Sweet tea (Rubus Suavissmus S. Lee) polysaccharides promote the longevity of Caenorhabditis elegans through autophagy-dependent insulin and mitochondrial pathways.

The fine structure of sweet tea polysaccharide (STP-60a) has been characterized. However, the biological activity of STP-60a has not been extensively explored. This study aims to evaluate the anti-aging activity of STP-60a using Caenorhabditis elegans (C. elegans) as a model and to investigate the underlying molecular mechanism. 400 μg/mL of STP-60a increased the mean lifespan of C. elegans by 22.88%, reduced the lipofuscin content by 33.01%, and improved the survival rate under heat stress and oxidative stress by 32.33% and 27.63%, respectively. Further research in lifespan-related mutants revealed that STP-60a exerted anti-aging effects mainly through insulin and mitochondrial signaling pathways. Through qRT-PCR and microscopic imaging of transgenic nematodes, we found that 400 μg/mL of STP-60a increased the expression of daf-16, skn-1, and hsf-1 downstream of the insulin pathway by 1.68-fold, 1.88-fold, and 1.03-fold, respectively, and promoted the accumulation of daf-16 and skn-1 in the nucleus. STP-60a also significantly regulated the function of the mitochondrial respiratory chain and unfolded protein recovery system. Furthermore, STP-60a activated the autophagy level in C. elegans, and the mutation of daf-2 or clk-1 inhibited the upregulation of autophagy genes by STP-60a, suggesting that autophagy acted as an effector of the insulin and mitochondrial pathways during STP-60a antiaging.