Gao Shang-mei, Peng Jie


Department of Cardiology, Chongqing Traditional Chinese Medicine Hospital, Chong Qing 400011, China


 Objective: To investigate the effect of timosaponin on myocardial blood vessels and to study its protective mechanism against myocardial ischemic injury, providing an important theoretical basis for the development of new drugs.

Methods: laboratory rats were selected for testing and then randomized into groups of six. Three groups were injected with 150 mg / kg, 300 mg / kg, 600 mg / kg concentration of timosaponin. The remaining three groups, one of which was injected with Di-ao- xin-xue-kang as a positive control, the remaining two groups served as experimental blank controls and model controls. The state of myocardial ischemic injury was simulated by injecting isoproterenol into the rat. The rats were given medication on time every day (required for all five groups except for the blank control), and the duration of treatment was five days. Five days later, the rats were dissected and the physicochemical degree of myocardial lesions was observed through experiments. At the same time, changes in serum levels of phosphocreatine kinase, lactate dehydrogenase, and aspartate aminotransferase were examined. At the same time, the activity of glutathione peroxidase, malondialdehyde, reactive oxygen species, superoxide dismutase, heme oxygenase-1, p53, Bcl-2 and Bax in myocardial tissue was detected in real time.

Results: experimental studies have found that for myocardial damage, timosaponin has a good inhibitory effect and protects myocardial blood vessels. Its mechanism of action is closely related to the inhibition of apoptosis and anti-free radicals. Anthraquinone saponins are effective in reducing the activity of these enzymes in the serum of myocardially injured animals. This indicates that the timosaponin has a function of protecting cardiomyocytes and inhibiting apoptosis. Its mechanism of action may be related to changes in the expression levels of p53 and Bax, and increased expression of Bcl-2. The results also showed that the content of HO-1 in the tissue increased slightly after myocardial ischemic injury, but the effect of timosaponin on it was not statistically significant. Therefore, the protective effect of timosaponin on myocardial ischemic injury may not involve changes in HO-1 or no favorable evidence has been found to be associated with HO-1. In summary, it has been proved by experiments that timosaponin has a protective effect on acute myocardial ischemia injury. The mechanism of action may be related to its anti-oxidation, improvement of myocardial cell zymogram, improvement of apoptotic proteins, inhibition of apoptosis and so on.

Conclusion: from the idea that the timosaponin has an effect on myocardial ischemic injury and has a protective effect on the myo- cardium, it is inspired by it, providing a theoretical basis for the development of new drugs in the future, and providing new medical means


Anogeneic saponin, myocardial ischemia, anti-peroxidation, apoptosis, mechanism of action