Phosphodiesterase Inhibitors: A Therapeutic Approach for Arsenic- Induced Neurotoxicity.

Drug metabolism and bioanalysis letters Pub Date : 2024-01-01 DOI:10.2174/0118723128343703250103063848

Sonia Bhatt, Ajay Pal Singh, Sokindra Kumar

{"title":"Phosphodiesterase Inhibitors: A Therapeutic Approach for Arsenic- Induced Neurotoxicity.","authors":"Sonia Bhatt, Ajay Pal Singh, Sokindra Kumar","doi":"10.2174/0118723128343703250103063848","DOIUrl":null,"url":null,"abstract":"Introduction: One of the world's most serious health issues is arsenic toxicity. Prolonged consumption of Arsenic contaminated water causes cognitive damage in the developing and adult brain. The present research investigated how sodium arsenite-induced neurotoxicity in SD rats was affected by rolipram, a PDE4 inhibitor, and vinpocetine, a PDE1 inhibitor.Methods: The arsenic concentration was determined, which indicates the accumulation of arsenic in blood. The low weight of the brain indicates the adverse effects on the brain, which was significantly improved by rolipram and vinpocetine. Biochemical markers (MDA, GSH, CAT, and SOD) and protein expression of CREB and P-CREB were studied in the hippocampal region of the brain.Results: The reduced antioxidant activity and elevated levels of inflammation were significantly improved by rolipram and vinpocetine administration. Additionally, rolipram and vinpocetine significantly increased the CREB and P-CREB expression in the hippocampi of rat brains.Conclusion: PDE4 and PDE1 inhibition in arsenic-induced neurotoxicity could be a novel approach and a new drug therapy for arsenic-induced neurotoxicity.","PeriodicalId":72844,"journal":{"name":"Drug metabolism and bioanalysis letters","volume":"17 2","pages":"67-75"},"PeriodicalIF":0.0000,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Drug metabolism and bioanalysis letters","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.2174/0118723128343703250103063848","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}

引用次数: 0

Abstract

Introduction: One of the world's most serious health issues is arsenic toxicity. Prolonged consumption of Arsenic contaminated water causes cognitive damage in the developing and adult brain. The present research investigated how sodium arsenite-induced neurotoxicity in SD rats was affected by rolipram, a PDE4 inhibitor, and vinpocetine, a PDE1 inhibitor.

Methods: The arsenic concentration was determined, which indicates the accumulation of arsenic in blood. The low weight of the brain indicates the adverse effects on the brain, which was significantly improved by rolipram and vinpocetine. Biochemical markers (MDA, GSH, CAT, and SOD) and protein expression of CREB and P-CREB were studied in the hippocampal region of the brain.

Results: The reduced antioxidant activity and elevated levels of inflammation were significantly improved by rolipram and vinpocetine administration. Additionally, rolipram and vinpocetine significantly increased the CREB and P-CREB expression in the hippocampi of rat brains.

Conclusion: PDE4 and PDE1 inhibition in arsenic-induced neurotoxicity could be a novel approach and a new drug therapy for arsenic-induced neurotoxicity.

查看原文本刊更多论文

磷酸二酯酶抑制剂：砷诱导神经毒性的治疗方法。

导言：砷中毒是世界上最严重的健康问题之一。长期饮用受砷污染的水会导致发育和成人大脑的认知损伤。本研究探讨了亚砷酸钠诱导的SD大鼠神经毒性是如何被罗利普兰（PDE4抑制剂）和长春西汀（PDE1抑制剂）影响的。方法：测定血砷浓度，测定血砷积累情况。大脑的低重量表明对大脑的不良影响，罗利普兰和长春西汀显著改善了这一点。研究脑海马区生化指标（MDA、GSH、CAT、SOD）及CREB、P-CREB蛋白表达。结果：罗利普兰和长春西汀可显著改善小鼠抗氧化活性降低和炎症水平升高。此外，罗利普兰和长春西汀显著增加了大鼠脑海马组织中CREB和P-CREB的表达。结论：抑制PDE4和PDE1可能是砷致神经毒性治疗的新途径和新药物。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Drug metabolism and bioanalysis letters

CiteScore

1.60

自引率

0.00%

发文量