Yushun Gong

Tea polyphenol epigallocatechin gallate inhibits Escherichia coli by increasing endogenous oxidative stress.

The antibacterial effects of tea polyphenol epigallocatechin gallate (EGCG), a common phytochemical with a number of potential health benefits, are well known. However, the mechanism of its bactericidal action remains unclear. Using E. coli as a model organism, it is argued here that H2O2 synthesis by EGCG is not attributed to its inhibitory effects. In contrast, the bactericidal action of EGCG was a result of increased intracellular reactive oxygen species and blunted adaptive oxidative stress response in E. coli due to the co-administration of antioxidant N-acetylcysteine, and not on account of exogenous catalase. Furthermore, we noted a synergistic bactericidal effect for EGCG when combined with paraquat. However, under anaerobic conditions, the inhibitory effect of EGCG was prevented. In conclusion, EGCG caused an increase in endogenous oxidative stress in E. coli, thereby inhibiting its growth, and hence the use of EGCG as a prooxidant is supported by this study.

TLC Separation of Catechins and Theaflavins on Polyamide Plates

The potential of polyamide as adsorbent for separation of nine compounds - (±)-catechin (DL-C), (-)-epicatechin (EC), (-)-epigallocat-echin (EGC), (-)-epicatechin gallate (ECg), (-)-epigallocatechin gal-late (EGCg), theaflavin (TF1), theaflavin 3-gallate (TF2A), theaflavin 3’-gallate (TF2B), and theaflavin 3,3’-digallate (TF3) - was studied. Polyamide TLC plates dried with a hair dryer, application as bands, and development in a horizontal chamber gave the best results. Detection was performed using iron(III) chloride- ethanol reagent. Twofold development with chloroform-methanol 2:3 (v/v) as mobile phase resulted in the separation of TF1, TF2A, TF2B, and TF3 from all the other compounds. EGCg, ECg, and EGC were separated but EC and DL-C were not separated from each other. The best mobile phase for each of the compounds is reported. The best separation of the five main catechins (EC, DL-C, EGC, ECg, and EGCg) was achieved by use of n-butanol-ace-tone-acetic acid 5:5:3 (v/v). In addition, separation of the flavonols myricetin, quercetin, kaempferol, and rutin and the phenolic acids gallic acid, chlorogenic acid, and caffeic acid was achieved by twofold development with chloroform-methanol 2:3 (v/v). The applicability of the method was checked by screening of extracts of green, black, oolong, and pu-erh tea.

Water extract of the fungi from Fuzhuan brick tea improves the beneficial function on inhibiting fat deposition

Abstract Fuzhuan brick tea (FBT) is traditionally consumed by the ethnic group in the border region of northwest China. The unique yellow fungal (Eurotium cristatum) growth phase is considered to be the key process point in the manufacture of the brick tea. The fungi from FBT are not only strongly correlated to the quality of brick tea, but also have the potential function of preventing obesity. The water extract of fungi (100 μg/mL) can significantly inhibit fat deposition in 3T3-L1 adipocyte and Caenorhabditis elegans. Furthermore, the inhibition of 3T3-L1 adipocyte formation was not due to the suppression on cell viability.

Epigallocatechin-3-gallate promotes healthy lifespan through mitohormesis during early-to-mid adulthood in Caenorhabditis elegans

The green tea polyphenol epigallocatechin-3-gallate (EGCG) is widely consumed as a dietary supplement. Its potential properties include slowing aging and extending lifespan, although how exactly this is achieved remains unclear. Here, we report that EGCG promoted healthy lifespan in Caenorhabditis elegans when administered throughout or only at early-to-mid adulthood. Specifically, EGCG extended lifespan in an inverted U-shaped dose-response manner. The life-extending mechanism was stimulated by EGCG-induced production of reactive oxygen species (ROS). Additionally, EGCG triggered mitochondrial biogenesis to restore mitochondrial function. The EGCG-induced increase in lifespan depends on known energy sensors such as AMPK/AAK-2, as well as SIRT1/SIR-2.1 and FOXO/DAF-16. Interestingly, aging decreased the response to EGCG and progressively neutralized its beneficial effects on longevity. Collectively, our findings link EGCG to the process of mitohormesis and suggest an inducible, AMPK/SIRT1/FOXO-dependent redox signaling module that could be invoked in different contexts to extend healthy lifespan. Its effectiveness is higher in younger adults and declines with age.