No abstract

Tea is the second most popular beverage in the world after water. Vast accumulative evidence attest that tea consumption may promote human health, such as antioxidant, anti-obesity, and anticancer activities. Therefore, tea phytochemicals have drawn exceeding attention from researchers in structure confirmation, formation mechanism, component clarification, and bioactivity screening of interested constituents. Particularly, most investigations of chemical or biochemical reactions of catechins have concentrated on the B ring of the C6–C3–C6 skeleton. Hence, in this perspective, we reviewed the profound findings of the carbon–carbon (C–C) connection from the unambiguous characterization of novel A-ring addition derivatives of tea catechins, including catechin–carbonyl and catechin–theanine conjugates and the C–C formation mechanisms, and offered our view of the potential effects of catechin–carbonyl interactions on flavor generation and bioactive action in tea.

The present study revealed the anti-aging properties of antcin M (ANM) and elucidated the molecular mechanism underlying the effects. We found that exposure of human normal dermal fibroblasts (HNDFs) to high-glucose (HG, 30 mM) for 3 days, accelerated G0/G1 phase arrest and senescence. Indeed, co-treatment with ANM (10 μM) significantly attenuated HG-induced growth arrest and promoted cell proliferation. Further molecular analysis revealed that ANM blocked the HG-induced reduction in G1-S transition regulatory proteins such as cyclin D, cyclin E, CDK4, CDK6, CDK2 and protein retinoblastoma (pRb). In addition, treatment with ANM eliminated HG-induced reactive oxygen species (ROS) through the induction of anti-oxidant genes, HO-1 and NQO-1 via transcriptional activation of Nrf2. Moreover, treatment with ANM abolished HG-induced SIPS as evidenced by reduced senescence-associated β-galactosidase (SA-β-gal) activity. This effect was further confirmed by reduction in senescence-associated marker proteins including, p21CIP1, p16INK4A, and p53/FoxO1 acetylation. Also, the HG-induced decline in aging-related marker protein SMP30 was rescued by ANM. Furthermore, treatment with ANM increased SIRT-1 expression, and prevented SIRT-1 depletion. This protection was consistent with inhibition of SIRT-1 phosphorylation at Ser47 followed by blocking its upstream kinases, p38 MAPK and JNK/SAPK. Further analysis revealed that ANM partially protected HG-induced senescence in SIRT-1 silenced cells. A similar effect was also observed in Nrf2 silenced cells. However, a complete loss of protection was observed in both Nrf2 and SIRT-1 knockdown cells suggesting that both induction of Nrf2-mediated anti-oxidant defense and SIRT-1-mediated deacetylation activity contribute to the anti-aging properties of ANM in vitro. Result of in vivo studies shows that ANM-treated C. elegens exhibits an increased survival rate during HG-induced oxidative stress insult. Furthermore, ANM significantly extended the life span of C. elegans. Taken together, our results suggest the potential application of ANM in age-related diseases or as a preventive reagent against aging process.

Curcumin (diferuloylmethane), a pharmacologically active substance derived from turmeric, exhibits anti-inflammatory, anticarcinogenic, and antioxidant properties. We examined the modulation of oxidative-stress resistance and associated regulatory mechanisms by curcumin in a Caenorhabditis elegans model. Our results showed that curcumin-treated wild-type C. elegans exhibited increased survival during juglone-induced oxidative stress compared with the control treatment. In addition, curcumin reduced the levels of intracellular reactive oxygen species in C. elegans. Moreover, curcumin induced the expression of the gst-4 and hsp-16.2 stress response genes. Lastly, our findings from the mechanistic study in this investigation suggest that the antioxidative effect of curcumin is mediated via regulation of age-1, akt-1, pdk-1, osr-1, unc-43, sek-1, skn-1, sir-2.1, and mev-1. Our study elucidates the diverse modes of action and signaling pathways that underlie the antioxidant activity exhibited by curcumin in vivo.