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 journalArticle

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 languageEnglish
Pages (from-to)919-932
Number of pages14
JournalKidney and Blood Pressure Research
Volume42
Issue number5
DOIs
Publication statusPublished - 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

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