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橙皮素-7-O-鼠李糖葡萄糖苷通过对抗离子调节、离子泵、氧化还原和脂质稳态破坏来改善敌敌畏诱导的大鼠心脏毒性。

Hesperetin-7-O-rhamnoglucoside ameliorates dichlorvos-facilitated cardiotoxicity in rats by counteracting ionoregulatory, ion pumps, redox, and lipid homeostasis disruptions.

作者信息

Akamo Adio J, Ojelabi Adetutu O, Somade Oluwatobi T, Kehinde Iyabode A, Taiwo Adewale M, Olagunju Boluwatife A, Akinsanya Mushafau A, Adebisi Adebisi A, Adekunbi Tobi S, Adenowo Abiola F, Anifowose Florence, Ajagun-Ogunleye Olufemi M, Eteng Ofem E, Akintunde Jacob K, Ugbaja Regina N

机构信息

Department of Medical Biochemistry, Faculty of Basic Medical Sciences, Lagos State University College of Medicine, Ikeja, Lagos State, Nigeria.

Clinical Biochemistry and Mechanistic Toxicology Research Cluster, Department of Biochemistry, Federal University of Agriculture, Abeokuta, Ogun State, Nigeria.

出版信息

Toxicol Rep. 2024 Jul 19;13:101698. doi: 10.1016/j.toxrep.2024.101698. eCollection 2024 Dec.

DOI:10.1016/j.toxrep.2024.101698
PMID:39140093
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11320608/
Abstract

The contamination of edible agricultural goods with pesticides, including dichlorvos (DVDP), poses a substantial public health risk, promoting severe morbidity and mortality, especially in developing countries. It has been shown that hesperidin (hesperetin-7-O-rhamnoglucoside or Hes-7-RGlc) preserves cytomembrane, redox, and lipid homeostasis; unfortunately, its function on dichlorvos-incited heart damage has not been investigated. This work explored the ameliorative influence of Hes-7-RGlc on DVDP-activated cardiotoxicity. For this end, forty-two rats were randomly appropriated into seven groups (6 rats/group): Control, DVDP alone (8 mg.kg⁻¹day⁻¹), DVDP supplied with either Hes-7-RGlc (50 and 100 mg.kg⁻¹day⁻¹) or the reference medication atropine (0.2 mg.kg⁻¹day⁻¹), and Hes-7-RGlc alone (50 and 10 mg.kg⁻¹day⁻¹) were the seven groups investigated. DVDP was administered orally for seven days, followed by fourteen days of Hes-7-RGlc therapy. Then the rats were euthanized, and their blood and hearts were removed. Hes-7-RGlc chemotherapy substantially (p<0.05) restored DVDP-elicited dynamics in plasma and cardiac/myocardium creatine kinase isoenzyme (CK-MB), major lipids (cholesterol, triacylglycerol, and phospholipids), electrolytes (Na⁺, K⁺, Ca²⁺, Mg²⁺, Cl⁻), and total protein. Hes-7-RGlc remedy decidedly (p<0.05) abolished DDVP-stimulated amplification in the cardiac concentration of H₂O₂, NO and malondialdehyde; annulled DVDP-educed decreases in heart GSH levels, activities of GST, SOD, catalase, and glutathione peroxidase, ion transporters (Na⁺/K⁺-ATPase and Ca²⁺/Mg²⁺-ATPase), ALT, AST, ALP, and LDH-1. Collectively, Hes-7-RGlc can be advocated as a natural supplementary candidate and blocker of DVDP-provoked heart deficits via its capacity to reverse disruptions of electrolytes, ion pumps, redox status, and lipid homeostasis.

摘要

包括敌敌畏(DVDP)在内的农药对食用农产品的污染构成了重大的公共卫生风险,会导致严重的发病率和死亡率,尤其是在发展中国家。研究表明,橙皮苷(橙皮素-7-O-鼠李糖葡萄糖苷或Hes-7-RGlc)可维持细胞膜、氧化还原和脂质稳态;遗憾的是,其对敌敌畏引发的心脏损伤的作用尚未得到研究。本研究探讨了Hes-7-RGlc对敌敌畏激活的心脏毒性的改善作用。为此,将42只大鼠随机分为7组(每组6只):对照组、单独使用敌敌畏组(8mg·kg⁻¹·天⁻¹)、同时给予敌敌畏和Hes-7-RGlc组(50和100mg·kg⁻¹·天⁻¹)或参考药物阿托品组(0.2mg·kg⁻¹·天⁻¹)、单独使用Hes-7-RGlc组(50和10mg·kg⁻¹·天⁻¹),共7组。口服敌敌畏7天,随后进行14天的Hes-7-RGlc治疗。然后对大鼠实施安乐死,并取出其血液和心脏。Hes-7-RGlc化疗显著(p<0.05)恢复了敌敌畏引起的血浆和心肌/心肌肌酸激酶同工酶(CK-MB)、主要脂质(胆固醇、三酰甘油和磷脂)、电解质(Na⁺、K⁺、Ca²⁺、Mg²⁺、Cl⁻)和总蛋白的动态变化。Hes-7-RGlc治疗明确(p<0.05)消除了敌敌畏刺激引起的心脏中H₂O₂、NO和丙二醛浓度的升高;消除了敌敌畏导致的心脏谷胱甘肽水平降低、谷胱甘肽S-转移酶、超氧化物歧化酶、过氧化氢酶和谷胱甘肽过氧化物酶活性降低、离子转运体(Na⁺/K⁺-ATP酶和Ca²⁺/Mg²⁺-ATP酶)、谷丙转氨酶、谷草转氨酶、碱性磷酸酶和乳酸脱氢酶-1降低。总体而言,Hes-7-RGlc可被推荐为一种天然补充剂候选物,通过其逆转电解质、离子泵、氧化还原状态和脂质稳态破坏的能力,成为敌敌畏引发的心脏缺陷的阻滞剂。

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