Cardiogen-20mg

The effect of the amino acids and cardiogen on the development of myocard tissue culture from young and old rats

The effect of 20 amino acids and the synthetic tetrapeptide cardiogen in concentration 10(-12) M was investigated in organotypic tissue culture on the cell proliferation and apoptosis development in myocard tissue explant in 3- and 24-months old rats. 7 of 20 amino acids stimulated the cell proliferation in the young rats. In the same time, only 2 amino acids were active in myocard culture from the old rats. The tetrapeptide cardiogen demonstrated the great stimulating effect on the proliferation both in tissues from young and old rats. The immunohistochemical study demonstrated a decrease of the p53 protein expression by cardiogen action. This fact can testify that cardiogen inhibits the apoptosis process in the myocard tissue.
Tumor-Modifying Effect of Cardiogen Peptide on M-1 Sarcoma in Senescent Rats

The tumor-modifying effect of cardiogen peptide was studied on rats with transplanted M-1 sarcoma. The level of apoptosis of tumor cells after cardiogen injections in all experimental groups was higher than in the control. The dose-dependent inhibition of M-1 sarcoma growth after injection of cardiogen was caused by the development of hemorrhagic necrosis and stimulation of tumor cell apoptosis. The parameters of proliferative activity indicate that inhibition of tumor growth was not caused by the direct cytostatic effect of the drug on the tumor. Morphological signs indicate a specific mechanism of cardiogen action, realized through the vascular network of the tumor.
Cardiogen and Prostate

The direct relationship between the aging process and the incidence and prevalence of both benign prostatic hyperplasia (BPH) and prostate cancer (PCa) implies that certain risk factors associated with the development of both diseases increase with the aging process. In particular, both diseases share an overly proliferative phenotype, suggesting that mechanisms that normally act to suppress cellular proliferation are disrupted or rendered dysfunctional as a consequence of the aging process. We propose that one such mechanism involves changes in the prostate microenvironment, which ‘evolves’ during the aging process and disrupts paracrine interactions between epithelial and associated stromal fibroblasts. We show that stromal fibroblasts isolated from the prostates of men 63-81 years of age at the time of surgery express and secrete higher levels of the CXCL12 chemokine compared with those isolated from younger men, and stimulate CXCR4-mediated signaling pathways that induce cellular proliferation. These studies represent an important first step towards a mechanistic elucidation of the role of aging in the etiology of benign and malignant prostatic diseases.

The effect of short peptides T-32, T-38 and cardiogen on the expression of signaling factors of the differentiation of human prostate’s fibroblasts (PFM), which are the main cells of its microenvironment–protein CXCL12, WEDC1 and ghrelin in aging cultures has been studied. Confocal laser microscopy has demonstrated that all the investigated peptides possess the ability to actively enhance the expression of the above markers, whose synthesis significantly reduced in senescent cultures. It has been shown that the rate of expression of the studied factors in older cultures (after 7 passages) under the action of the peptides have a tendency to even higher than those of controls (young culture, after 1 passage). Thus, peptide T-38 is the most active among the investigated ones. These studies show promise for detailed development of methods of peptides’ regulation of aging and age-correction of violations of functioning of the prostate gland.