Hemvala Chirdchupunseree

Chulalongkorn University, Bangkok, Bangkok, Thailand

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Publications (3)4.55 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: The purposes of this study were to investigate the inhibitory effects of two lignans, phyllanthin and hypophyllanthin, on the function of P-glycoprotein (P-gp) and multidrug resistance protein 2 (MRP2), using the in-vitro model of Caco-2 cells. In addition, the effect of prolonged exposure to these two compounds on the expression of active P-gp was also determined. The activity of P-gp and MRP2 was determined in the uptake assays by monitoring the intracellular accumulation of their specific substrates (calcein acetoxymethyl ester and 5(6)-carboxy-2',7'-dichlorofluorescein diacetate, respectively) with fluorescence spectroscopy. Hypophyllanthin and phyllanthin inhibited P-gp function with comparable potencies, but neither compound affected MRP2 activity. When the lignans were washed out before addition of substrate, the inhibitory action of both compounds against P-gp function was lost. These results suggested the reversibility of the inhibition. Moreover, prolonged exposure of the Caco-2 cells to both lignans (up to 7 days) had no effect on P-gp function. Phyllanthin and hypophyllanthin directly inhibited P-gp activity and did not interfere with MRP2 activity. It was likely that both phyllanthin and hypophyllanthin could reversibly inhibit P-gp function.
    The Journal of pharmacy and pharmacology. 02/2013; 65(2):292-9.
  • Marisa Inchoo, Hemvala Chirdchupunseree, Pornpen Pramyothin, Suree Jianmongkol
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    ABSTRACT: The purpose of this study was to investigate the modulating effects of phyllanthin and hypophyllanthin on vascular tension, using in the in vitro model of isolated rat aorta. Our results indicated that both phyllanthin and hypophyllanthin significantly relaxed the sustained contraction induced by phenylephrine (PE) in a concentration-dependent manner. In addition, endothelial removal had no significant influence on the vasorelaxation responses of the aortic rings toward these two compounds. Furthermore, both compounds inhibited the contraction of aortic muscle provoked by either PE (1 μM) or KCl (40 mM) as well as the spontaneous contraction of the Ca²⁺-depleted muscle. In high K⁺-Ca²⁺ free solution, phyllanthin (100 μM), but not hypophyllanthin, significantly inhibited the contractile responses upon cumulative addition of CaCl₂. Both compounds (100 μM) significantly inhibited PE-induced contraction in Ca²⁺-free condition, but could not affect caffeine-induced contraction. Taken together, phyllanthin and hypophyllanthin could modulate the vascular tension via the endothelium-independent mechanisms. The modulating effects of both compounds were possibly involved with the blockade of Ca²⁺ entry into vascular smooth muscle cells and inhibition of PE-mediated Ca²⁺ release from sarcoplasmic reticulum.
    Fitoterapia 08/2011; 82(8):1231-6. · 2.23 Impact Factor
  • Hemvala Chirdchupunseree, Pornpen Pramyothin
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    ABSTRACT: To investigate the protective effect of phyllanthin (a known principal constituent of Phyllanthus amarus Schum. et Thonn.) on ethanol-induced rat liver cell injury. Primary culture of rat hepatocytes (24h culturing) were pretreated with phyllanthin (1, 2, 3 and 4 microg/ml) for 24h. After 24h pretreatment, cells were treated with ethanol (80 microl/ml) for 2h. Ethanol decreased %MTT, increased the release of transaminases (ALT and AST) with the increase in the production of intracellular ROS and lipid peroxidation. Phyllanthin demonstrated its role in protection by antagonizing the above effect induced by ethanol. Phyllanthin also restored the antioxidant capability of rat hepatocytes including level of total glutathione, and activities of superoxide dismutase (SOD) and glutathione reductase (GR) which were reduced by ethanol. These results suggested the hepatoprotective effect of phyllanthin against ethanol-induced oxidative stress causing rat liver cell damage through its antioxidant activity.
    Journal of ethnopharmacology 03/2010; 128(1):172-6. · 2.32 Impact Factor