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Black tea (C. sinensis) consumption is well associated with enhanced endothelial function (EF) and reduced cardiovascular (CV) risk. This clinical end benefit is endorsed to flavonoids in tea. The black tea flavonoid composition varies across geographies and may impact its health benefits. Moreover, the underlying functional species and a precise working mechanism responsible for the observed health benefit also remain to be investigated. In this Article, we investigated the effect of black teas from various geographies (WoBTs) on different working mechanisms (antioxidant potential and endothelial function) proposed to influence certain risk factors of CVH, in vitro. Pearson correlation analysis showed that the antioxidant benefits are fairly influenced by majority of tea actives such as catechins, theaflavins, thearubigins, and phenolic acids, while NO potentiating effects are mainly regulated by catechins in black tea. The data also suggest that the net vascular function benefit of black tea is majorly influenced by NO enhancement, while mildly contributed by its antioxidant benefit.

Green tea is often associated with glycemic control benefit. However, the available evidence is not conclusive. In this study, we systematically assessed the contribution of main green tea extract (GTE) ingredients to the inhibition of carbohydrate digestive enzyme and intestinal glucose transport, which are two intervention options for postprandial blood glucose control. A catechin mixture (CM) solution containing seven catechins and epigallocatechin gallate (EGCG) solution was prepared based on the contents of individual catechins in the GTE as determined by high-performance liquid chromatography. The inhibitory potency of GTE, CM, and EGCG on α-amylase or α-glucosidase was compared in cell-free system. GTE’s inhibitory potency was mainly attributed to catechins, among which, EGCG accounted for at least 80 % of the α-amylase inhibitory activity and 90 % of the α-glucosidase inhibitory activity of GTE. In addition, the fluorescence quenching of the digestive enzymes by EGCG revealed that the binding site of EGCG-α-amylase was 1.2, and that for EGCG-α-glucosidase to be 2.0. The inhibitory potency of GTE, CM, and EGCG on glucose transport was assessed in Caco-2 monolayer system. Under the simulated fasting state, there was significant difference between the test materials regarding inhibitory potency according to two-way ANOVA (P > 0.05). Under the simulated fed state, CM showed stronger inhibition than EGCG only at the highest test concentration (25.7 μg/mL), while no significant difference was observed between CM and the GTE. In conclusion, our results suggest that green tea’s postprandial hypoglycemic potential can be attributed to its catechins.

Consumption of tea ( Camellia sinensis ) improves vascular function and is linked to lowering the risk of cardiovascular disease. Endothelial nitric oxide is the key regulator of vascular functions in endothelium. In this study, we establish that l-theanine, a non-protein amino-acid found in tea, promotes nitric oxide (NO) production in endothelial cells. l-theanine potentiated NO production in endothelial cells was evaluated using Griess reaction, NO sensitive electrode and a NO specific fluorescent probe (4-amino-5-methylamino-2',7'-difluororescein diacetate). l-Theanine induced NO production was partially attenuated in presence of l-NAME or l-NIO and completely abolished using eNOS siRNA. eNOS activation was Ca 2+ and Akt independent, as assessed by fluo-4AM and immunoblotting experiments, respectively and was associated with phosphorylation of eNOS Ser 1177. eNOS phosphorylation was inhibited in the presence of ERK1/2 inhibitor, PD-98059 and partially inhibited by PI3K inhibitor, LY-294002 and Wortmanin suggesting PI3K-ERK1/2 dependent pathway. Increased NO production was associated with vasodilation in ex ovo (chorioallantoic membrane) model. These results demonstrated that l-theanine administration in vitro activated ERK/eNOS resulting in enhanced NO production and thereby vasodilation in the artery. The results of our experiments are suggestive of l-theanine mediated vascular health benefits of tea.

The effects of Ocimum sanctum (Lamiaceae), Tulsi on the cellular oxidative state in a hepatocyte cell line (HepG2) and its putative potency to enhance endogenous antioxidant defenses were investigated. Cells were incubated with aqueous extracts of Tulsi (1–100 μg·ml−1) between 4 and 48 h, and biochemical markers of OS were determined. Tulsi up to 100 μg·ml−1 concentrations had no effect either on cytotoxicity or cell proliferation but increased the levels of glutathione (18%–32%) and antioxidant capacity (19%–31%) of cells and enhanced activities of endogenous antioxidant enzymes. Results suggested that aqueous extract of Tulsi reduced the basal OS in HepG2 cells, by induction of antioxidant enzymes and enhancing levels of antioxidant molecules either of which can potentially effect faster dissipation of ROS.

Arjuna (Terminalia arjuna) is a medicinal plant used in many polyherbal hepatoprotective formulations. Although widely claimed to be antioxidant, data supporting such actions of Arjuna are limited. In the present study, we have investigated the efficacy of the aqueous extract of T. arjuna (AETA) using a standard pro-oxidant [tertiary butyl hydroperoxide (TBHP)] in HepG2 cells. Cells were incubated with AETA (5–100 µg/ml) for a range of time points (4–24 h) with or without TBHP (500 μM), and biochemical markers of oxidative stress (OS) were determined. Cells incubated with TBHP showed the significant induction of OS response in cytosol manifested as lipid hydroperoxide (76%–198%) and the generation of reactive oxygen species (60%–127%). Diminished levels of reduced glutathione (35%–60%) and total antioxidant capacity (20%–61%) suggested an altered redox state. Significant perturbations in the activities of antioxidant enzymes such as catalase (30%–56%), superoxide dismutase (25%–68%), glutathione S-transferase (29%–67%), glutathione peroxidase (24%–68%) and glutathione reductase (38%–49%) were discernible suggesting the ongoing OS in the cells. However, cells treated with AETA (100 µg/ml) along with TBHP offered significant protection by reducing levels of lipid hydroperoxide (33%–62%) and ROS (69%) and by increasing antioxidant capacity (54%–81%) and levels of reduced glutathione (49%–82%). Further, it also enhanced the activities of endogenous antioxidant enzymes (superoxide dismutase, 60%; catalase, 35%–82%; glutathione peroxidase, 42–65 %; glutathione reductase, 48%–62%; and glutathione S-transferase, 22%–100%). Taken together, these data suggest that Arjuna can protect against the oxidative damage induced by TBHP and may be effectively used as a hepatoprotective adjuvant to abrogate OS in vivo. Copyright © 2012 John Wiley & Sons, Ltd.

Two natural homogalacturonan (HG) pectins (MW ca. 20 kDa) were isolated from green tea based on their immunomodulatory activity. The crude tea polysaccharides (TPS1 and TPS2) were obtained from green tea leaves by hot water extraction and followed by 40% and 70% ethanol precipitation, respectively. Two homogenous water soluble polysaccharides (TPS1-2a and TPS1-2b) were obtained from TPS1 after purification with gel permeation, which gave a higher phagocytic effect than TPS2. A combination of composition, methylation and configuration analyses, as well as NMR (nuclear magnetic resonance) spectroscopy revealed that TPS1-2a and TPS1-2b were homogalacturonan (HG) pectins consisting of a backbone of 1,4-linked α-d-galacturonic acid (GalA) residues with 28.4% and 26.1% of carboxyl groups as methyl ester, respectively. The immunological assay results demonstrated that TPS1-2, which consisted mainly of HG pectins, showed phagocytosis-enhancing activity in HL-60 cells.

Nitric oxide (NO), produced by endothelial nitric-oxide synthase (eNOS), is recognized as a central anti-inflammatory and anti-atherogenic principle in the vasculature. Decreased availability of NO in the vasculature promotes the progression of cardiovascular diseases. Epidemiological and clinical studies have demonstrated that natural products, in daily diet or phytomedical preparations, may improve vascular function by enhancing NO production and bioavailability. Phyto-ingredients in tea, cocoa, pomegranate and soy are known to positively influence eNOS activity and/or endothelial function, in vitro and in vivo. In this review, we discuss the common pathways modulating endothelial NO production to provide a basis for subsequent mechanistic discussions. We herein also discuss about the mechanism and clinical efficacy of the mentioned dietary ingredients. In summary, there is increasing evidence that several single natural products and plant extracts influence endothelial NO production. Identification of such compounds and characterization of their cellular actions may increase our knowledge of the regulation of endothelial NO production and could provide valuable clues for the prevention or treatment of cardiovascular diseases.