Catechins blunt the effects of oxldl and its primary metabolite phosphatidylcholine hydroperoxide on endothelial dysfunction through inhibition of oxidative stress and restoration of eNOS in rats

Hao Hsiang Chang; Chen Yen Chien; Kuo Hsin Chen; Shih Chung Huang; Chiang Ting Chien

doi:10.1159/000485082

Catechins blunt the effects of oxldl and its primary metabolite phosphatidylcholine hydroperoxide on endothelial dysfunction through inhibition of oxidative stress and restoration of eNOS in rats

Hao Hsiang Chang, Chen Yen Chien, Kuo Hsin Chen, Shih Chung Huang, Chiang Ting Chien

Research output: Contribution to journal › Article

3 Citations (Scopus)

Abstract

Background/Aims: We explored the effects of catechins (decaffeinated green tea extracts containing (-)-epicatechin, (-)-epigallocatechin, (-)-epicatechin gallate and (-)-epigallocatechin gallate) on atherosclerosis risk factors, oxidized low-density lipoprotein (oxLDL) and its primary metabolite, phosphatidylcholine hydroperoxide (PCOOH) induced oxidative injury in cultured endothelial cell line and rats. Methods: We used endothelial cell line and male Wistar rats to determine the effect of catechins on oxLDL or PCOOH induced oxidative injury including apoptosis, H ₂ O ₂ level, vascular responses and urinary 8-isoprostane and nitrite/nitrate concentration. Plasma catechins concentration was determined by a CoulArray HPLC. Responses of aortic and renal vasoconstriction were evaluated by a transonic meter and a full-field laser perfusion imager. Results: PCOOH administration significantly increased H ₂ O ₂ amounts and cell apoptosis and decreased endothelial nitric oxide synthase (eNOS) expression in the cultured endothelial cells. Catechins pretreatment significantly reduced PCOOH-elevated H ₂ O ₂ amounts, endothelial cell apoptosis and partly recovered eNOS expression. Intravenous administration of oxLDL, PCOOH or H ₂ O ₂ , not native LDL, significantly decreased renal and aortic blood flow associated with enhanced ICAM-1 expression and 4-hydroxynoneal (4-HNE) accumulation, and decreased eNOS expression in the male Wistrar rats. One hour after oral intake of green tea extracts, 4 peaks of catechins were found in the rat plasma. The increased plasma catechins significantly inhibited oxLDL-, PCOOH- or H ₂ O ₂ -induced renal and aortic vasoconstriction, decreased urinary 8-isoprostane levels, renal ICAM-1 expression and 4-HNE accumulation, and restored nitrite/nitrate amounts and eNOS activity. Conclusions: Our data suggests that catechins pretreatment decrease PCOOH-induced endothelial apoptosis and arterial vasoconstriction through the action of H ₂ O ₂ inhibition and eNOS restoration.

Original language	English
Pages (from-to)	919-932
Number of pages	14
Journal	Kidney and Blood Pressure Research
Volume	42
Issue number	5
DOIs	https://doi.org/10.1159/000485082
Publication status	Published - 2018 Jan 1

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Keywords

Catechins
Endothelial cells
Nitric oxide
Oxidative stress
PCOOH
Vasoconstriction

ASJC Scopus subject areas

Nephrology
Cardiology and Cardiovascular Medicine

Cite this

Chang, H. H., Chien, C. Y., Chen, K. H., Huang, S. C., & Chien, C. T. (2018). Catechins blunt the effects of oxldl and its primary metabolite phosphatidylcholine hydroperoxide on endothelial dysfunction through inhibition of oxidative stress and restoration of eNOS in rats. Kidney and Blood Pressure Research, 42(5), 919-932. https://doi.org/10.1159/000485082

Catechins blunt the effects of oxldl and its primary metabolite phosphatidylcholine hydroperoxide on endothelial dysfunction through inhibition of oxidative stress and restoration of eNOS in rats. / Chang, Hao Hsiang; Chien, Chen Yen; Chen, Kuo Hsin; Huang, Shih Chung; Chien, Chiang Ting.

In: Kidney and Blood Pressure Research, Vol. 42, No. 5, 01.01.2018, p. 919-932.

Research output: Contribution to journal › Article

Chang, Hao Hsiang ; Chien, Chen Yen ; Chen, Kuo Hsin ; Huang, Shih Chung ; Chien, Chiang Ting. / Catechins blunt the effects of oxldl and its primary metabolite phosphatidylcholine hydroperoxide on endothelial dysfunction through inhibition of oxidative stress and restoration of eNOS in rats. In: Kidney and Blood Pressure Research. 2018 ; Vol. 42, No. 5. pp. 919-932.

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abstract = " Background/Aims: We explored the effects of catechins (decaffeinated green tea extracts containing (-)-epicatechin, (-)-epigallocatechin, (-)-epicatechin gallate and (-)-epigallocatechin gallate) on atherosclerosis risk factors, oxidized low-density lipoprotein (oxLDL) and its primary metabolite, phosphatidylcholine hydroperoxide (PCOOH) induced oxidative injury in cultured endothelial cell line and rats. Methods: We used endothelial cell line and male Wistar rats to determine the effect of catechins on oxLDL or PCOOH induced oxidative injury including apoptosis, H 2 O 2 level, vascular responses and urinary 8-isoprostane and nitrite/nitrate concentration. Plasma catechins concentration was determined by a CoulArray HPLC. Responses of aortic and renal vasoconstriction were evaluated by a transonic meter and a full-field laser perfusion imager. Results: PCOOH administration significantly increased H 2 O 2 amounts and cell apoptosis and decreased endothelial nitric oxide synthase (eNOS) expression in the cultured endothelial cells. Catechins pretreatment significantly reduced PCOOH-elevated H 2 O 2 amounts, endothelial cell apoptosis and partly recovered eNOS expression. Intravenous administration of oxLDL, PCOOH or H 2 O 2 , not native LDL, significantly decreased renal and aortic blood flow associated with enhanced ICAM-1 expression and 4-hydroxynoneal (4-HNE) accumulation, and decreased eNOS expression in the male Wistrar rats. One hour after oral intake of green tea extracts, 4 peaks of catechins were found in the rat plasma. The increased plasma catechins significantly inhibited oxLDL-, PCOOH- or H 2 O 2 -induced renal and aortic vasoconstriction, decreased urinary 8-isoprostane levels, renal ICAM-1 expression and 4-HNE accumulation, and restored nitrite/nitrate amounts and eNOS activity. Conclusions: Our data suggests that catechins pretreatment decrease PCOOH-induced endothelial apoptosis and arterial vasoconstriction through the action of H 2 O 2 inhibition and eNOS restoration. ",

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AU - Chen, Kuo Hsin

AU - Huang, Shih Chung

AU - Chien, Chiang Ting

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10.1159/000485082