Lung injury caused by cobra venom factor is reduced in rats raised on an essential fatty acid-deficient diet.
Lung injury caused by cobra venom factor is reduced in rats raised on an essential fatty acid-deficient diet.
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在缺乏必需脂肪酸的饮食中饲养的大鼠中，由眼镜蛇毒因子引起的肺损伤减少。
DOI：
10.1152/ajpheart.1989.257.4.h1192
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发表时间：
1989
期刊：
影响因子：
--
通讯作者：
Ward,PA
中科院分区：
文献类型：
--
作者：
Morganroth,ML;Schoeneich,SO;Till,GO;Pickett,W;Ward,PA
花生四烯酸代谢物似乎参与了由眼镜蛇毒因子（CVF）诱导的补体和多形核白细胞（PMN）激活引起的肺损伤。这些研究旨在评估饮食诱导的花生四烯酸缺乏对cvf诱导的肺损伤的影响。在必需脂肪酸缺乏（EFAD）饮食中饲养的大鼠显示出预期的脂肪酸组成变化，包括血浆花生四烯酸水平降低和5,8,11-二十碳三烯酸水平升高。在以EFAD喂养的完整大鼠中，cvf诱导的肺损伤减弱。当使用正常饮食饲养的大鼠的血液和切除的肺时，CVF引起肺血管收缩和急性肺损伤，肺实质和肺泡灌洗液中125i标记的牛血清白蛋白积累增加。EFAD喂养的大鼠的血液灌注或切除肺的血液灌注均降低了cvf诱导的肺动脉加压反应和肺损伤。无论是正常饮食饲养的大鼠还是EFAD饮食饲养的大鼠所切除的肺，当从正常饮食饲养的大鼠身上获得血液灌注液时，肺血管收缩和肺损伤并未减轻。EFAD喂养大鼠获得的pmn在体外显示出超氧化物产生减少，随机迁移和趋化性受损。相比之下，β -葡糖醛酸酶释放量与对照大鼠的pmn相似。这些数据表明，EFAD饮食诱导的cvf诱导的肺动脉高压和急性肺损伤的衰减是由于血液中效应细胞的缺陷，而不是修饰的肺靶组织。
Arachidonate metabolites appear to be involved in lung injury caused by cobra venom factor (CVF)-induced complement and polymorphonuclear leukocyte (PMN) activation. These studies were designed to assess the effects of a dietary-induced deficiency of arachidonic acid on CVF-induced lung injury. Rats raised on an essential fatty acid-deficient (EFAD) diet exhibited the expected changes in fatty acid composition including decreased plasma levels of arachidonic acid and increased levels of 5,8,11-eicosatrienoic acid. In intact rats raised on the EFAD diet, CVF-induced lung injury was attenuated. When blood and excised lungs from rats raised on the normal diet were used, CVF caused pulmonary vascular constriction and acute lung injury, as evidenced by increased 125I-labeled bovine serum albumin accumulation in lung parenchyma and alveolar lavage fluid. The CVF-induced pulmonary artery pressor response and lung injury were reduced when blood perfusate or blood perfusate and excised lungs were obtained from rats raised on the EFAD diet. The pulmonary vascular constriction and lung injury were not attenuated when the blood perfusate was obtained from rats raised on the normal diet, irrespective of whether the excised lungs were obtained from rats raised on the normal or EFAD diet. PMNs obtained from rats raised on the EFAD diet demonstrated decreased superoxide production as well as impaired random migration and chemotaxis in vitro. In contrast, beta-glucuronidase release was quantitatively similar to PMNs from control rats. These data indicate that the EFAD diet-induced attenuation of CVF-induced pulmonary hypertension and acute lung injury is due to defective effector cells in blood rather than modified pulmonary target tissue.
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DOI：
10.1073/pnas.80.3.702
发表时间：
1983-02
影响因子：
11.1
作者：
C. Privalle;J. Crivello;C. Jefcoate
通讯作者：
C. Privalle;J. Crivello;C. Jefcoate
培养的 Leydig 肿瘤细胞上的心房钠尿因子受体：配体结合和光亲和标记。
影响因子：
2.9
作者：
Pandey,KN;Inagami,T;Misono,KS
通讯作者：
Misono,KS
表皮生长因子可激活培养的 Leydig 肿瘤细胞中的类固醇生物合成，而不影响 cAMP 水平，并增强绒毛膜促性腺激素和 cAMP 类固醇生物合成的激活。
DOI：
--
发表时间：
1987
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Ascoli,M;Euffa,J;Segaloff,DL
通讯作者：
Segaloff,DL
促性腺激素反应性鼠 Leydig 肿瘤细胞中心房钠尿因子对孕酮分泌的抑制和环核苷酸的调节。
DOI：
10.1016/0006-291x(85)90975-1
发表时间：
1985
影响因子：
3.1
作者：
Pandey,KN;Kovacs,WJ;Inagami,T
通讯作者：
Inagami,T
影响因子：
2.1
作者：
L. Pon;L. Epstein;N. Orme-Johnson
通讯作者：
L. Pon;L. Epstein;N. Orme-Johnson