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Contributions of Nrf2 to Puerarin Prevention of Cardiac Hypertrophy and its Metabolic Enzymes Expression in Rats.
Zhao, Gan-Jian; Hou, Ning; Cai, Shao-Ai; Liu, Xia-Wen; Li, Ai-Qun; Cheng, Chuan-Fang; Huang, Yin; Li, Li-Rong; Mai, Yun-Pei; Liu, Shi-Ming; Ou, Cai-Wen; Xiong, Zhen-Yu; Chen, Xiao-Hui; Chen, Min-Sheng; Luo, Cheng-Feng.
Afiliación
  • Zhao GJ; The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou Institute of Cardiovascular Disease (G.-J.Z., A.-Q.L., C.-F.C., Y.H., L.-R.L., S.-M.L., C.-F.L.), School of Pharmaceutical Sciences and the Fifth Affiliated Hospital, Guangzhou Medical University (N.H., X.-W.L., Y.-P.M.), The
  • Hou N; The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou Institute of Cardiovascular Disease (G.-J.Z., A.-Q.L., C.-F.C., Y.H., L.-R.L., S.-M.L., C.-F.L.), School of Pharmaceutical Sciences and the Fifth Affiliated Hospital, Guangzhou Medical University (N.H., X.-W.L., Y.-P.M.), The
  • Cai SA; The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou Institute of Cardiovascular Disease (G.-J.Z., A.-Q.L., C.-F.C., Y.H., L.-R.L., S.-M.L., C.-F.L.), School of Pharmaceutical Sciences and the Fifth Affiliated Hospital, Guangzhou Medical University (N.H., X.-W.L., Y.-P.M.), The
  • Liu XW; The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou Institute of Cardiovascular Disease (G.-J.Z., A.-Q.L., C.-F.C., Y.H., L.-R.L., S.-M.L., C.-F.L.), School of Pharmaceutical Sciences and the Fifth Affiliated Hospital, Guangzhou Medical University (N.H., X.-W.L., Y.-P.M.), The
  • Li AQ; The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou Institute of Cardiovascular Disease (G.-J.Z., A.-Q.L., C.-F.C., Y.H., L.-R.L., S.-M.L., C.-F.L.), School of Pharmaceutical Sciences and the Fifth Affiliated Hospital, Guangzhou Medical University (N.H., X.-W.L., Y.-P.M.), The
  • Cheng CF; The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou Institute of Cardiovascular Disease (G.-J.Z., A.-Q.L., C.-F.C., Y.H., L.-R.L., S.-M.L., C.-F.L.), School of Pharmaceutical Sciences and the Fifth Affiliated Hospital, Guangzhou Medical University (N.H., X.-W.L., Y.-P.M.), The
  • Huang Y; The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou Institute of Cardiovascular Disease (G.-J.Z., A.-Q.L., C.-F.C., Y.H., L.-R.L., S.-M.L., C.-F.L.), School of Pharmaceutical Sciences and the Fifth Affiliated Hospital, Guangzhou Medical University (N.H., X.-W.L., Y.-P.M.), The
  • Li LR; The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou Institute of Cardiovascular Disease (G.-J.Z., A.-Q.L., C.-F.C., Y.H., L.-R.L., S.-M.L., C.-F.L.), School of Pharmaceutical Sciences and the Fifth Affiliated Hospital, Guangzhou Medical University (N.H., X.-W.L., Y.-P.M.), The
  • Mai YP; The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou Institute of Cardiovascular Disease (G.-J.Z., A.-Q.L., C.-F.C., Y.H., L.-R.L., S.-M.L., C.-F.L.), School of Pharmaceutical Sciences and the Fifth Affiliated Hospital, Guangzhou Medical University (N.H., X.-W.L., Y.-P.M.), The
  • Liu SM; The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou Institute of Cardiovascular Disease (G.-J.Z., A.-Q.L., C.-F.C., Y.H., L.-R.L., S.-M.L., C.-F.L.), School of Pharmaceutical Sciences and the Fifth Affiliated Hospital, Guangzhou Medical University (N.H., X.-W.L., Y.-P.M.), The
  • Ou CW; The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou Institute of Cardiovascular Disease (G.-J.Z., A.-Q.L., C.-F.C., Y.H., L.-R.L., S.-M.L., C.-F.L.), School of Pharmaceutical Sciences and the Fifth Affiliated Hospital, Guangzhou Medical University (N.H., X.-W.L., Y.-P.M.), The
  • Xiong ZY; The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou Institute of Cardiovascular Disease (G.-J.Z., A.-Q.L., C.-F.C., Y.H., L.-R.L., S.-M.L., C.-F.L.), School of Pharmaceutical Sciences and the Fifth Affiliated Hospital, Guangzhou Medical University (N.H., X.-W.L., Y.-P.M.), The
  • Chen XH; The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou Institute of Cardiovascular Disease (G.-J.Z., A.-Q.L., C.-F.C., Y.H., L.-R.L., S.-M.L., C.-F.L.), School of Pharmaceutical Sciences and the Fifth Affiliated Hospital, Guangzhou Medical University (N.H., X.-W.L., Y.-P.M.), The
  • Chen MS; The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou Institute of Cardiovascular Disease (G.-J.Z., A.-Q.L., C.-F.C., Y.H., L.-R.L., S.-M.L., C.-F.L.), School of Pharmaceutical Sciences and the Fifth Affiliated Hospital, Guangzhou Medical University (N.H., X.-W.L., Y.-P.M.), The
  • Luo CF; The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou Institute of Cardiovascular Disease (G.-J.Z., A.-Q.L., C.-F.C., Y.H., L.-R.L., S.-M.L., C.-F.L.), School of Pharmaceutical Sciences and the Fifth Affiliated Hospital, Guangzhou Medical University (N.H., X.-W.L., Y.-P.M.), The
J Pharmacol Exp Ther ; 366(3): 458-469, 2018 09.
Article en En | MEDLINE | ID: mdl-29945930
ABSTRACT
Previous evidence has suggested that puerarin may attenuate cardiac hypertrophy; however, the potential mechanisms have not been determined. Moreover, the use of puerarin is limited by severe adverse events, including intravascular hemolysis. This study used a rat model of abdominal aortic constriction (AAC)-induced cardiac hypertrophy to evaluate the potential mechanisms underlying the attenuating efficacy of puerarin on cardiac hypertrophy, as well as the metabolic mechanisms of puerarin involved. We confirmed that puerarin (50 mg/kg per day) significantly attenuated cardiac hypertrophy, upregulated Nrf2, and decreased Keap1 in the myocardium. Moreover, puerarin significantly promoted Nrf2 nuclear accumulation in parallel with the upregulated downstream proteins, including heme oxygenase 1, glutathione transferase P1, and NAD(P)Hquinone oxidoreductase 1. Similar results were obtained in neonatal rat cardiomyocytes (NRCMs) treated with angiotensin II (Ang II; 1 µM) and puerarin (100 µM), whereas the silencing of Nrf2 abolished the antihypertrophic effects of puerarin. The mRNA and protein levels of UGT1A1 and UGT1A9, enzymes for puerarin metabolism, were significantly increased in the liver and heart tissues of AAC rats and Ang II-treated NRCMs. Interestingly, the silencing of Nrf2 attenuated the puerarin-induced upregulation of UGT1A1 and UGT1A9. The results of chromatin immunoprecipitation-quantitative polymerase chain reaction indicated that the binding of Nrf2 to the promoter region of Ugt1a1 or Ugt1a9 was significantly enhanced in puerarin-treated cardiomyocytes. These results suggest that Nrf2 is the key regulator of antihypertrophic effects and upregulation of the metabolic enzymes UGT1A1 and UGT1A9 of puerarin. The autoregulatory circuits between puerarin and Nrf2-induced UGT1A1/1A9 are beneficial to attenuate adverse effects and maintain the pharmacologic effects of puerarin.
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Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Regulación Enzimológica de la Expresión Génica / Cardiomegalia / Factor 2 Relacionado con NF-E2 / Isoflavonas Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Año: 2018 Tipo del documento: Article
Texto completo
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Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Regulación Enzimológica de la Expresión Génica / Cardiomegalia / Factor 2 Relacionado con NF-E2 / Isoflavonas Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Año: 2018 Tipo del documento: Article