PMID- 23084641 OWN - NLM STAT- MEDLINE DCOM- 20130326 LR - 20220409 IS - 1879-0739 (Electronic) IS - 0271-5317 (Linking) VI - 32 IP - 9 DP - 2012 Sep TI - Green tea extract reverses endothelial dysfunction and reduces atherosclerosis progression in homozygous knockout low-density lipoprotein receptor mice. PG - 684-93 LID - S0271-5317(12)00164-9 [pii] LID - 10.1016/j.nutres.2012.08.003 [doi] AB - 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 muL/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 alpha 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. CI - Copyright (c) 2012 Elsevier Inc. All rights reserved. FAU - Minatti, Jaqueline AU - Minatti J AD - Department of Nutrition, Health Sciences Center, Federal University of Santa Catarina, Florianopolis, SC, Brazil. FAU - Wazlawik, Elisabeth AU - Wazlawik E FAU - Hort, Mariana A AU - Hort MA FAU - Zaleski, Fernanda L AU - Zaleski FL FAU - Ribeiro-do-Valle, Rosa M AU - Ribeiro-do-Valle RM FAU - Maraschin, Marcelo AU - Maraschin M FAU - da Silva, Edson L AU - da Silva EL LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20120903 PL - United States TA - Nutr Res JT - Nutrition research (New York, N.Y.) JID - 8303331 RN - 0 (Antioxidants) RN - 0 (Biomarkers) RN - 0 (Ccl2 protein, mouse) RN - 0 (Chemokine CCL2) RN - 0 (Lipoproteins, LDL) RN - 0 (Plant Extracts) RN - 0 (Receptors, LDL) RN - 0 (Tea) RN - 0 (Triglycerides) RN - 0 (Tumor Necrosis Factor-alpha) RN - 8R1V1STN48 (Catechin) RN - BQM438CTEL (epigallocatechin gallate) RN - EC 2.6.1.2 (Alanine Transaminase) SB - IM MH - Alanine Transaminase/metabolism MH - Animals MH - Antioxidants/*pharmacology MH - Aorta/drug effects/metabolism MH - Atherosclerosis/*drug therapy/pathology MH - Biomarkers/blood MH - Catechin/*analogs & derivatives/pharmacology MH - Chemokine CCL2/blood MH - Disease Models, Animal MH - Endothelium, Vascular/*drug effects/physiopathology MH - Female MH - Inflammation/drug therapy/pathology MH - Lipoproteins, LDL/blood MH - Male MH - Mice MH - Mice, Inbred C57BL MH - Mice, Knockout MH - Plant Extracts/*pharmacology MH - Receptors, LDL/genetics MH - Tea/*chemistry MH - Triglycerides/blood MH - Tumor Necrosis Factor-alpha/blood EDAT- 2012/10/23 06:00 MHDA- 2013/03/27 06:00 CRDT- 2012/10/23 06:00 PHST- 2011/12/11 00:00 [received] PHST- 2012/07/31 00:00 [revised] PHST- 2012/08/03 00:00 [accepted] PHST- 2012/10/23 06:00 [entrez] PHST- 2012/10/23 06:00 [pubmed] PHST- 2013/03/27 06:00 [medline] AID - S0271-5317(12)00164-9 [pii] AID - 10.1016/j.nutres.2012.08.003 [doi] PST - ppublish SO - Nutr Res. 2012 Sep;32(9):684-93. doi: 10.1016/j.nutres.2012.08.003. Epub 2012 Sep 3.