文献检索，用中文搜 PubMed

Suppr 超能文献

核心技术专利：CN118964589B侵权必究

核心技术专利：CN118964589B侵权必究

Clayton L, Hiley C, D'Souza R J, Jones P W, Davies S J, Strange R C, Aber G M

Renal Laboratory, School of Postgraduate Medicine, University of Keele, England.

Free Radic Res Commun. 1993;18(2):107-13. doi: 10.3109/10715769309147347.

The effect of H2O2 (4.7 x 10(-9) -4.7 x 10(-3) M) on prostanoid production by isolated glomeruli from normotensive (WKY) and, spontaneously hypertensive rats (SHR) has been studied. 2. Oxidant stress significantly increased synthesis of prostaglandin E2 (PGE2), I2 (PGI2) and thromboxane A2 (TxA2) by glomeruli from both strains whereas the ratio (PGE2 + PGI2)/TxA2 increased in only SHR. 3. Pre-incubation of glomeruli with the angiotensin converting enzyme inhibitors captopril or lisinopril, had virtually no effect on H2O2-induced synthesis of individual prostanoids nor on the ratio (PGE2 + PGI2)/TxA2 by glomeruli from either WKY or SHR. 4. The findings suggest that H2O2-induced changes in glomerular function may be mediated, in part, by PGs but fail to support the suggestion that the ability of ACEI to protect glomeruli from H2O2-induced damage is determined by PGs.

研究了过氧化氢（4.7×10⁻⁹ - 4.7×10⁻³ M）对正常血压大鼠（WKY）和自发性高血压大鼠（SHR）分离肾小球前列腺素生成的影响。2. 氧化应激显著增加了两种品系肾小球中前列腺素E2（PGE2）、I2（PGI2）和血栓素A2（TxA2）的合成，而仅在SHR中（PGE2 + PGI2）/TxA2比值增加。3. 用血管紧张素转换酶抑制剂卡托普利或赖诺普利预孵育肾小球，对WKY或SHR肾小球中H2O2诱导的单个前列腺素合成以及（PGE2 + PGI2）/TxA2比值几乎没有影响。4. 研究结果表明，H2O2诱导的肾小球功能变化可能部分由前列腺素介导，但不支持血管紧张素转换酶抑制剂保护肾小球免受H2O2诱导损伤的能力由前列腺素决定这一观点。

Clayton L, Hiley C, D'Souza R J, Jones P W, Davies S J, Strange R C, Aber G M

Renal Laboratory, School of Postgraduate Medicine, University of Keele, England.

Free Radic Res Commun. 1993;18(2):107-13. doi: 10.3109/10715769309147347.

The effect of H2O2 (4.7 x 10(-9) -4.7 x 10(-3) M) on prostanoid production by isolated glomeruli from normotensive (WKY) and, spontaneously hypertensive rats (SHR) has been studied. 2. Oxidant stress significantly increased synthesis of prostaglandin E2 (PGE2), I2 (PGI2) and thromboxane A2 (TxA2) by glomeruli from both strains whereas the ratio (PGE2 + PGI2)/TxA2 increased in only SHR. 3. Pre-incubation of glomeruli with the angiotensin converting enzyme inhibitors captopril or lisinopril, had virtually no effect on H2O2-induced synthesis of individual prostanoids nor on the ratio (PGE2 + PGI2)/TxA2 by glomeruli from either WKY or SHR. 4. The findings suggest that H2O2-induced changes in glomerular function may be mediated, in part, by PGs but fail to support the suggestion that the ability of ACEI to protect glomeruli from H2O2-induced damage is determined by PGs.

研究了过氧化氢（4.7×10⁻⁹ - 4.7×10⁻³ M）对正常血压大鼠（WKY）和自发性高血压大鼠（SHR）分离肾小球前列腺素生成的影响。2. 氧化应激显著增加了两种品系肾小球中前列腺素E2（PGE2）、I2（PGI2）和血栓素A2（TxA2）的合成，而仅在SHR中（PGE2 + PGI2）/TxA2比值增加。3. 用血管紧张素转换酶抑制剂卡托普利或赖诺普利预孵育肾小球，对WKY或SHR肾小球中H2O2诱导的单个前列腺素合成以及（PGE2 + PGI2）/TxA2比值几乎没有影响。4. 研究结果表明，H2O2诱导的肾小球功能变化可能部分由前列腺素介导，但不支持血管紧张素转换酶抑制剂保护肾小球免受H2O2诱导损伤的能力由前列腺素决定这一观点。