• 제목/요약/키워드: Ang II

검색결과 335건 처리시간 0.025초

정상인(正常人) 혈청(血淸)의 Propionibacterium acnes Serotype I 및 Serotype II에 대한 항체(抗體) (Agglutinating Antibody to Propionibacterium acnes Serotype I and Serotype II in Normal Human Sera)

  • 최철순;서용열;양용태
    • 대한미생물학회지
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    • 제14권1호
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    • pp.63-69
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    • 1979
  • Antibodies to Propionibacterium acnes(Corynebacterium parvum) serotype I and serotype II in normal human sera were measured using a microtitre bacterial agglutination test. Of 168 sera tested, 53 sera(31.0%) exhibited higher agglutinin titres to serotype I than to serotype II and 34 sera(20.2%) gave higher titers to serotype II than to serotype I. Eighty-one sera(48.3%), however, showed similar antibody titres to both types. Antibodies to serotype I(x) and serotype II(y) showed high correlation(r=0.73, p<0.01) and regression equation was Y=1,078+0.73X. The mean antibody titre($log_2$) of 529 normal sera(male 447 and female 82) to serotype I was $5.49{\pm}1.36$, but there was no significant difference between male($5.45{\pm}1.36$) and female($5.74{\pm}1.36$). Bacterial agglutinin to Propionibacterium acnes in normal sera belonged to a 2-mercaptoethanol resistant IgG class.

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Epigallocatechin-3-gallate Regulates NADPH Oxidase Expression in Human Umbilical Vein Endothelial Cells

  • Ahn, Hee-Yul;Kim, Chan-Hyung;Ha, Tae-Sun
    • The Korean Journal of Physiology and Pharmacology
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    • 제14권5호
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    • pp.325-329
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    • 2010
  • Vascular NADPH oxidase plays a pivotal role in producing superoxide in endothelial cells and thus acts in the initiation and development of inflammatory cardiovascular diseases such as atherosclerosis. Epigallocatechin-3-gallate (EGCG), the major catechin derived from green tea, has multiple beneficial effects for treating cardiovascular disease but the effect of EGCG on the expression of vascular NADPH oxidase remains unknown. In this study, we investigated the mechanism(s) by which EGCG might inhibit the expression of subunits of NADPH oxidase, namely $p47^{phox}$, $p67^{phox}$ and $p22^{phox}$, induced by angiotensin II (Ang II) in human umbilical vein endothelial cells. Ang II increased the expression levels of $p47^{phox}$, $p67^{phox}$, and $p22^{phox}$, but EGCG counteracted this effect on $p47^{phox}$. Moreover, EGCG did not affect the production of reactive oxygen species induced by Ang II. These data suggest a novel mechanism whereby EGCG might provide direct vascular benefits for treating inflammatory cardiovascular diseases.

Losartan Inhibits Vascular Smooth Muscle Cell Proliferation through Activation of AMP-Activated Protein Kinase

  • Kim, Jung-Eun;Choi, Hyoung-Chul
    • The Korean Journal of Physiology and Pharmacology
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    • 제14권5호
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    • pp.299-304
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    • 2010
  • Losartan is a selective angiotensin II (Ang II) type 1 ($AT_1$) receptor antagonist which inhibits vascular smooth muscle cells (VSMCs) contraction and proliferation. We hypothesized that losartan may prevent cell proliferation by activating AMP-activated protein kinase (AMPK) in VSMCs. VSMCs were treated with various concentrations of losartan. AMPK activation was measured by Western blot analysis and cell proliferation was measured by MTT assay and flowcytometry. Losartan dose- and time-dependently increased the phosphorylation of AMPK and its downstream target, acetyl-CoA carboxylase (ACC) in VSMCs. Losartan also significantly decreased the Ang II- or 15% FBS-induced VSMC proliferation by inhibiting the expression of cell cycle associated proteins, such as p-Rb, cyclin D, and cyclin E. Compound C, a specific inhibitor of AMPK, or AMPK siRNA blocked the losartan-induced inhibition of cell proliferation and the $G_0/G_1$ cell cycle arrest. These data suggest that losartan-induced AMPK activation might attenuate Ang II-induced VSMC proliferation through the inhibition of cell cycle progression.

Whey Protein Attenuates Angiotensin II-Primed Premature Senescence of Vascular Smooth Muscle Cells through Upregulation of SIRT1

  • Hwang, Jung Seok;Han, Sung Gu;Lee, Chi-Ho;Seo, Han Geuk
    • 한국축산식품학회지
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    • 제37권6호
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    • pp.917-925
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    • 2017
  • Whey protein, a by-product of milk curdling, exhibits diverse biological activities and is used as a dietary supplement. However, its effects on stress-induced vascular aging have not yet been elucidated. In this study, we found that whey protein significantly inhibited the Ang II-primed premature senescence of vascular smooth muscle cells (VSMCs). In addition, we observed a marked dose- and time-dependent increase in SIRT1 promoter activity and mRNA in VSMCs exposed to whey protein, accompanied by elevated SIRT1 protein expression. Ang II-mediated repression of SIRT1 level was dose-dependently reversed in VSMCs treated with whey protein, suggesting that SIRT1 is involved in preventing senescence in response to this treatment. Furthermore, resveratrol, a well-defined activator of SIRT1, potentiated the effects of whey protein on Ang II-primed premature senescence, whereas sirtinol, an inhibitor of SIRT1, exerted the opposite. Taken together, these results indicated that whey protein-mediated upregulation of SIRT1 exerts an anti-senescence effect, and can thus ameliorate Ang II-induced vascular aging as a dietary supplement.

Activating transcription factor 4 aggravates angiotensin II-induced cell dysfunction in human vascular aortic smooth muscle cells via transcriptionally activating fibroblast growth factor 21

  • Tao, Ke;Li, Ming;Gu, Xuefeng;Wang, Ming;Qian, Tianwei;Hu, Lijun;Li, Jiang
    • The Korean Journal of Physiology and Pharmacology
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    • 제26권5호
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    • pp.347-355
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    • 2022
  • Abdominal aortic aneurysm (AAA) is a life-threatening disorder worldwide. Fibroblast growth factor 21 (FGF21) was shown to display a high level in the plasma of patients with AAA; however, its detailed functions underlying AAA pathogenesis are unclear. An in vitro AAA model was established in human aortic vascular smooth muscle cells (HASMCs) by angiotensin II (Ang-II) stimulation. Cell counting kit-8, wound healing, and Transwell assays were utilized for measuring cell proliferation and migration. RT-qPCR was used for detecting mRNA expression of FGF21 and activating transcription factor 4 (ATF4). Western blotting was utilized for assessing protein levels of FGF21, ATF4, and markers for the contractile phenotype of HASMCs. ChIP and luciferase reporter assays were implemented for identifying the binding relation between AFT4 and FGF21 promoters. FGF21 and ATF4 were both upregulated in Ang-II-treated HASMCs. Knocking down FGF21 attenuated Ang-II-induced proliferation, migration, and phenotype switch of HASMCs. ATF4 activated FGF21 transcription by binding to its promoter. FGF21 overexpression reversed AFT4 silencing-mediated inhibition of cell proliferation, migration, and phenotype switch. ATF4 transcriptionally upregulates FGF21 to promote the proliferation, migration, and phenotype switch of Ang-II-treated HASMCs.

Preparation of SnS Thin Films by MOCVD Method Using Single Source Precursor, Bis(3-mercapto-1-propanethiolato) Sn(II)

  • Park, Jong-Pil;Song, Mi-Yeon;Jung, Won-Mok;Lee, Won-Young;Lee, Jin-Ho;Kim, Hang-Geun;Shim, Il-Wun
    • Bulletin of the Korean Chemical Society
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    • 제33권10호
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    • pp.3383-3386
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    • 2012
  • SnS thin films were deposited on glasses through metal organic chemical vapor deposition (MOCVD) method at relatively mild conditions, using bis(3-mercapto-1-propanethiolato) tin(II) precursor without toxic $H_2S$ gas. The MOCVD process was carried out in the temperature range of $300-400^{\circ}C$ and the average grain size in fabricated SnS films was about 500 nm. The optical band gap of the SnS film was about 1.3 eV which is in optimal range for harvesting solar radiation energy. The precursor and SnS films were characterized through infrared spectroscopy, nuclear magnetic resonance spectroscopy, DIP-EI mass spectroscopy, elemental analyses, thermal analysis, X-ray diffraction, and field emission scanning electron microscopic analyses.

비소세포폐암 수술 후 세포분화도가 재발에 영향을 미친다 (Cell Differentiation Might Predict the Recurrence in Surgically Resected Non-Small Cell Lung Carcinoma)

  • 강형구;조성근;이혜민;박성운;이병욱;이재희;김보민;박인원
    • Tuberculosis and Respiratory Diseases
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    • 제68권1호
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    • pp.10-15
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    • 2010
  • Background: Lung cancer is the most common cause of cancer mortality in Korea. The TNM stage at presentation in patients with non-small cell lung cancer (NSCLC) has the greatest impact on prognosis. Patients who undergo a complete resection for NSCLC are likely to develop recurrent and/or metastatic disease. There are several factors influencing the development of recurrence. We explored risk factors of recurrence in patients with stages I and II NSCLC, who had undergone curative resection. Methods: We reviewed patients who had complete surgical resection as definitive treatment for stage I or II. Patients followed up for more than 36 months. We evaluated several factors which might have relationship with recurrence, such as patient's demographic factors, TNM staging, pathologic finding, tumor markers and surgical technique. Results: A total of 75 patients were enrolled for analysis, of whom 58 were men and 17 were women with mean age of 61 (range, 37 to 76) years. The average size of tumors was 3.9 cm (0.7 to 10 cm). There were 64 patients with stage I NSCLC and 11 with stage II NSCLC. Among 64 patients with stage I NSCLC, 35 patients showed recurrences whereas 8 patients have recurred in stage II NSCLC. Grade of differentiation of tumor was closely related to the recurrence. Seventy-five percent of patients who had poor tumor differentiation experienced a recurrence. In contrast, 3 patients of twelve had recurrences, who revealed differentiation in their tissue (p<0.05). Conclusion: Tumor differentiation could be a predictive factor for tumor recurrence in patients who have undergone curative resection for stage I or II NSCLC.

Effects of Central Interleukin-1 on the Cardiovascular Response in Hemorrhaged Rats

  • Kang, Joon-Ho;Jang, Jae-Hee;Ahn, Dong-Kuk;Park, Jae-Sik
    • The Korean Journal of Physiology and Pharmacology
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    • 제8권2호
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    • pp.89-94
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    • 2004
  • The arterial pressure is regulated by the nervous and humoral mechanisms. The neuronal regulation is mostly carried out by the autonomic nervous system through the rostral ventrolateral medulla (RVLM), a key area for the cardiovascular regulation, and the humoral regulation is mediated by a number of substances, including the angiotensin (Ang) II and vasopressin. Recent studies suggest that central interleukin-1 (IL-1) activates the sympathetic nervous system and produces hypertension. The present study was undertaken to elucidate whether IL-1 and Ang II interact in the regulation of cardiovascular responses to the stress of hemorrhage. Thus, Sprague-Dawley rats were anesthetized and both femoral arteries were cannulated for direct measurement of arterial pressure and heart rate (HR) and for inducing hemorrhage. A guide cannula was placed into the lateral ventricle for injection of IL-1 $(0.1,\;1,\;10,\;20\;ng/2\;{\mu}l)$ or Ang II $(600\;ng/10\;{\mu}l)$. A glass microelectrode was inserted into the RVLM to record the single unit spike potential. Barosensitive neurons were identified by an increased number of single unit spikes in RVLM following intravenous injection of nitroprusside. I.c.v. $IL-1\;{\beta}$ increased mean arterial pressure (MAP) in a dose-dependent fashion, but HR in a dose-independent pattern. The baroreceptor reflex sensitivity was not affected by i.c.v. $IL-1\;{\beta}$. Both i.c.v. $IL-1\;{\alpha}\;and\;{\beta}$ produced similar increase in MAP and HR. When hemorrhage was induced after i.c.v. injection of $IL-1\;{\beta}$, the magnitude of MAP fall was not different from the control. The $IL-1\;{\beta}$ group showed a smaller decrease in HR and a lower spike potential count in RVLM than the control. MAP fall in response to hemorrhage after i.c.v. injection of Ang II was not different from the control. When both IL-1 and Ang II were simultaneously injected i.c.v., however, MAP fall was significantly smaller than the control, and HR was increased rather than decreased. These data suggest that IL-1, a defense immune mediator, manifests a hypertensive action in the central nervous system and attenuates the hypotensive response to hemorrhage by interaction with Ang II.