Phytomedicine : international journal of phytotherapy and phytopharmacology · 2018
Protective role and mechanism of snakegourd peel against myocardial infarction in rats.
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Yang Guanlin, Min Dongyu, Yan Junwei, Yang Ming, Lin Guijun
Аннотация
BACKGROUND: Injection of snakegourd peel (SP), an herb used in traditional Chinese medicine, is used to treat coronary artery disease and stable angina in China. However, its therapeutic role and mechanism of action for the treatment of myocardial infarction (MI) is not fully understood.
PURPOSE: The present study was designed to investigate the effect of SP on MI-induced cardiac injury and elucidate its underlying molecular mechanisms.
METHODS: To create an in vivo model of MI, we ligated the left coronary artery of Wistar rats. For our in vitro model of MI, we treated primary neonatal rat ventricular myocytes with hypoxia. Myocardial infarct size was measured by triphenyltetrazolium chloride (TTC) staining. Intracellular calcium concentration (Ca2+) was measured by confocal microscopy, and cardiomyocyte apoptosis was assessed by TUNEL assay. Western blot was applied to determine protein levels.
RESULTS: Three days post-MI, SP significantly improved MI-induced impairment of cardiac function, as indicated by increased left ventricular systolic pressure (LVSP), maximum rate of left ventricular pressure rise and fall (± dp/dt max), and decreased left ventricular end-diastolic pressure (LVEDP). In addition, SP treatment markedly reduced the infarct size and serum lactate dehydrogenase (LDH) activity; inhibited cardiomyocyte apoptosis and Caspase-3 activation both in vivo and in vitro; and decreased intracellular calcium overload, Cav1.2, phosphorylated JNK (p-JNK), and p38 MAPK (p-p38 MAPK) levels in ischemic myocardium.
CONCLUSION: SP alleviated cardiac ischemic injury and inhibited cardiomyocyte apoptosis by attenuating intracellular calcium overload, suppressing Caspase-3 activation, and downregulating protein expression of p-JNK and p-p38MAPK. These results suggest that SP may serve as a potential novel therapeutic drug for MI.
PURPOSE: The present study was designed to investigate the effect of SP on MI-induced cardiac injury and elucidate its underlying molecular mechanisms.
METHODS: To create an in vivo model of MI, we ligated the left coronary artery of Wistar rats. For our in vitro model of MI, we treated primary neonatal rat ventricular myocytes with hypoxia. Myocardial infarct size was measured by triphenyltetrazolium chloride (TTC) staining. Intracellular calcium concentration (Ca2+) was measured by confocal microscopy, and cardiomyocyte apoptosis was assessed by TUNEL assay. Western blot was applied to determine protein levels.
RESULTS: Three days post-MI, SP significantly improved MI-induced impairment of cardiac function, as indicated by increased left ventricular systolic pressure (LVSP), maximum rate of left ventricular pressure rise and fall (± dp/dt max), and decreased left ventricular end-diastolic pressure (LVEDP). In addition, SP treatment markedly reduced the infarct size and serum lactate dehydrogenase (LDH) activity; inhibited cardiomyocyte apoptosis and Caspase-3 activation both in vivo and in vitro; and decreased intracellular calcium overload, Cav1.2, phosphorylated JNK (p-JNK), and p38 MAPK (p-p38 MAPK) levels in ischemic myocardium.
CONCLUSION: SP alleviated cardiac ischemic injury and inhibited cardiomyocyte apoptosis by attenuating intracellular calcium overload, suppressing Caspase-3 activation, and downregulating protein expression of p-JNK and p-p38MAPK. These results suggest that SP may serve as a potential novel therapeutic drug for MI.