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Topical Administration of ACE Inhibitor Interrupts the Progression of Cataract in Two Kidney One Clip Induced Hypertensive Cataract Model
Current Eye Research ( IF 1.7 ) Pub Date : 2021-11-12 , DOI: 10.1080/02713683.2021.2002911
Jaya Shree 1, 2 , Amrita Singh 1, 3 , Rajesh Choudhary 1, 4 , Devi Prasad Pandey 5 , Surendra H Bodakhe 1
Affiliation  

ABSTRACT

Purpose

Previously, we assessed that hypertension increases cataractogenesis. In the present study, we evaluated the effect of oral and topical administration of enalapril on two kidney one clip (2K1C)-induced hypertensive cataract model by evaluating the biochemical alteration of lenticular antioxidants, ionic content, ATPase activity, protein content and careful examination of the lenticular opacity.

Materials and Method

Animals were divided into normal and hypertensive animals. Hypertensive animals were divided into hypertensive control group (0.3% CMC), enalapril (oral) treatment group (20 mg/kg/day; p.o), and enalapril (topical) treatment group (0.1% w/v on the eye cornea) for a period of twelve weeks. During experimental study blood pressure, heart rate and morphology of the eyes were monitored biweekly. After twelve weeks, lenses were photographed and various catractogenic biochemical parameters were assessed.

Results

Enalapril (oral) treatment conserved the blood pressure (systolic and diastolic), restored the level of antioxidants, restored the lipid peroxidation marker, nitrite content, ionic content, ATPase function, protein content, and thus delayed the cataract formation. While, enalapril (topical) treatment exhibited anti-cataract effect without affecting the systolic and diastolic blood pressure that could be by restoring the antioxidant level, maintaining the ionic balance, balancing the protein levels, and by inhibiting the upregulated ocular renin angiotensin system. The overall results suggest that enalapril (topical) treatment showed conspicuous effect than enalapril (oral) treatment in adjourning the cataract formation.

Conclusion

Based on the results, it may be concluded that upregulated ocular RAS by increasing oxidative stress and by misbalancing the lenticular ionic and protein content may lead to cataract formation in hypertensive condition.



中文翻译:

ACE 抑制剂的局部给药中断了两个肾一夹诱发的高血压白内障模型中白内障的进展

摘要

目的

以前,我们评估了高血压会增加白内障的发生。在本研究中,我们通过评估晶状体抗氧化剂、离子含量、ATP酶活性、蛋白质含量的生化变化和仔细检查,评估了口服和局部给药依那普利对两个肾一夹(2K1C)诱导的高血压白内障模型的影响。透镜不透明度。

材料和方法

动物分为正常动物和高血压动物。高血压动物分为高血压对照组(0.3% CMC)、依那普利(口服)治疗组(20 mg/kg/天;口服)和依那普利(局部)治疗组(0.1% w/v在眼角膜上)为期十二周。在实验研究期间,每两周监测一次血压、心率和眼睛的形态。十二周后,对晶状体拍照并评估各种致导管生化参数。

结果

依那普利(口服)治疗可以保护血压(收缩压和舒张压),恢复抗氧化剂水平,恢复脂质过氧化标志物、亚硝酸盐含量、离子含量、ATP酶功能、蛋白质含量,从而延缓白内障的形成。而依那普利(局部)治疗在不影响收缩压和舒张压的情况下表现出抗白内障作用,这可能是通过恢复抗氧化水平、维持离子平衡、平衡蛋白质水平和抑制上调的眼肾素血管紧张素系统来实现的。总体结果表明,依那普利(局部)治疗在延缓白内障形成方面显示出比依那普利(口服)治疗显着的效果。

结论

基于这些结果,可以得出结论,通过增加氧化应激和不平衡晶状体离子和蛋白质含量来上调眼部 RAS 可能导致高血压条件下的白内障形成。

更新日期:2021-11-12
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