المؤلفون: Hae Jin Kee, Myung Ho Jeong, Zhe Hao Piao, Sin Young Choi, Chun Ping Liu, Bin Liu, Li Jin, Gwi Ran Kim, Yuhee Ryu, Simei Sun

المصدر: Journal of Cellular and Molecular Medicine

مصطلحات موضوعية: Male, 0301 basic medicine, Apoptosis, Blood Pressure, Essential hypertension, Rats, Inbred WKY, chemistry.chemical_compound, Atrial natriuretic peptide, Rats, Inbred SHR, Natriuretic Peptide, Brain, Myocytes, Cardiac, p300-CBP Transcription Factors, Gallic acid, bcl-2-Associated X Protein, biology, Caspase 3, cardiac hypertrophy, Angiotensin II, spontaneously hypertensive rats (SHR), Brain natriuretic peptide, Isoenzymes, Nitric oxide synthase, Hypertension, cardiovascular system, Molecular Medicine, Original Article, Hypertrophy, Left Ventricular, Atrial Natriuretic Factor, Signal Transduction, medicine.medical_specialty, Cardiotonic Agents, Cell Line, 03 medical and health sciences, Gallic Acid, Internal medicine, Ca2+/calmodulin-dependent protein kinase, medicine, Animals, Antihypertensive Agents, Ca2+/calmodulin‐dependent protein kinase II, Original Articles, Cell Biology, medicine.disease, Rats, 030104 developmental biology, Endocrinology, Gene Expression Regulation, chemistry, biology.protein, Nitric Oxide Synthase, Tumor Suppressor Protein p53, Calcium-Calmodulin-Dependent Protein Kinase Type 2

الوصف: Hypertension causes cardiac hypertrophy and leads to heart failure. Apoptotic cells are common in hypertensive hearts. Ca2+/calmodulin‐dependent protein kinase II (CaMKII) is associated with apoptosis. We recently demonstrated that gallic acid reduces nitric oxide synthase inhibition‐induced hypertension. Gallic acid is a trihydroxybenzoic acid and has been shown to have beneficial effects, such as anti‐cancer, anti‐calcification and anti‐oxidant activity. The purpose of this study was to determine whether gallic acid regulates cardiac hypertrophy and apoptosis in essential hypertension. Gallic acid significantly lowered systolic and diastolic blood pressure in spontaneously hypertensive rats (SHRs). Wheat germ agglutinin (WGA) and H&E staining revealed that gallic acid reduced cardiac enlargement in SHRs. Gallic acid treatment decreased cardiac hypertrophy marker genes, including atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP), in SHRs. The four isoforms, α, β, δ and γ, of CaMKII were increased in SHRs and were significantly reduced by gallic acid administration. Gallic acid reduced cleaved caspase‐3 protein as well as bax, p53 and p300 mRNA levels in SHRs. CaMKII δ overexpression induced bax and p53 expression, which was attenuated by gallic acid treatment in H9c2 cells. Gallic acid treatment reduced DNA fragmentation and the TUNEL positive cells induced by angiotensin II. Taken together, gallic acid could be a novel therapeutic for the treatment of hypertension through suppression of CaMKII δ‐induced apoptosis.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::0fd0c03e67ab3a1e36bf6670923376bdTest
https://doi.org/10.1111/jcmm.13419Test

المؤلفون: Sin Young Choi, Gwi Ran Kim, Yuhee Ryu, Simei Sun, Jae Yeong Cho, Hae Jin Kee, Ming Quan Lin, Myung Ho Jeong, Li Jin, Zhe Hao Piao

المصدر: Journal of Hypertension. 35:1502-1512

مصطلحات موضوعية: Male, 0301 basic medicine, Antioxidant, Physiology, Heart Ventricles, medicine.medical_treatment, Histone Deacetylase 2, Blood Pressure, Histone Deacetylase 1, Mice, 03 medical and health sciences, chemistry.chemical_compound, Fibrosis, Gallic Acid, NG-Nitroarginine Methyl Ester, Internal Medicine, medicine, Animals, Gallic acid, Histone deacetylase 5, Ventricular Remodeling, Histone deacetylase 2, business.industry, medicine.disease, Ng-nitro-L-arginine methyl ester, HDAC1, Rats, 030104 developmental biology, chemistry, Biochemistry, Hypertension, Nitric Oxide Synthase, Cardiology and Cardiovascular Medicine, business

الوصف: Gallic acid, a natural chemical found in plants, has been reported to show antioxidant, anticancer, and anti-inflammatory effects. We investigated the efficacy of a short-term or long-term treatment with gallic acid in N-nitro-L-arginine methyl ester (L-NAME)-induced hypertensive mice and the underlying regulatory mechanism.Hypertension was sufficiently induced after 2 weeks of L-NAME administration. Cardiac remodeling was assessed by echocardiography. Hypertrophic markers, transcription factors, and fibrosis-related gene expression were evaluated by quantitative real-time polymerase chain reaction and western blotting.Gallic acid effectively lowered SBP, regardless of the administration route (intraperitoneal or oral). L-NAME increased the left ventricular (LV) thickness without an increase in the total heart weight. Weekly echocardiography demonstrated that gallic acid significantly reduced LV posterior wall and septum thickness in chronic L-NAME mice from 3 to 7 weeks. The administration of gallic acid to mice showed a dual preventive and therapeutic effect on the L-NAME-induced LV remodeling. The effect was associated with the suppression of the gene expression of hypertrophy markers and the GATA-binding factor 6 (GATA6) transcription factor. Short-term or long-term treatment with gallic acid attenuated cardiac fibrosis and reduced the expression of histone deacetylase 1 and 2 in H9c2 cells and in rat primary cardiac fibroblasts, as well as in vivo. Small interfering RNA knockdown confirmed the association of these enzymes with L-NAME-induced cardiac remodeling and fibrosis.These results suggested that gallic acid may be a potential therapeutic agent for the treatment of cardiovascular diseases with hypertension and cardiac fibrosis.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a55b615687603aee17f6d3b645aee114Test
https://doi.org/10.1097/hjh.0000000000001327Test

المؤلفون: Hae Jin Kee, Myung Ho Jeong, Gwi Ran Kim, Simei Sun, Zhe Hao Piao, Young Mi Seok, Sin Young Choi, Li Jin, Bin Liu, Ming Quan Lin, Yuhee Ryu

المصدر: SCIENTIFIC REPORTS(7)
Scientific Reports, Vol 7, Iss 1, Pp 1-14 (2017)
Scientific Reports

مصطلحات موضوعية: Male, 0301 basic medicine, medicine.medical_specialty, lcsh:Medicine, Blood Pressure, Cardiomegaly, 030204 cardiovascular system & hematology, Left ventricular hypertrophy, Essential hypertension, medicine.disease_cause, Article, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Gallic Acid, Rats, Inbred SHR, Internal medicine, Renin–angiotensin system, medicine, Animals, Humans, cardiovascular diseases, lcsh:Science, Multidisciplinary, NADPH oxidase, biology, Chemistry, GATA4, Angiotensin II, lcsh:R, Blood Pressure Determination, Heart, medicine.disease, Malondialdehyde, GATA4 Transcription Factor, Rats, Oxidative Stress, 030104 developmental biology, Endocrinology, Blood pressure, Gene Expression Regulation, Hypertension, NADPH Oxidase 2, Homeobox Protein Nkx-2.5, biology.protein, cardiovascular system, lcsh:Q, Oxidative stress

الوصف: Gallic acid (GA) has been reported to have beneficial effects on cancer, vascular calcification, and diabetes-induced myocardial dysfunction. We hypothesized that GA controls hypertension via oxidative stress response regulation in an animal model for essential hypertension. Spontaneously hypertensive rats (SHRs) were administered GA for 16 weeks. GA treatment lowered elevated systolic blood pressure in SHRs through the inhibition of vascular contractility and components of the renin-angiotensin II system. In addition, GA administration reduced aortic wall thickness and body weight in SHRs. In SHRs, GA attenuated left ventricular hypertrophy and reduced the expression of cardiac-specific transcription factors. NADPH oxidase 2 (Nox2) and GATA4 mRNA expression was induced in SHR hearts and angiotensin II-treated H9c2 cells; this expression was downregulated by GA treatment. Nox2 promoter activity was increased by the synergistic action of GATA4 and Nkx2-5. GA seems to regulate oxidative stress by inhibiting the DNA binding activity of GATA4 in the rat Nox2 promoter. GA reduced the GATA4-induced Nox activity in SHRs and angiotensin II-treated H9c2 cells. GA administration reduced the elevation of malondialdehyde levels in heart tissue obtained from SHRs. These findings suggest that GA is a potential therapeutic agent for treating cardiac hypertrophy and oxidative stress in SHRs.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::23585899b4d6652c5681d93ca50df413Test
http://open-repository.kisti.re.kr/cube/handle/open_repository/479323.doTest

المؤلفون: Yuhee Ryu, Li Jin, Zhe Hao Piao, Hae Jin Kee, Gwi Ran Kim, Myung Ho Jeong, Sin Young Choi, Ming Quan Lin

المصدر: Korean Circulation Journal

مصطلحات موضوعية: 0301 basic medicine, medicine.medical_specialty, 030204 cardiovascular system & hematology, 03 medical and health sciences, 0302 clinical medicine, L-NAME, Internal medicine, Internal Medicine, medicine, Histone deacetylase 5, business.industry, Angiotensin II, Class II histone deacetylases, HDAC8, HDAC6, HDAC3, HDAC4, 030104 developmental biology, Endocrinology, Blood pressure, Spontaneously hypertensive rats, Hypertension, Original Article, Histone deacetylase, Cardiology and Cardiovascular Medicine, business

الوصف: Background and objectives Dysregulation of histone deacetylase expression and enzymatic activity is associated with a number of diseases. It has been reported that protein levels of histone deacetylase (HDAC)1 and HDAC5 increase during human pulmonary hypertension, and that the enzymatic activity of HDAC6 is induced in a chronic hypertensive animal model. This study investigated the protein expression profiles of class I and II a/b HDACs in three systemic hypertension models. Subjects and methods We used three different hypertensive animal models: (i) Wistar-Kyoto rats (n=8) and spontaneously hypertensive rats (SHR; n=8), (ii) mice infused with saline or angiotensin II to induce hypertension, via osmotic mini-pump for 2 weeks, and (iii) mice that were allowed to drink L-NG-nitro-L-arginine methyl ester (L-NAME) to induce hypertension. Results SHR showed high systolic, diastolic, and mean blood pressures. Similar increases in systolic blood pressure were observed in angiotensin II or L-NAME-induced hypertensive mice. In SHR, class IIa HDAC (HDAC4, 5, and 7) and class IIb HDAC (HDAC6 and 10) protein expression were significantly increased. In addition, a HDAC3 protein expression was induced in SHR. However, in L-NAME mice, class IIa HDAC protein levels (HDAC4, 5, 7, and 9) were significantly reduced. HDAC8 protein levels were significantly reduced both in angiotensin II mice and in SHR. Conclusion These results indicate that dysregulation of class I and class II HDAC protein is closely associated with chronic hypertension.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::cbb880fd3fd8882e81c5ceae236750fcTest
https://pubmed.ncbi.nlm.nih.gov/28567090Test