心血管和肾脏的影响抑制环氧酶在转基因老鼠窝藏老鼠renin-2基因(TGR [mREN2] 27)。

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程ZJ Finckenberg P Louhelainen M, Merasto年代,Tikkanen我Vapaatalo H, Mervaala EM

心血管和肾脏的影响抑制环氧酶在转基因老鼠窝藏老鼠renin-2基因(TGR [mREN2] 27)。

欧元J杂志。2003年2月14日,461 (2):159 - 69。

PubMed ID
12586211 (在PubMed
]
文摘

目前的研究调查了的角色cyclooxygenase-synthetized前列腺素类angiotensin-II-induced炎症反应和血管损伤的发病机制在转基因老鼠窝藏老鼠renin-2基因(mREN2老鼠)。五到六个,杂合的mREN2老鼠收到下列药物治疗8周:(1)控制;(2)cyclooxygenase-2抑制剂(MF-tricyclic [3 - (3, 4-difluorophenyl) 4 - (4 - (methylsulfonyl)苯基)2 (5 h) -furanone), 14毫克公斤(1)订单。);(3)cyclooxygenase-1 / cyclooxygenase-2抑制剂(苏灵大,14毫克公斤(1)订单。);(4)血管紧张素ⅱ受体拮抗剂洛沙坦40毫克公斤订单。(1));(5)MF-tricyclic +洛沙坦;(6)苏灵大+洛沙坦。血压正常的老鼠Sprague-Dawley担任控制。mREN2老鼠发达明显高血压、心脏肥大、蛋白尿与血压正常的人相比Sprague-Dawley控制。mREN2老鼠表现出明显的血管周的炎症和形态学损伤肾脏和心脏。 Both MF-tricyclic and sulindac further increased blood pressure and albuminuria in mREN2 rats. Neither MF-tricyclic nor sulindac were able to prevent angiotensin-II-induced perivascular inflammation and morphological changes in the heart or in the kidneys. Myocardial and renal cyclooxygenase-2 mRNA expressions were decreased in mREN2 rats, whereas no difference was found in cyclooxygenase-1 mRNA expressions. Sulindac increased both cyclooxygenase-1 and cyclooxygenase-2 gene expressions, whereas MF-tricyclic increased only cyclooxygenase-2 gene expressions. Losartan normalized blood pressure, cardiac hypertrophy, albuminuria, inflammatory response and morphological changes in mREN2 rats, both in the presence and absence of cyclooxygenase inhibitors. Our findings indicate that cyclooxygenase does not play a central role in the pathogenesis of angiotensin-II-induced inflammatory response and vascular injury in mREN2 rats.

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药物靶点
药物 目标 生物 药理作用 行动
苏灵大 前列腺素合成酶1 G / H 蛋白质 人类
未知的
抑制剂
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