• 제목/요약/키워드: Ang II

검색결과 334건 처리시간 0.022초

Flavonoids의 약리작용(II) -항염작용과 창상치유 억제작용과의 상관성- (Pharmacological Activities of Flavonoids(II) -Relationships of Anti-inflammatory and Antigranulomatous Actions-)

  • 김창종;서수경;주재현;조승길
    • 약학회지
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    • 제34권6호
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    • pp.407-414
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    • 1990
  • The relationships of inhibitory activities of inflammation and wound healing of flavonoids were studied in vitro and in vivo. Generally flavonoids have not only significantly anti-inflammatory activity in carrageenin-induced paw edema and Freund's complete adjuvant-induced arthritis, but also inhibitory activity of wound healing. The more inhibitory activities of wound healing flavonoids have, the more they have the anti-inflammatory activities; apigenin > guercetin > flovone > rutin > hesperidin > naringin. Their inhibitory mechanism seems to be inhibition of the inflammatory cell infiltration and fibroblast proliferation, and so they decreased the granulomatous activity and tensile strength.

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Ginsenoside Re inhibits myocardial fibrosis by regulating miR-489/myd88/NF-κB pathway

  • Jinghui Sun;Ru Wang;Tiantian Chao;Jun Peng;Chenglong Wang;Keji Chen
    • Journal of Ginseng Research
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    • 제47권2호
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    • pp.218-227
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    • 2023
  • Background: Myocardial fibrosis (MF) is an advanced pathological manifestation of many cardiovascular diseases, which can induce heart failure and malignant arrhythmias. However, the current treatment of MF lacks specific drugs. Ginsenoside Re has anti-MF effect in rat, but its mechanism is still not clear. Therefore, we investigated the anti-MF effect of ginsenoside Re by constructing mouse acute myocardial infarction (AMI) model and AngII induced cardiac fibroblasts (CFs) model. Methods: The anti-MF effect of miR-489 was investigated by transfection of miR-489 mimic and inhibitor in CFs. Effect of ginsenoside Re on MF and its related mechanisms were investigated by ultrasonographic, ELISA, histopathologic staining, transwell test, immunofluorescence, Western blot and qPCR in the mouse model of AMI and the AngII-induced CFs model. Results: MiR-489 decreased the expression of α-SMA, collagenI, collagen III and myd88, and inhibited the phosphorylation of NF-κB p65 in normal CFs and CFs treated with AngII. Ginsenoside Re could improve cardiac function, inhibit collagen deposition and CFs migration, promote the transcription of miR-489, and reduce the expression of myd88 and the phosphorylation of NF-κB p65. Conclusion: MiR-489 can effectively inhibit the pathological process of MF, and the mechanism is at least partly related to the regulation of myd88/NF-κB pathway. Ginsenoside Re can ameliorate AMI and AngII induced MF, and the mechanism is at least partially related to the regulation of miR-489/myd88/NF-κB signaling pathway. Therefore, miR-489 may be a potential target of anti-MF and ginsenoside Re may be an effective drug for the treatment of MF.

Wogonin attenuates vascular remodeling by inhibiting smooth muscle cell proliferation and migration in hypertensive rat

  • Yang Yang;Shan Huang;Jun Wang;Xiao Nie;Ling Huang;Tianfa Li
    • The Korean Journal of Physiology and Pharmacology
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    • 제28권1호
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    • pp.39-48
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    • 2024
  • Wogonin, extracted from the roots of Scutellaria baicalensis Georgi, has been shown to suppress collagen deposition in spontaneously hypertensive rats (SHRs). This study was performed to investigate the role and mechanism of wogonin underlying vascular remodeling in SHRs. After injection of SHRs with 40 mg/kg of wogonin, blood pressure in rats was measured once a week. Masson's trichrome staining was conducted to observe the changes in aortas and mesenteric arteries. Vascular smooth muscle cells (VSMCs) isolated from rat thoracic aortas were treated with Angiotensin II (Ang II; 100 nM) in the presence or absence of varying concentrations of wogonin. The viability and proliferation of VSMCs were examined using Cell Counting Kit-8 assay and 5-ethynyl-2'-deoxyuridine assay, respectively. The migration of VSMCs was examined using wound healing assay and transwell assay. We found that wogonin administration alleviated hypertension, increased lumen diameter, and reduced the thickness of the arterial media in SHRs. Ang II treatment enhanced the viability of VSMCs, which was inhibited by wogonin in a concentration-dependent manner. Wogonin reversed Ang II-induced increases in the viability, proliferation, and migration of VSMCs. Moreover, wogonin inhibited Ang II-induced activation of mitogen-activated protein kinase (MAPK) signaling in VSMCs. Overall, wogonin repressed the proliferative and migratory capacity of VSMCs by regulating the MAPK signaling pathway, thereby attenuating vascular remodeling in hypertensive rats, indicating that wogonin might be a therapeutic agent for the treatment of vascular diseases.

Dronedarone Attenuates Ang II-Induced Myocardial Hypertrophy Through Regulating SIRT1/FOXO3/PKIA Axis

  • Cheng Chen;Song Hu;Heng-Jing Hu;Zhi-Xuan Liu;Xin-Teng Wu;Tao Zou;Hua Su
    • Korean Circulation Journal
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    • 제54권4호
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    • pp.172-186
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    • 2024
  • Background and Objectives: Long-term pathological myocardial hypertrophy (MH) seriously affects the normal function of the heart. Dronedarone was reported to attenuate left ventricular hypertrophy of mice. However, the molecular regulatory mechanism of dronedarone in MH is unclear. Methods: Angiotensin II (Ang II) was used to induce cell hypertrophy of H9C2 cells. Transverse aortic constriction (TAC) surgery was performed to establish a rat model of MH. Cell size was evaluated using crystal violet staining and rhodamine phalloidin staining. Reverse transcription quantitative polymerase chain reaction and western blot were performed to detect the mRNA and protein expressions of genes. JASPAR and luciferase activity were conducted to predict and validate interaction between forkhead box O3 (FOXO3) and protein kinase inhibitor alpha (PKIA) promoter. Results: Ang II treatment induced cell hypertrophy and inhibited sirtuin 1 (SIRT1) expression, which were reversed by dronedarone. SIRT1 overexpression or PKIA overexpression enhanced dronedarone-mediated suppression of cell hypertrophy in Ang II-induced H9C2 cells. Mechanistically, SIRT1 elevated FOXO3 expression through SIRT1- mediated deacetylation of FOXO3 and FOXO3 upregulated PKIA expression through interacting with PKIA promoter. Moreover, SIRT1 silencing compromised dronedarone-mediated suppression of cell hypertrophy, while PKIA upregulation abolished the influences of SIRT1 silencing. More importantly, dronedarone improved TAC surgery-induced MH and impairment of cardiac function of rats via affecting SIRT1/FOXO3/PKIA axis. Conclusions: Dronedarone alleviated MH through mediating SIRT1/FOXO3/PKIA axis, which provide more evidences for dronedarone against MH.

환경온도(環境溫度)에 따른 운동(運動)수행전후 전해질(電解質) 및 호르몬의 성분변화(成分變化) (The element changes of Electrolytes and Hormones Pre & Post the Performance of Exercises Induces by Environment Temperature)

  • 이재식
    • 한국산업융합학회 논문집
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    • 제3권2호
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    • pp.155-166
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    • 2000
  • In order to elucidate the interrelationship between electrolytes and exercise the investigation was undertaken to determine the electrolyte levels in young males took on varied environmental temperatures ($13^{\circ}C$, $24^{\circ}C$ or $34^{\circ}C$). 10 healthy young males were used for the experiments. Our results showed the following significant changes; 1. The raising of the environmental temperature, the weight reduction were increased due to marked sweating. 2. In the electrolytes of serum, decreased the $K^+$ concentration at $13^{\circ}C$, but increased the $Na^+$ or $Cl^-$ concentration at $24^{\circ}C$, and increased the $Na^+$ or $Cl^-$, or $Mg^{+}^{+}$ concentrations at $34^{\circ}C$. 3. The raising of environmental temperature appear to be increased PRA,Ang I, Ang II and ALD levels, whereas no changed ADH level. 4. Serum levels of PRA, Ang I, Ang II and ALD were incresed after exercise, and their increments were incresed paralel ttie incresed environmental temperature. However, there no significant change in ADH, level. In conclusion, exercise induced not only changes of serum electrolytes levels such as $Na^+$, $Cl^-$, $K^+$, $Mg^{+}^{+}$, but also serum hormonal changes such as PRA, Ang I, Ang II, ALD. However, ADH level was not changed significantly, These changes were more prominent in exercise at hot temperature than in lower temperature.

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Localization of Angiotensin II in Korean Bovine Follicles and Its Effects on IVM/IVF of Oocytes

  • Quen, J. H.;Kim, S. K.
    • 한국동물번식학회:학술대회논문집
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    • 한국동물번식학회 2004년도 춘계학술발표대회
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    • pp.252-252
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    • 2004
  • 1. The concentrations of Ang. Ⅱ were 7.2±0.91 × 10³, 3.8±0.34 × 10³, 3.5±0.30 × 10³, 2.8±0.22 × 10³ pg/㎖ in bovine follicular fluids from 1∼3 ㎜, 3∼5 ㎜, 5∼7 ㎜ and 8∼10 ㎜ follicles, respectively. However, the concentrations of Ang. Ⅱ decreased in follicular fluids from large follicles. (omitted)

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Da-125 a New Antitumor Agent, Inhibits Topoisomerase II as Topoisomerase Poison and DNA Intercalator Simultaneously

  • Seo, Jin-Wook;Lee, Hak-Sung;Lee, Min-Jun;Kim, Mi-Ra;Shin, Cha-Gyun
    • Archives of Pharmacal Research
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    • 제27권1호
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    • pp.77-82
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    • 2004
  • DA-125, a novel derivative of adriamycin, is known for its anti-cancer activity. In this study, the inhibitory mechanism of DA-125 on topoisomerase was investigated in the simian virus 40 (SV40) replicating CV-1 cell by studying the SV40 DNA replication intermediates and DNA-topoisomerase complexes. DNA-protein complexes that were formed in the drug-treated cells were quantitated by using a glass filter assay. SV40 DNA replication intermediates that were accumulated in the drug-treated CV-1 cell were analyzed in a high resolution gel. DA-125 did not accumulate B-dimers of SV40 DNA replication intermediates which were found in the adriamycin-treated CV-1 cells. DA-125 induced a dose-dependent formation of the DNA-protein complexes, while adriamycin did not. When adriamycin and etoposide (VP16) were added to the SV40-infected cells at the same time, adriamycin blocked the formation of the DNA-protein complexes induced by VP16 in a dose-dependent manner. However, DA-125 blocked the formation of the DNA-protein complexes induced by VP16 up to the maximum level of the DNA-protein complexes that were induced by DA-125 alone. Adriamycin and DA-125 did not inhibit the formation of the DNA-protein complexes that were caused by camptothecin, a known topoisomerase I poison. DA-125 is bifunctional in inhibiting topoisomerase II because it simultaneously has the properties of the topoisomerase II poison and the DNA intercalator. As a topoisomerase II poison, DA-125 alone induced dose-dependent formation of the DNA-protein complexes. However, as a DNA intercalator, it quantitatively inhibited the formation of the DNA-protein complexes induced by a strong topoisomerase II poison VP16. Furthermore considering that the levels of the DNA-protein complex induced by VP16 were decreased by DA-125 in terms of the topoisomerase II poison, we suggest that DA-125 has a higher affinity to the drug-binding sites of DNA than VP16 has.

Deposition of CuInSe2 Thin Films Using Stable Copper and Indium-selenide Precursors through Two-stage MOCVD Method

  • Park, Jong-Pil;Kim, Sin-Kyu;Park, Jae-Young;Ok, Kang-Min;Shim, Il-Wun
    • Bulletin of the Korean Chemical Society
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    • 제30권4호
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    • pp.853-856
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    • 2009
  • Highly polycrystalline copper indium diselenide (CuInSe2, CIS) thin films were deposited on glass or ITO glass substrates by two-stage metal organic chemical vapor deposition (MOCVD) at relatively mild conditions, using Cuand In/Se-containing precursors. First, pure Cu thin film was prepared on glass or ITO glass substrates by using a single-source precursor, bis(ethylbutyrylacetate)copper(II) or bis(ethylisobutyrylacetato)copper(II). Second, on the resulting Cu films, tris(N,N-ethylbutyldiselenocarbamato)indium(III) was treated to produce CuInSe2 films by MOCVD method at 400 ${^{\circ}C}$. These precursors are very stable in ambient conditions. In our process, it was quite easy to obtain high quality CIS thin films with less impurities and uniform thickness. Also, it was found that it is easy to control the stoichiometric ratio of relevant elements on demands, leading to Cu or In rich CIS thin films. These CIS films were analyzed by XRD, SEM, EDX, and Near-IR spectroscopy. The optical band gap of the stoichiometric CIS films was about 1.06 eV, which is within an optimal range for harvesting solar radiation energy.

황금 지상부의 항산화 및 항 알러지 활성 성분 (Antioxidant and Antiallergic Activity of Compounds from the Aerial Parts of Scutellaria baicalensis Georgi)

  • 차자현;김현욱;김성건;정성희;황완균
    • 약학회지
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    • 제50권2호
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    • pp.136-143
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    • 2006
  • Roots of Scutellaria baicalensis have been used for fever remedy; diuresis, antiphlogistic. For the investigation of the active component from aerial parts of Scutellaria baicalensis, MeOH extracts from aerial parts of Scutellaria baicalensis were suspended with $H_2O$, and partitioned by $CHCl_3$. In order to investigate the efficacy of antioxidative activity the activity guided fraction and isolation of physiologically active substance were peformed. Its $H_2O,\;30\%,\;60\%$ MeOH and MeOH fractions were examined on antioxidative activity using DPPH method and TBARS assay; It was revealed that $30\%\;and\;60\%$ MeOH fractions have significant anti-oxidative activity. its fractions testing type I allergy, compound 48/80 induced systemic anaphylaxis was applied. As a result, compared with reference (cromolygate), these fraction significantly inhibited systemic anaphylaxis by $71\%\;and\;57\%$, respectively. From $30\%,\;60\%$ MeOH fraction, five compounds were isolated and elucidated apigenin 6-C-${\alpha}$-L-arabinopyranosyl-8-C-${\beta}$-D-glucopyranoside (isoschaftside, I), scutellarein 7-O-${\beta}$-D-glucuronopyranoside (scutellarin, II), apigenin 7-O- ${\beta}$-D-glucuronopyranoside (III), isoscutellarein 8-O-${\beta}$-D-glucuronopyranoside (IV), kaempferol 3-O-${\beta}$-D-glucopyranoside (V) through their physicochemical data and spectroscopic methods. We measured radical scavenging activity with DPPH method and anti-lipid peroxidative efficacy on human LDL with TBARS assay. [$I] showed antioxidant activities in order. Type I allergy compound 48/80 induced systemic anaphylaxis was applied. $[V inhibited systemic anaphylaxis in order.