Introduction. Despite the absence of a generally accepted theory explaining the mechanisms of aging, existing scientific data indicate a close relationship between aging and chronic low-grade inflammation (low-grade inflammation). This theory of inflammatory aging (inflame-aging) suggests that aging is accompanied by the development of a chronic inflammatory phenotype, which ultimately leads to fibroplastic transformation of tissues, which manifests itself in a functional deficiency of organs and, in particular, the bladder.

Aims. To study the role of free radical oxidation, endothelial dysfunction and low-level age-associated inflammation as universal mechanisms of cellular senescence in the process of age-related detrusor rearrangement in experimental animals.

Materials and methods. Two groups of laboratory animals were used in the experiment: group 1 (30-month-old white mongrel rats, n=10) and group 2 (10- month-old white mongrel rats, n=10). Markers of low-level age-associated inflammation (TNF-α, IL-6, IL1RA), endothelial dysfunction (ET-1, IL-1β, ESM1), profibrotic status (TGF beta 1 and CTGF), and free radical oxidation (8-isoprostane) were determined in blood and bladder homogenate, malonic dialdehyde, diene conjugates).The Student's criterion was used to compare two groups with a normal distribution.

Results and discussion. It was shown that with age in experimental animals, the levels of inflammation markers (TNF-α, IL-6, IL1RA), endothelial dysfunction (ET-1, IL-1β, ESM1), lipid peroxidation (diene conjugates, silicone dialdehyde) and profibrotic cytokines (TGF beta 1 and CTGF) increased, while the levels of antioxidant activity (catalase) decreased statistically significantly.This pattern was revealed both at the systemic (blood plasma) and organ levels (bladder wall).

Conclusion. The results of our experimental study confirm the role of chronic low-level inflammation in fibrosis-mediated inflammatory aging of organs and, in particular, in age-associated bladder reconstruction.