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阿司匹林和水杨酸钠对糖尿病大鼠白内障形成的影响。

Effect of aspirin and sodium salicylate on cataract development in diabetic rats.

作者信息

Shastri G V, Thomas M, Victoria A J, Selvakumar R, Kanagasabapathy A S, Thomas K

机构信息

Christian Medical College & Hospital, Vellore, India.

出版信息

Indian J Exp Biol. 1998 Jul;36(7):651-7.

PMID:9782780
Abstract

The role of acetylation in the antiglycating and anticataract effects of aspirin (ASA) is explored by comparing ASA's effects with that of sodium salicylate (SS), a nonacetyl analog of ASA, on cataract development in diabetic rats. Streptozocin diabetic rats were provided with either ASA or SS, orally, for 24 weeks. Appropriate drug controls, normal controls and diabetic controls were run in parallel. Periodic estimations of blood glucose, glycated hemoglobin and assessments of cataract progression were done. After 24 weeks lenses were removed, homogenised and separated into water soluble fraction and urea soluble fraction. The glycated lens proteins in each fraction was quantified. Results were analysed statistically and interpreted in relation to serum salicylate levels. Both ASA and SS did not influence blood glucose levels. In the untreated diabetic groups the onset and progression of cataract was quicker and complete within 16 weeks. Both ASA and SS delayed the onset and progression in diabetic rats, but ASA's effect was more pronounced than that of SS. The levels of glycated Hb and lens proteins in diabetic rats were significantly reduced by ASA and not by SS for the same serum salicylate levels. ASA's anticataract potential far exceeds that of SS and it is ASA, and not SS, that inhibits protein glycation. Thus the results favour the hypothesis that acetylation plays a major role in ASA's anticataract effect via inhibition of glycation.

摘要

通过比较阿司匹林(ASA)及其非乙酰类似物水杨酸钠(SS)对糖尿病大鼠白内障发展的影响,探讨乙酰化在阿司匹林抗糖化和抗白内障作用中的作用。给链脲佐菌素诱导的糖尿病大鼠口服ASA或SS,持续24周。同时设置适当的药物对照组、正常对照组和糖尿病对照组。定期测定血糖、糖化血红蛋白,并评估白内障进展情况。24周后取出晶状体,匀浆并分离成水溶性部分和尿素溶性部分。对每个部分中的糖化晶状体蛋白进行定量。对结果进行统计学分析,并结合血清水杨酸盐水平进行解释。ASA和SS均不影响血糖水平。在未治疗的糖尿病组中,白内障的发生和进展更快,在16周内就完全形成。ASA和SS均能延缓糖尿病大鼠白内障的发生和进展,但ASA的效果比SS更明显。在相同血清水杨酸盐水平下,ASA能显著降低糖尿病大鼠的糖化血红蛋白和晶状体蛋白水平,而SS则不能。ASA的抗白内障潜力远远超过SS,并且是ASA而非SS抑制了蛋白质糖化。因此,结果支持这样的假说,即乙酰化通过抑制糖化在ASA的抗白内障作用中起主要作用。

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