Abstract
Objective: Arginase inhibition could be a potential therapeutic approach for endothelial dysfunction. Syzygium cumini (L.) Skeels leaves containphenolic acids and flavonoids, which have been predicted to exhibit arginase inhibitory activity. Moreover, these leaves contain tannins, which canform complexes with enzymes and lead to false-positive results during biological testing. Therefore, this study was conducted to evaluate the arginaseinhibitory activity of S. cumini leaf extract and fractions as well as to elucidate the effects of tannins on this activity.Methods: S. cumini leaves were fractionated using n-hexane, ethyl acetate, and methanol. A colorimetric method was employed to evaluate arginaseinhibitory activity. Tannin elimination was performed through the gelatin precipitation method. Total phenolic and flavonoid contents of the fractionswere calculated using the Folin–Ciocalteu and aluminum chloride methods, respectively.Results: Ethyl acetate and methanol fractions showed arginase inhibitory activity with half-maximal inhibitory concentrations (IC50) of 46.96 and15.35 μg/mL, respectively. The methanol fraction was positive for tannins. After tannin elimination, this fraction exhibited less potent arginaseinhibitory activity, with an IC50 value of 53.03 μg/mL. The ethyl acetate fraction showed higher total phenolic and flavonoid contents than the methanolfraction.Conclusion: Tannins affected the arginase inhibitory activity of the methanol fraction of S. cumini leaves; however, the ethyl acetate fraction did notcontain tannins and could inhibit arginase activity.
Highlights
The endothelium plays an important role as the central hub for vascular structure, tone, and homeostasis regulation in cardiovascular physiology
The methanol fraction was positive for tannins
The methanol fraction was positive for tannins and tannin elimination was performed through the gelatin precipitation method [19]
Summary
The endothelium plays an important role as the central hub for vascular structure, tone, and homeostasis regulation in cardiovascular physiology. Endothelial dysfunction could serve as a predictor of various vascular diseases that lead to pathological conditions. Endothelial dysfunction is characterized by depleted levels of nitric oxide (NO) – a potent vasodilator biomarker [1]. NO synthesis is catalyzed by endothelial NO synthase (eNOS) from the amino acid L-arginine with cofactor tetrahydrobiopterin (BH4) [2]. L-arginine is utilized by arginase as a substrate to produce L-ornithine and urea. Competition between eNOS and arginase may occur under pathophysiological conditions. Increased expression and/or activity of arginase in endothelial cells can disrupt NO synthesis [3]
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