutase（ SOD） was detected by xanthine oxidase method， the content of malondialdehyde（ MDA） was detected by thiobarbital acid method， and the apoptosis of cardiomyocytes was detected by TUNEL. Results Compared with the control group， LVSP and SOD levels in the model group were decreased， while NT-proBNP， cTnI， LVEDP， p38MAPK， p-p38MAPK and MDA levels were increased. Compared with the model group， LVSP and SOD levels in Shenqi Dingji decoction low-dose group were higher， while NT-proBNP， cTnI， LVEDP， p38MAPK， p-p38MAPK and MDA levels were lower. Compared with Shenqi Dingji decoction low-dose group， LVSP and SOD levels in the Shenqi Dingji decoction high-dose group were increased， while NT-proBNP， cTnI， LVEDP， p38MAPK， p-p38MAPK and MDA levels were decreased. The nuclei of normal myocardium were blue and apoptotic bodies were green. There were a large number of viable cardiomyocytes in the control group， but no apoptosis was observed. The normal myocardium in the model group decreased obviously and there were a lot of apoptotic bodies. Compared with the model group， the apoptosis in the low dose group and the high dose group of Shenqi Dingji decoction was decreased. Conclusion Shenqi Dingji decoction can improve the heart function andachieve therapeutic effect in CHF rats. As a result， its mechanism may be related to the regulation of the expression of NT-proBNP and p38MAPK