Arginase Inhibition by Ethylacetate Extract of<i>Caesalpinia sappan</i>Lignum Contributes to Activation of Endothelial Nitric Oxide Synthase

Shin, Woosung; Cuong, To Dao; Lee, Jeong Hyung; Min, Byung‐Sun; Jeon, Byeong Hwa; Lim, Hyun Kyo; Ryoo, Sungwoo

doi:10.4196/kjpp.2011.15.3.123

Cited by 25 publications

(23 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Hence, the inhibition of arginase activity can be additional therapeutic targets for the management of ED as this could increase the bioavailability of L-arginine, contribute to the production of NO via reaction catalyzed by NOS, where overall result could facilitate penile erection. Inhibition of arginase activity by the studied extracts is in line with some reports of plant extracts, which are rich in phenolics including epicatechin, quercetin, quercitrin and isoquercitrin and their arginase inhibitory potential (Shin et al 2011;Oboh et al 2015;Akomolafe et al 2016). Hence, the observed high flavonoid content and abundant presence of flavonoid compounds such as (-)-epicatechin, rutin, quercetin and quercitrin in UPP may be responsible for its higher arginase inhibitory activity.…”

Section: Discussionsupporting

confidence: 66%

Modulation of some markers of erectile dysfunction and malonaldehyde levels in isolated rat penile tissue with unripe and ripe plantain peels: identification of the constituents of the plants using HPLC

Oboh

Ademiluyi

Oyeleye

et al. 2017

Pharmaceutical Biology

View full text Add to dashboard Cite

Section: Discussionsupporting

confidence: 66%

Modulation of some markers of erectile dysfunction and malonaldehyde levels in isolated rat penile tissue with unripe and ripe plantain peels: identification of the constituents of the plants using HPLC

Oboh

Ademiluyi

Oyeleye

et al. 2017

Pharmaceutical Biology

View full text Add to dashboard Cite

“…Endothelial function is modulated by vasodilators and vasoconstrictors in vivo . It is well established that nitric oxide (NO) produced in vascular endothelial cells has a potent vasodilator effect [3-5] and plays an important role in vascular resistance and growth [6]. Administration of L-arginine analogues such as N G -nitro-L-arginine methyl ester hydrochloride (L-NAME) inhibits nitric oxide synthase (NOS) activity and hence NO biosynthesis, leading to hypertension [7-10].…”

Section: Introductionmentioning

confidence: 99%

Effect of Lutein on L-NAME-Induced Hypertensive Rats

Sung

Kim

et al. 2013

Korean J Physiol Pharmacol

View full text Add to dashboard Cite

We investigated the antihypertensive effect of lutein on NG-nitro-L-arginine methyl ester hydrochloride (L-NAME)-induced hypertensive rats. Daily oral administration of L-NAME (40 mg/kg)-induced a rapid progressive increase in mean arterial pressure (MAP). L-NAME significantly increased MAP from the first week compared to that in the control and reached 193.3±9.6 mmHg at the end of treatment. MAP in the lutein groups was dose-dependently lower than that in the L-NAME group. Similar results were observed for systolic and diastolic blood pressure of L-NAME-induced hypertensive rats. The control group showed little change in heart rate for 3 weeks, whereas L-NAME significantly reduced heart rate from 434±26 to 376±33 beats/min. Lutein (2 mg/kg) significantly prevented the reduced heart rate induced by L-NAME. L-NAME caused hypertrophy of heart and kidney, and increased plasma lipid peroxidation four-fold but significantly reduced plasma nitrite and glutathione concentrations, which were significantly prevented by lutein in a dose-dependent manner. These findings suggest that lutein affords significant antihypertensive and antioxidant effects against L-NAME-induced hypertension in rats.

show abstract

“…Modulation of endothelial nitric oxide synthase (eNOS) activation is a target protein for treating cardiovascular disorder [21-23]. The p66shc adaptor protein has an inhibitory role in eNOS activity [24] and endothelial vasomotor function [10].…”

Section: Discussionmentioning

confidence: 99%

Tat-Mediated p66shc Transduction Decreased Phosphorylation of Endothelial Nitric Oxide Synthase in Endothelial Cells

Lee

Joo

et al. 2012

Korean J Physiol Pharmacol

Self Cite

View full text Add to dashboard Cite

We evaluated the role of Tat-mediated p66shc transduction on the activation of endothelial nitric oxide synthase in cultured mouse endothelial cells. To construct the Tat-p66shc fusion protein, human full length p66shc cDNA was fused with the Tat-protein transduction domain. Transduction of TAT-p66shc showed a concentration- and time-dependent manner in endothelial cells. Tat-mediated p66shc transduction showed increased hydrogen peroxide and superoxide production, compared with Tat-p66shc (S/A), serine 36 residue mutant of p66shc. Tat-mediated p66shc transduction decreased endothelial nitric oxide synthase phosphorylation in endothelial cells. Furthermore, Tat-mediated p66shc transduction augmented TNF-α-induced p38 MAPK phosphorylation in endothelial cells. These results suggest that Tat-mediated p66shc transduction efficiently inhibited endothelial nitric oxide synthase phosphorylation in endothelial cells.

show abstract

Arginase Inhibition by Ethylacetate Extract ofCaesalpinia sappanLignum Contributes to Activation of Endothelial Nitric Oxide Synthase

Cited by 25 publications

References 34 publications

Modulation of some markers of erectile dysfunction and malonaldehyde levels in isolated rat penile tissue with unripe and ripe plantain peels: identification of the constituents of the plants using HPLC

Modulation of some markers of erectile dysfunction and malonaldehyde levels in isolated rat penile tissue with unripe and ripe plantain peels: identification of the constituents of the plants using HPLC

Effect of Lutein on L-NAME-Induced Hypertensive Rats

Tat-Mediated p66shc Transduction Decreased Phosphorylation of Endothelial Nitric Oxide Synthase in Endothelial Cells

Contact Info

Product

Resources

About