Why the study?
Does tetramethylpyrazine phosphate improve cardiac function and reduce oxidative stress in rats with isoproterenol-induced heart failure?
Does tetramethylpyrazine phosphate improve cardiac function and reduce oxidative stress in rats with isoproterenol-induced heart failure?
In a rat model of isoproterenol-induced heart failure, tetramethylpyrazine phosphate improved cardiac function and reduced myocardial fibrosis, potentially through reduction of oxidative stress and inflammation.
The aim of the study was to determine the effect of tetramethylpyrazine phosphate tablets (TPT), a Chinese medicine used for cardiovascular disease, on immunity activity and oxidative injury in rats. Heart failure (HF) was induced by isoproterenol (ISO). After the animal model was established, the rats were administered the TPT by gavage (once a day). The results indicated that TPT improved left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), ±dP/dt, heart weight/body weight. TPT could decrease the levels of tumor necrosis factor-α (TNF-α) and interleukin 6 (IL-6). Furthermore, it also could raise the activities of catalase, superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), but reduce malonyldialdehyde (MDA) level. The results indicated that TPT improved cardiac function and myocardial fibrosis from myocardial injury, and this cardioprotection might be attributed to a reduction of oxidative stress and regulation of inflammation mediators.
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Guo et al. (2012) studied this question.
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