Green tea extract reverses endothelial dysfunction and reduces atherosclerosis progression in homozygous knockout low-density lipoprotein receptor mice.
The aim of this study was to evaluate the effects of green tea extract (GTE) administration on vascular reactivity and atherosclerosis progression in low-density lipoprotein receptor knockout mice. We hypothesized that GTE intake may ameliorate atherosclerosis by improving endothelial dysfunction. Animals (n = 12 per group) were fed a hypercholesterolemic diet and received either water or GTE at a dose of 50, 100, or 300 mg/kg once a day by gavage (100 μL/10 g weight). After 4 weeks, atherosclerosis extension and vascular reactivity were evaluated in the aorta, and the levels of lipids, monocyte chemotactic protein-1 (MCP-1), and tumor necrosis factor α were measured in the plasma. Administration of GTE at a dose of 50 mg/kg significantly decreased the area of atherosclerotic lesions by 35%, improved the vascular reactivity in the isolated thoracic aorta, and lowered the plasma levels of both MCP-1 and triglycerides. Delivery of 100 mg/kg of GTE only promoted vasocontraction and vasorelaxation (P < .05), whereas a dose of 300 mg/kg was ineffective. Maximum contraction and relaxation negatively correlated with the lesion area (r = -0.755 and -0.767, respectively), whereas the plasma levels of MCP-1 and triglycerides positively correlated with plaque size (r = 0.549 and 0.421, respectively). In summary, our results supported the hypothesis that administration of GTE at low doses may contribute to a decrease in atherosclerosis progression by reversing endothelial dysfunction.
Department of Nutrition, Health Sciences Center, Federal University of Santa Catarina, Florianópolis, SC, Brazil.
Jaqueline
J
Minatti
Elisabeth
E
Wazlawik
Mariana A
MA
Hort
Fernanda L
FL
Zaleski
Rosa M
RM
Ribeiro-do-Valle
Marcelo
M
Maraschin
Edson L
EL
da Silva
D000410:Alanine Transaminase / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D001011:Aorta / Q000187:drug effects / Q000378:metabolism; D050197:Atherosclerosis / Q000188:drug therapy* / Q000473:pathology; D015415:Biomarkers / Q000097:blood; D002392:Catechin / Q000031:analogs & derivatives* / Q000494:pharmacology; D018932:Chemokine CCL2 / Q000097:blood; D004195:Disease Models, Animal; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000503:physiopathology; D005260:Female; D007249:Inflammation / Q000188:drug therapy / Q000473:pathology; D008077:Lipoproteins, LDL / Q000097:blood; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D010936:Plant Extracts / Q000494:pharmacology*; D011973:Receptors, LDL / Q000235:genetics; D013662:Tea / Q000737:chemistry*; D014280:Triglycerides / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
D000975:Antioxidants; D015415:Biomarkers; C491768:Ccl2 protein, mouse; D018932:Chemokine CCL2; D008077:Lipoproteins, LDL; D010936:Plant Extracts; D011973:Receptors, LDL; D013662:Tea; D014280:Triglycerides; D014409:Tumor Necrosis Factor-alpha; D002392:Catechin; C045651:epigallocatechin gallate; D000410:Alanine Transaminase