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Dong-YoonLim,Eun-SookLee,Hyeon-GyoonPark,Byeong-CheolKim,Soon-PyoHong,EunBangLee 대한약학회 2003 Archives of Pharmacal Research Vol.26 No.3
The present study was conducted to investigate the effects of green tea extract (GTE) on arterial blood pressure and contractile responses of isolated aortic strips of the normotensive rats and to establish the mechanism of action. The phenylephrine (10-6~10-5 M)-induced contractile responses were greatly inhibited in the presence of GTE (0.3~1.2 mg/mL) in a dose-dependent fashion. Also, high potassium (3.5´10-2~5.6´10-2 M)-induced contractile responses were depressed in the presence of 0.6~1.2 mg/mL of GTE, but not affected in low concentration of GTE (0.3 mg/mL). However, epigallocatechin gallate (EGCG, 4~12 mg/mL) did not affect the contractile responses evoked by phenylephrine and high K+. GTE (5~20 mg/kg) given into a femoral vein of the normotensive rat produced a dose-dependent depressor response, which is transient. Interestingly, the infusion of a moderate dose of GTE (10 mg/kg/30 min) made a significant reduction in pressor responses induced by intravenous norepinephrine. However, EGCG (1 mg/kg/30 min) did not affect them. Collectively, these results obtained from the present study demonstrate that intravenous GTE causes a dose-dependent depressor action in the anesthetized rat at least partly through the blockade of adrenergic a1-receptors. GTE also causes the relaxation in the isolated aortic strips of the rat via the blockade of adrenergic a1-receptors, in addition to the unknown direct mechanism. It seems that there is a big difference in the vascular effect between GTE and EGCG.
Sang-WookKim,Hyun-MeeOh,김범수,Hun-TaegChung,Weon-CheolHan,Eun-CheolKim,Tae-HyeonKim,Geom-SeogSeo,June-HyungLyou,Yong-HoNah,정재창,Suck-CheiChoi,전창덕 생화학분자생물학회 2003 Experimental and molecular medicine Vol.35 No.1
Tumor target-derived soluble secretary factor has been known to influence macrophage activation to induce nitric oxide (NO) production. Since heme oxigenase-1 (HO-1) is induced by a variety of con-ditions associated with oxidative stress, we ques-tioned whether soluble factor from tumor cels induces HO-1 through NO-dependent mechanism in macrophages. We designated this factor as a because of its ability to activate macrophages to induce iNOS. Although TMAF alone showed mod-est activity, TMAF in combination with IFN-γ signi-ficantly induced iNOS expression and NO syn-thesis. Simultaneously, TMAF induced HO-1 and this induction was slightly augmented by IFN-γ. Surprisingly, however, induction of HO-1 by TMAF was not inhibited by the treatment with the highly selective iNOS inhibitor, 1400 W, indicating that pendent mechanism. While rIFN-γ alone induced iNOS, it had no efect on HO-1 induction by itself. Colectively, the current study reveals that soluble factor from tumor target cells induces HO-1 en-zyme in macrophages. However, overall biological significance of this phenomenon remains to be determined.