Long-term diabetic complications are exacerbated by post-prandial hyperglycemia which could be ameliorated by α-glucosidase inhibitor including oxyresveratrol. Puag-Haad is an aqueous extract from Artocarpus lakoocha Roxb. containing ~65% oxyresveratrol. Oxyresveratrol is an inhibitor of isolated yeast α-glucosidase enzyme but has not been tested on intact gut enterocytes where the enzyme is membrane-bound. Accordingly, differentiated Caco-2 cells that contain the native enzyme were used to test maltose hydrolysis in the present study. The results demonstrated that purified yeast α-glucosidase was non-competitively inhibited by oxyresveratrol (Ki 54.4 AE 0.7 μg/mL) and Puag-Haad (2.7 AE 0.1 μg/mL) compared to 153.8 AE 4.3 μg/mL acarbose, an anti-diabetic drug. In differentiated Caco-2 cells, both oxyresveratrol and Puag-Haad inhibited maltose hydrolysis with lesser potency compared to acarbose. Thus, although weaker than acarbose, oxyresveratrol and Puag-Haad do not inhibit pancreatic amylase which might be a therapeutic asset in preventing fermentation of unabsorbed carbohydrate causes abdominal bloating, flatulence, or diarrhea. Oxyresveratrol and Puag-Haad may help control postprandial hyperglycemia with low risk of gastrointestinal side effects.

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Reduction of intestinal glucose absorption might result from either delayed carbohydrate digestion or blockage of glucose transporters. Previously, oxyresveratrol was shown to inhibit α-glucosidase, but its effect on glucose transporters has not been explored. The present study aimed to assess oxyresveratrol-induced inhibition of the facilitative glucose transporter 2 and the active sodium-dependent glucose transporter 1. An aqueous extract of Artocarpus lacucha, Puag Haad, which is oxyresveratrol-enriched, was also investigated. Glucose transport was measured by uptake into Caco-2 cells through either glucose transporter 2 or sodium-dependent glucose transporter 1 according to the culture conditions. Oxyresveratrol (40 to 800 µM) dose-dependently reduced glucose transport, which appeared to inhibit both glucose transporter 2 and sodium-dependent glucose transporter 1. Puag Haad at similar concentrations also inhibited these transporters but with greater efficacy. Oxyresveratrol and Puag Haad could help reduce postprandial hyperglycemic peaks, which are considered to be most damaging in diabetics.

Objective: Artocarpuslakoocha Roxb. Is a traditional medical plant native to Southeast Asia and used as a dried aqueous extract so-called puaghaad. Its role (and its major ingredient, oxyresveratrol) as an antioxidant neuroprotectant were explored.Methods: Differentiated SH-SY5Y neuroblastoma cells in 96-well plates were challenged with 200 µM H2O2 for 4h and either Trolox (100 µM), oxyresveratrol (5-100 µM), or puaghaad (1.2-25 µg/ml) applied 2h before H2O2 or for 20 h after H2O2Results: Continuous presence of both H washout. Cell viability, mitochondrial function, intracellular ROS, and lipid peroxidation were assessed.2O 2 and antioxidant reduced mitochondrial function by ~50% but only by 30% with antioxidant. Sustained 24 h H2O2 showed no recoveries with antioxidants. Cell viability was modestly restored when antioxidants accompanied H2O2 for 4 h and both washed for another 20 h, but little recovery of mitochondrial function even though antioxidants removed ROS and prevent lipid peroxidation. Antioxidants added for 20 h after H2O2 Conclusion:These results show that mitochondrial protection was illusive, yet both tested compounds, puaghaad and oxyresveratrol, improved cell viability and especially ROS levels and lipid peroxidation. The potency oxyresveratrol on theredox-sensitive expression of antioxidant enzymes and its pharmacokinetics suggests that oral puaghaad could provide effective protection in transient neurodegenerative disease. marginally improve mitochondria and modestly restore cell viability, but lipid peroxidation was completely reversed.