Background: The approach from the point of view of the evolutionary perspective of finding targets for therapeutic effects among the components of the cellular destruction system is critical both in the treatment of rheumatological diseases and in gerontology.

Objectives: To identify the relationships between the pathways of cell death in synovial fluid (SF) of people of different age groups with SDCT.

Methods: SF was analyzed in patients of two age groups. Group N 1 of patients: 10 SLE (43±2.3 years), 13 RA (45±1.6 years), 7 SSD (35±1.8 years) and 8 donors (42±2.7 years, postmortem). Group N 2 (age) of patients: 9 SLE (69±1.8 years), 10 RA (65±1.6 years), 5 SSD (65±0.7 years) and 9 donors (66±2.3 years, postmortem). SF treated with 0.1% Triton-x-100, resuspended in 0.1% citrate buffer (pH = 7.4) and centrifuged at 25000 g for 30 minutes. The supernatant has been used in the experiment. The activity of adenosine monophosphate-activated protein kinase (AMPK) was evaluated by Western blotting. The level of p53 protein was analyzed by the enzyme immunoassay method using ELISA kit (eBioscience, (USA). The content of 8-hydroxy-2-deoxyguanosine (8-OH-dG) was evaluated using the EIA Kit (USA). Quantitative determination of cytochrome C (Cyt c) was carried using the ELISA kit. Active forms of oxygen free radicals (АFRF) were registered by EPR.

Results: An interaction was established between the pathways of cell death in SDCT (mostly distinctive in SLE), age-related changes and clinical manifestations of the autoimmune process were established. The severity of cell death types depends on the nosological form of SDCT (tab.1).