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银杏叶提取物761与缺血再灌注糖尿病大鼠视网膜离子失衡的恢复

EGb 761 and the recovery of ion imbalance in ischemic reperfused diabetic rat retina.

作者信息

Szabo M E, Droy-Lefaix M T, Doly M

机构信息

University of Connecticut, Farmington, Conn., USA.

出版信息

Ophthalmic Res. 1995 Mar-Apr;27(2):102-9. doi: 10.1159/000267606.

Abstract

We studied the effects of a free-radical scavenger, EGb 761, on electrolyte shifts (Na+, Ca2+, and K+) induced by ischemia and reperfusion in the retinas obtained from streptozotocin-induced diabetic rats. Eyes were subjected to 90 min ischemia followed by 24 h of reperfusion by clamping and releasing the central retinal artery. Ten days before the induction of ischemia and reperfusion, diabetic rats received a daily dose of 25, 50, and 100 mg/kg p.o. of EGb 761, respectively (n = 12 in each group). In the drug-free diabetic control group, 90 min ischemia followed by 24 h of reperfusion resulted in an increase in retinal Na+ and Ca2+ (measured by atomic absorption spectrophotometry) compared to nonischemic control values of 73 +/- 4 and 2.6 +/- 0.3 mumol/g dry weight to 113 +/- 5 (p < 0.05) and 5.3 +/- 0.3 mumol/g dry weight (p < 0.05), respectively. Tissue K+ content was significantly reduced compared to its nonischemic diabetic control value of 268 +/- 7 to 213 +/- 6 mumol/g dry weight (p < 0.05). EGb 761 dose-dependently reduced reperfusion-induced ion imbalance, improving the recovery of ion content in diabetic rat retina. EGb 761 did not reduce blood glucose in streptozotocin-induced diabetic rats. Therefore we may conclude that these protective effects of EGb 761 are independent of blood glucose content or of the severity of diabetes and protect against electrolyte shifts directly in retinal cells.

摘要

我们研究了自由基清除剂EGb 761对链脲佐菌素诱导的糖尿病大鼠视网膜缺血再灌注所引起的电解质变化(Na+、Ca2+和K+)的影响。通过夹闭和松开视网膜中央动脉使眼睛经历90分钟的缺血,随后进行24小时的再灌注。在诱导缺血再灌注前10天,糖尿病大鼠分别每日口服25、50和100 mg/kg的EGb 761(每组n = 12)。在无药物的糖尿病对照组中,与非缺血对照组相比,90分钟缺血后再灌注24小时导致视网膜Na+和Ca2+增加(通过原子吸收分光光度法测量),非缺血对照组的Na+和Ca2+值分别为73±4和2.6±0.3 μmol/g干重,缺血再灌注后分别增至113±5(p < 0.05)和5.3±0.3 μmol/g干重(p < 0.05)。组织K+含量与非缺血糖尿病对照组的268±7 μmol/g干重相比显著降低至213±6 μmol/g干重(p < 0.05)。EGb 761剂量依赖性地减少再灌注诱导的离子失衡,改善糖尿病大鼠视网膜中离子含量的恢复。EGb 761未降低链脲佐菌素诱导的糖尿病大鼠的血糖。因此我们可以得出结论,EGb 761的这些保护作用与血糖含量或糖尿病严重程度无关,而是直接保护视网膜细胞免受电解质变化的影响。

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