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기해진,Yuhee Ryu,Young Mi Seok,최신영,Simei Sun,Gwi Ran Kim,정명호 대한고혈압학회 2019 Clinical Hypertension Vol.25 No.3
Background: The dysregulation of histone deacetylase (HDAC) protein expression or its enzyme activity is implicated in a variety of diseases. Cardiac HDAC6 and HDAC8 enzyme activity induced by deoxycorticosterone acetate (DOCA) hypertension was attenuated by sodium valproate, a pan-HDAC inhibitor. However, the HDAC6- selective inhibitor, tubastatin A, did not attenuate angiotensin II-induced hypertension. The purpose of this study was to investigate whether PCI34051, an HDAC8-selective inhibitor, can modulate angiotensin II-induced hypertension and its regulatory mechanism. Methods: An angiotensin II-regulated mouse model was used in this study. Animals received vehicle or PCI34051 (3 mg·kg − 1 ·day− 1 ) via intraperitoneal injection. Systolic blood pressure was measured by the tail-cuff method. Blood vessel thickness was measured following hematoxylin and eosin staining, VCAM-1 immunohistochemistry was performed in the aortas, and mRNA expression of renin-angiotensin system components, inflammation markers, and NADPH oxidase (Nox) was determined by RT-PCR. The effect of PCI34051 on vasorelaxation was studied in rat aortic rings, and its effect on nitric oxide (NO) production was determined using DAF-FM DA, a fluorescent dye, in human umbilical vascular endothelial cells (HUVECs). Results: PCI34051 administration reduced systolic blood pressure via downregulation of angiotensin II receptor type 1 (AT1) mRNA expression. PCI34051 treatment attenuated vascular hypertrophy by decreasing E2F3 and GATA6 mRNA expression. Vascular relaxation after PCI34051 treatment was more dependent on vascular endothelial cells and it was blocked by an NO synthase (NOS) inhibitor. In addition, NO production increased in HUVECs after PCI34051 treatment; this was decreased by the NOS inhibitor. The expression of inflammatory molecules and adhesion molecules VCAM-1 and ICAM-1 decreased in the aortas of angiotensin II-infused mice after PCI34051 administration. However, PCI34051 did not affect Nox or its regulatory subunits. Conclusions: PCI34051 lowered high blood pressure through modulation of arterial remodeling, vasoconstriction, and inflammation in an angiotensin II-induced hypertension model. We suggest that HDAC8 could be a potential therapeutic target for hypertension.
기해진,김귀란,Ming Quan Lin,최신영,류유희,Li Jin,Zhe Hao Piao,정명호 대한심장학회 2017 Korean Circulation Journal Vol.47 No.3
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. Materials 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.
기해진,황영선,김강화,홍윤호 한국축산식품학회 1998 한국축산식품학회지 Vol.18 No.1
In order to study the tenderizing effect of the proteolytic enzyme, ficin, from fig fruit (Ficus carica L), the enzyme was purified from fig latex by precipitation and chromatography. The ficin separated from Bongraesi showed single band on SDS-PAGE. However, the ficin from Masui showed tow bands. The specific activity of ficin purified from Bongraesi species was 2.8 unit/mg protein and that from Masui species was 6.5 unit / mg protein. The amounts of ficin purified from 50 mL of crude latex of Bongraesi and Masui were 1,760 mg and 657 mg, respectively. the water holding capacity of beef decreased to the large extent, when sugar Bongraesi latex and Masui latex were added. The hardness of beef showed decreasing tendency with the time, however, after 60 min, it decreased and thereafter increased a little after 120 min. the hardness of beef decreased sharply with addition of the latex of Bongraesi and Masui. The Masui has more tenderizing effect than the Bongraesi. When meat was mixed with tenderizing agent(ficin) and not heated, the change of color showed significant difference (p<0.01). when meat was mixed with tenderizing agent(ficin) and heated, the toughness showed significant difference (p<0.01) and the softness showed significant difference (p<0.001).