| With the increasing aging population, Circulatory diseases have become a threat to human health. Currently there are about 300 million people in China each year dying of cardiovascular diseases. Many heart diseases coexist with varying degrees of myocardial fibrosis.The pathogenesis of myocardial fibrosis is regulated by many factors. Some studies show close relationship between oxidative stress and myocardial fibrosis. Oxidative stress can activate the MAPK pathway, and then activate the transcription factor, promoting cardiac cells and fibroblasts to secret fibrogenic cytokines in autocrine and paracrine ways etc. Myocardial fibrosis is the key process of development of the compensation to decompensation, which will gradually, causes an irreversible myocardial damage, ultimately leading to cardiac failure, so that the survival rate decreased. Therefore, the development of myocardial fibrosis has become a hot topic in medical study to early intervention and reversal. Now the recognized drugs commonly used for cardiac fibrosis are ACEI, AT1 receptor blockers, aldosterone antagonists, calcium antagonists, statins, and so on, but inferior efficacy and serious side effects remain a problem to be resolved. Therefore, the development of traditional Chinese medicine with better efficacy, fewer side effects for myocardial fibrosis has important clinical significance. Myocardial fibrosis is chest pain in areas of traditional Chinese medicine, the characteristic of whose pathogenesis is that the vacuity false is mixed. About the treatment, we mainly adopt replenishing Qi and nourishing yin, activating blood and resolving stasis, supplement by Shu Bi expectorant, moving Qi to relieve pain, dredging channels and activating collaterals, to get the effect of treating the etiology together with performance. NXKKFY preparations are Traditional Chinese Medicine, developed by the department of traditional Chinese medicine of the First Hospital of Jilin University in Buyang Huanwu Tang based on years of clinical research, by adding or subtracting coronary heart disease from a Chinese herbal formula, mainly for the treatment of coronary heart disease - blood stasis type, can nourish Qi and blood, and strengthen body resistance. NXKKFY, since launched in 2000, has treated tens of thousands of patients, can improve clinical symptoms and signs, and no adverse reactions reported yet. In recent years, several studies indicating NXKKFY significantly acts against myocardial ischemia and cerebral ischemia-reperfusion injury, but NXKKFY on myocardial fibrosis is lack of researches. The main purpose of this study is to confirm the anti-oxidation mechanism the effect of NXKKFY by establishing rat models of myocardial fibrosis, through the detection of rat HW / BW, SOD, MDA, NO and NOS, etc.In this study, rats were divided into six groups, namely control group, myocardial fibrosis model group, the captopril group, NXKKFY large, medium and small dose group. Normal 10, and the remaining 15 rats in each group. In this study we used the method of drug control and observed the effect of NXKKFY4.4g/ml, 2.2g/ml, 1.1g/ml dose and captopril on HW / BW, SOD activity, MDA, serum NO, NOS activity in rats with myocardial fibrosis and then analyzed NXKKFY's anti-myocardial fibrosis through anti-oxidation mechanism.In this study, superoxide dismutase (SOD) and malondialdehyde (MDA) were chosen as the primary endpoints needed to be compared. SOD can be combined with in vivo multi-oxidase and can effectively remove all kinds of free radicals and block lipid peroxidation and oxygen free radicals to terminate chain reactions, reducing its impact on tissue cells and the ultrastructural damage. In the circulatory system, it is effective in reducing the irreversible damage of myocardial cells, thereby protecting myocardial cells. The activity of SOD represents free radical scavenging level.MDA is the metabolite of fatty acid peroxidation in the cell membrane caused by oxygen free radicals, leading damage to the organization. And as lipid peroxidation metabolites and the concentration of MDA partly reflects the degree of tissue oxidative damage. In our study, xanthine oxidase, thiobarbituric acid colorimetry and other methods were used to detect the serum and myocardial tissue SOD activity and MDA concentration , serum NO levels, NOS activity, combined with pathological examination, to study and evaluate the effect of NXKKFY on myocardial fibrosis in rats and to explore the mechanism of NXKKFY against myocardial fibrosis.The results showed that: HW / BW of model group was significantly higher than that of normal (P <0.05), which shows that the model was successfully established; the captopril group and NXKKFY large dose group was significantly lower than that of model (P <0.05); HW/BW of NXKKFY medium and small dose group were lower than that of model group, but no significant difference found, and compared with the normal group there are still significant differences (P> 0.05). NXKKFY in each dose group can raise the serum and myocardial tissue SOD activity, decrease MDA levels, and increase serum NO concentration and NOS activity, NKKFY has most obvious effect in high dose group (P <0.05), compared with the captopril group , there is no significant statistical difference (P> 0.05). Histopathological evaluation showed: when cardiac fibrosis happens, myocardial collagens grow to different degrees, but NXKKFY groups improved myocardial cell damage, and especially the role of high-dose group is obvious.In summary, this study of myocardial fibrosis in rats observed NXKKFY for antioxidant enzyme system and cardiac tissue pathological changes during myocardial fibrosis process, and from the perspective of modern pharmacology, analyzed the mechanism of NXKKFY against myocardial fiber. The results show that the NXKKFY can improve myocardial fibrosis in rats related with the body SOD, MDA, NO and NOS levels and can significantly alleviate the degree of myocardial fibrosis, suggest that NXKKFY probably acts by regulating free radicals in the body to reverse myocardial fibrosis, which provides a pharmacological basis for the treatment of myocardial fibrosis. This study not only provides valuable experimental information for the treatment of myocardial fibrosis by NXKKFY, but also supplies a new direction and new ideas for the further development of drugs against myocardial fibrosis.
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