Student Research Committee, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Toxicology Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Cardiovasc Toxicol. 2024 Jun;24(6):539-549. doi: 10.1007/s12012-024-09864-3. Epub 2024 May 4.
NaAsO is known as a harmful pollutant all over the world, and many chronic heart diseases can be attributed to its prolonged exposure in NaAsO-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)-induced cardiotoxicity. Forty male mice were randomly divided into 4 groups: (I) Control; (II) BET (500 mg/kg); (III) NaAsO (50 ppm); and (IV) NaAsO + BET. NaAsO 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-intoxicated mice, thereby attenuating oxidative stress-induced damage and inflammation.
砷酸钠(NaAsO)是一种全球范围内的有害污染物,许多慢性心脏病可归因于长期暴露于受 NaAsO 污染的水中。因此,考虑到甜菜碱(BET)的抗炎和抗氧化作用,在这项研究中,我们的团队研究了这种植物化学物质对亚砷酸钠(NaAsO)诱导的心脏毒性的心脏保护作用。40 只雄性小鼠被随机分为 4 组:(I)对照组;(II)BET(500mg/kg);(III)NaAsO(50ppm);和(IV)NaAsO+BET。给动物喂食 NaAsO 8 周,但在最后两周给予 BET。断头后,测量炎症因子和生化参数,并进行 Western blot 分析。BET 降低丙氨酸氨基转移酶、肌酸激酶 MB、硫代巴比妥酸反应物质水平、炎症因子(肿瘤坏死因子-α)含量和核因子 kappa B 表达的活性水平。此外,BET 增加了心脏总巯基和过氧化氢酶、超氧化物歧化酶和谷胱甘肽过氧化物酶的活性水平以及核因子红系-2 的表达。因此,BET 的给药改善了氧化和抗氧化途径失衡以及 NaAsO 中毒小鼠中观察到的组织病理学改变所带来的有害影响,从而减轻了氧化应激诱导的损伤和炎症。