{"title":"甜菜碱通过抗氧化和抗炎途径保护小鼠免受亚砷酸钠引发的心脏毒性的影响","authors":"Saeedeh Shariati, Maryam Shirani, Reza Azadnasab, Layasadat Khorsandi, Mohammad Javad Khodayar","doi":"10.1007/s12012-024-09864-3","DOIUrl":null,"url":null,"abstract":"<p><p>NaAsO<sub>2</sub> is known as a harmful pollutant all over the world, and many chronic heart diseases can be attributed to its prolonged exposure in NaAsO<sub>2</sub>-contaminated water. Therefore, considering the anti-inflammatory and antioxidant effects of betaine (BET), in this study, our team investigated the cardioprotective effects of this phytochemical agent on sodium arsenite (NaAsO<sub>2</sub>)-induced cardiotoxicity. Forty male mice were randomly divided into 4 groups: (I) Control; (II) BET (500 mg/kg); (III) NaAsO<sub>2</sub> (50 ppm); and (IV) NaAsO<sub>2</sub> + BET. NaAsO<sub>2</sub> was given to the animals for 8 weeks, but BET was given in the last two weeks. After decapitation, inflammatory factors and biochemical parameters were measured, and Western blot analyses were performed. BET decrease the activity level of alanine aspartate aminotransferase, creatine kinase MB, thiobarbituric acid reactive substances level, inflammatory factors (tumor necrosis factor-α) content, and nuclear factor kappa B expression. Furthermore, BET increased cardiac total thiol and activity levels of catalase, superoxide dismutase, and glutathione peroxidase and nuclear factor erythroid-2 expression. Hence, the administration of BET ameliorated the deleterious effects stemming from the imbalance of oxidative and antioxidant pathways and histopathological alterations observed in NaAsO<sub>2</sub>-intoxicated mice, thereby attenuating oxidative stress-induced damage and inflammation.</p>","PeriodicalId":9570,"journal":{"name":"Cardiovascular Toxicology","volume":" ","pages":"539-549"},"PeriodicalIF":3.4000,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Betaine Protects Mice from Cardiotoxicity Triggered by Sodium Arsenite Through Antioxidative and Anti-inflammatory Pathways.\",\"authors\":\"Saeedeh Shariati, Maryam Shirani, Reza Azadnasab, Layasadat Khorsandi, Mohammad Javad Khodayar\",\"doi\":\"10.1007/s12012-024-09864-3\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>NaAsO<sub>2</sub> is known as a harmful pollutant all over the world, and many chronic heart diseases can be attributed to its prolonged exposure in NaAsO<sub>2</sub>-contaminated water. Therefore, considering the anti-inflammatory and antioxidant effects of betaine (BET), in this study, our team investigated the cardioprotective effects of this phytochemical agent on sodium arsenite (NaAsO<sub>2</sub>)-induced cardiotoxicity. Forty male mice were randomly divided into 4 groups: (I) Control; (II) BET (500 mg/kg); (III) NaAsO<sub>2</sub> (50 ppm); and (IV) NaAsO<sub>2</sub> + BET. NaAsO<sub>2</sub> was given to the animals for 8 weeks, but BET was given in the last two weeks. After decapitation, inflammatory factors and biochemical parameters were measured, and Western blot analyses were performed. BET decrease the activity level of alanine aspartate aminotransferase, creatine kinase MB, thiobarbituric acid reactive substances level, inflammatory factors (tumor necrosis factor-α) content, and nuclear factor kappa B expression. Furthermore, BET increased cardiac total thiol and activity levels of catalase, superoxide dismutase, and glutathione peroxidase and nuclear factor erythroid-2 expression. Hence, the administration of BET ameliorated the deleterious effects stemming from the imbalance of oxidative and antioxidant pathways and histopathological alterations observed in NaAsO<sub>2</sub>-intoxicated mice, thereby attenuating oxidative stress-induced damage and inflammation.</p>\",\"PeriodicalId\":9570,\"journal\":{\"name\":\"Cardiovascular Toxicology\",\"volume\":\" \",\"pages\":\"539-549\"},\"PeriodicalIF\":3.4000,\"publicationDate\":\"2024-06-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Cardiovascular Toxicology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1007/s12012-024-09864-3\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/5/4 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q2\",\"JCRName\":\"CARDIAC & CARDIOVASCULAR SYSTEMS\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cardiovascular Toxicology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s12012-024-09864-3","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/5/4 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"CARDIAC & CARDIOVASCULAR SYSTEMS","Score":null,"Total":0}
引用次数: 0
摘要
众所周知,NaAsO2 是一种对全世界都有害的污染物,许多慢性心脏病都可归因于长期暴露于被 NaAsO2 污染的水中。因此,考虑到甜菜碱(BET)的抗炎和抗氧化作用,我们的研究小组在本研究中探讨了这种植物化学物质对亚砷酸钠(NaAsO2)诱导的心脏毒性的保护作用。将 40 只雄性小鼠随机分为 4 组:(I) 对照组;(II) BET(500 毫克/千克)组;(III) NaAsO2(50 ppm)组;(IV) NaAsO2 + BET 组。给动物注射 NaAsO2 8 周,但在最后两周注射 BET。断头后,测量炎症因子和生化指标,并进行 Western 印迹分析。BET降低了丙氨酸天冬氨酸氨基转移酶活性水平、肌酸激酶MB、硫代巴比妥酸活性物质水平、炎症因子(肿瘤坏死因子-α)含量和核因子卡巴B的表达。此外,BET 还能提高心脏总硫醇和过氧化氢酶、超氧化物歧化酶、谷胱甘肽过氧化物酶的活性水平以及核因子红细胞-2 的表达。因此,服用 BET 可改善 NaAsO2 中毒小鼠体内氧化和抗氧化途径失衡所产生的有害影响以及组织病理学改变,从而减轻氧化应激引起的损伤和炎症。
Betaine Protects Mice from Cardiotoxicity Triggered by Sodium Arsenite Through Antioxidative and Anti-inflammatory Pathways.
NaAsO2 is known as a harmful pollutant all over the world, and many chronic heart diseases can be attributed to its prolonged exposure in NaAsO2-contaminated water. Therefore, considering the anti-inflammatory and antioxidant effects of betaine (BET), in this study, our team investigated the cardioprotective effects of this phytochemical agent on sodium arsenite (NaAsO2)-induced cardiotoxicity. Forty male mice were randomly divided into 4 groups: (I) Control; (II) BET (500 mg/kg); (III) NaAsO2 (50 ppm); and (IV) NaAsO2 + BET. NaAsO2 was given to the animals for 8 weeks, but BET was given in the last two weeks. After decapitation, inflammatory factors and biochemical parameters were measured, and Western blot analyses were performed. BET decrease the activity level of alanine aspartate aminotransferase, creatine kinase MB, thiobarbituric acid reactive substances level, inflammatory factors (tumor necrosis factor-α) content, and nuclear factor kappa B expression. Furthermore, BET increased cardiac total thiol and activity levels of catalase, superoxide dismutase, and glutathione peroxidase and nuclear factor erythroid-2 expression. Hence, the administration of BET ameliorated the deleterious effects stemming from the imbalance of oxidative and antioxidant pathways and histopathological alterations observed in NaAsO2-intoxicated mice, thereby attenuating oxidative stress-induced damage and inflammation.
期刊介绍:
Cardiovascular Toxicology is the only journal dedicated to publishing contemporary issues, timely reviews, and experimental and clinical data on toxicological aspects of cardiovascular disease. CT publishes papers that will elucidate the effects, molecular mechanisms, and signaling pathways of environmental toxicants on the cardiovascular system. Also covered are the detrimental effects of new cardiovascular drugs, and cardiovascular effects of non-cardiovascular drugs, anti-cancer chemotherapy, and gene therapy. In addition, Cardiovascular Toxicology reports safety and toxicological data on new cardiovascular and non-cardiovascular drugs.