Saponins from bitter melon (BMS) exert potential bioactivities and pharmacological activities, including anti-oxidation and lifespan extension. However, the exact mechanisms of BMS in response to oxidative stress remain unknown. Results demonstrated that bitter melon saponins could strengthen locomotive activities (body bend and head thrashing) accompanied by delaying the muscle fiber damage with age in Caenorhabditis elegans . In addition, BMS inhibited the ROS accumulation, improved the activities of antioxidant enzymes like SOD (by 57.90% and 94.34% for 100 μg/ml and 200 μg/ml BMS, respectively) and CAT (by 51.45% and 56.91% for 100 μg/ml and 200 μg/ml BMS, respectively), and extend the lifespan of N2 and CL2006 worms under paraquat-induced oxidative stress. Mechanism study suggested that BMS modulated the mRNA expressions of oxidation-related regulators, like the upregulation of cat-1 , hsf-1 , sir-2.1, and hlh-30. Furthermore, gene-deficient mutants verified that IIS (insulin/insulin-like growth factor-1 signaling) pathway linked with sir-2.1 and hlh-30 factors were involved in the BMS's lifespan-extension effects under oxidative stress. In general, this study supplemented the explanation of BMS in promoting oxidation-resistance and lifespan-extension activities, which could be served as a potential candidate for anti-aging. Practical applications Our previous studies have suggested that saponins from bitter melon exhibited fat-lowering activity in C. elegans . However, little was known about the mechanism underlying the anti-oxidation effects of BMS in C. elegans. Current results indicated that the IIS pathway linked with sir-2.1 and hlh-30 transcriptional factors jointly to increase the lifespan in BMS' responses to oxidative stress. Our findings are beneficial to understand the main nutritional ingredients in bitter melon, which are ideal and expected in functional foods for aging.
High-sugar diets are associated with multiple health risks, such as obesity, metabolic disorders, and cardiovascular diseases. To mitigate the adverse effects of high sugar intake on biological health, aspartame (ASP) is widely used as one of the sugar substitutes. In this study, we used Caenorhabditis elegans ( C. elegans ) as the model to reveal the specific mechanism by which ASP affects healthy lifespan. Our results showed that ASP (1, 10, 100 μmol/L) significantly extended the lifespan of C. elegans and improved health indicators in dose dependent manner, including reduced lipofuscin accumulation and enhanced motility, but did not influence the fertility of worms. Furthermore, by screening the classic signaling pathways, we discovered ASP extended healthspan via mechanistic target of rapamycin complex 1 (mTORC1) pathway. In addition, we found that ASP inhibited mTORC1 activity to promote the nuclear translocation of helix-loop-helix protein 30 (HLH-30), the nematode homolog of transcription factor EB (TFEB), and subsequently upregulated autophagy-related genes such as autophagy-related gene 5 ( atg-5 ), beclin 1 ( bec-1 ), LC3, GABARAP, GATE-16 family member 1 ( lgg-1 ) and LC3, GABARAP, GATE-16 family member 2 ( Lgg-2 ). This ultimately activated the autophagy process, thereby delaying aging. This finding elucidates that ASP induces autophagy to enhance healthspan in C. elegans dependent on the mTORC1/TFEB pathway, offering a novel approach for anti-aging research.
危险品化学品经营许可证（带存储）