[Peptides prevent the forming of secretory phenotype of chondrocytes associated with the aging.]

Myakisheva SN, Linkova NS, Kozhevnikova EO, Polyakova VO, Ryzhak GA · Advances in Gerontology (Uspekhi Gerontologii)

Ageing raised p16 4.3-fold, p21 4.5-fold, p53 5-fold and IL-1-alpha 3.8-fold, and lowered Sirt1 4.3-fold. The two preparations did not do the same things. AED lowered all three pro-apoptotic proteins — p16 by 3 and 2.8-fold at the two doses, p21 by 5.1 to 5.2-fold at both, p53 by 2.2 and 2.5-fold — and raised Sirt1 3.6 and 4.6-fold, but moved neither TNF-alpha nor IL-1-alpha. The cartilage complex lowered the apoptotic proteins too (p16 4.7-fold, p21 4.1-fold and p53 3.9-fold at 2,000 ng/ml) and is the only one of the two that touched the cytokines: TNF-alpha 1.9-fold at 2,000 ng/ml, IL-1-alpha 1.6 and 1.9-fold at the two doses. Neither preparation changed any marker in cultures from the young rats.

Population

Primary chondrocytes from the intervertebral discs of young (3-month) and old (20-month) outbred white rats, used at the fourth passage

Intervention

AED tripeptide (Cartalax) at 200 and 2,000 ng/ml, or the cartilage polypeptide complex (CPC, the Sigumir substance) at the same two concentrations

Comparator

Untreated cultures from the old rats, and cultures from the young rats as the ageing reference

Limitations

The cells are rat, not human, and they come from intervertebral discs rather than articular cartilage, so this is a spinal-disc model read across to joint cartilage. Immunocytochemical expression area is the only readout — no matrix synthesis, no mechanical endpoint. Institute-authored, in a Russian-language journal tied to that institute. The paper's own closing summary divides the labour more cleanly than its results do, crediting AED with the apoptotic markers and the complex with the cytokines and Sirt1, where AED also raised Sirt1 and the complex also lowered the apoptotic markers; the real asymmetry is that AED did nothing to either cytokine.