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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., (Copyright © 2013 Elsevier Inc. All rights reserved.)

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.)

Context: Amla [Emblica officinalis Gaertn. (Euphorbiaceae)], a major constituent of several herbal formulations, is a well-known hepatoprotectant. Despite its extensive use, mechanistic understanding of its antioxidant action is rather limited., Objective: In the current study, we investigated the effects of E. officinalis extracts (from dried fruits) on cellular oxidative state using a hepatocyte cell line (HepG2). We hypothesize that E. officinalis aqueous extracts have potency to modulate basal oxidative markers and enhance endogenous antioxidant defenses., Materials and Methods: Cells were incubated with aqueous extracts of E. officinalis (1-100 μg/ml) for varied time points (4-24 h) and biochemical markers of oxidative stress were determined in cell lysate., Discussion: Aqueous extracts of E. officinalis at 100 μg/ml can significantly modulate the basal levels of oxidative markers and enhance antioxidant defenses of the cells., Conclusions: Our findings clearly indicate the propensity of E. officinalis aqueous extracts to improve endogenous antioxidant defenses in HepG2 cells. Although further studies are required to assess their efficacy under experimentally induced oxidative, our data suggest that the hepatoprotective effects of E. officinalis reported earlier may be largely due to its potential to enhance the antioxidant defenses in vivo., Results: Because E. officinalis up to 100 μg/ml concentrations had no effect on cell viability; it was considered noncytotoxic. Incubation with E. officinalis for 24 h resulted in significant diminution in the levels of lipid hydroperoxide (18-42%) and reactive oxygen species (11-29%). Furthermore; E. officinalis increased the levels of glutathione (GSH; 18-32%); antioxidant capacity (19-31%); and activities of antioxidant enzymes (superoxide dismutase; 25-41%; catalase; 39-50%; GSH peroxidase; 20-35%; GSH reductase; 26-35%; and GSH S-transferase; 12-30%).

Background: Lower post-prandial glucose (PPG) and insulin (PPI) responses to foods are associated with reduced diabetes risk and progression. Several plant extracts have been proposed to reduce PPG or PPI by inhibiting enzymes or transporters involved in carbohydrate digestion and uptake. This study evaluates a range of such extracts, consumed with a carbohydrate load, for their effects on PPG, PPI and indicators of (gastrointestinal) tolerance. Methods: Interventions were extracts of mulberry fruit (MFE, 1.5 g), mulberry leaf (MLE, 1.0 g), white bean (WBE, 3.0 g), apple (AE, 2.0 g), elderberry (EE, 2.0 g), turmeric (TE, 0.18 g), AE + TE, and EE + TE. Each of these 8 individual extracts or combinations were added to a rice porridge containing ~ 50 g available carbohydrate (control). In a within-subject (randomised, balanced incomplete block) design, individual subjects received the control and a subset of 4 of the 8 extracts or combinations. Participants were 72 apparently healthy adults (mean [SD] age 31.2 [5.5] yr, body mass index 22.1 [2.0] kg/m2). The primary outcome was the percentage change in 2-h PPG (positive incremental area under the curve) relative to control. Secondary measures were the 2-h PPI response, 7-h breath hydrogen, measures of gastrointestinal discomfort, and urine glucose. Results: In the 65 subjects who completed the control and at least one intervention treatment, additions of AE, MFE and MLE produced statistically significant reductions in PPG vs control (p < 0.05; mean effect − 24.1 to − 38.1%). All extracts and combinations except TE and WBE significantly reduced PPI (p < 0.01; mean effect − 17.3% to − 30.4%). Rises in breath hydrogen > 10 ppm were infrequent, but statistically more frequent than control only for MLE (p = 0.02). Scores for gastrointestinal discomfort were extremely low and not different from control for any treatment, and no glucosuria was observed. Conclusions: Additions of AE, MFE and MLE to rice robustly reduced PPG and PPI. EE significantly reduced only PPI, while TE and WBE showed no significant efficacy for PPG or PPI. Breath hydrogen responses to MLE suggest possible carbohydrate malabsorption at the dose used, but there were no explicit indications of intolerance to any of the extracts. Trial registration: ClinicalTrials.gov identifier NCT04258501. Registered 6 February 2020 - Retrospectively registered. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM PUBLISHER]