食用农产品被农药污染,包括敌敌畏(DVDP),会带来巨大的公共卫生风险,促进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-鼠李糖苷或Hes-7-RGlc)可以保留细胞膜,氧化还原,和脂质稳态;不幸的是,它对敌敌畏引起的心脏损伤的作用尚未得到研究。这项工作探索了Hes-7-RGlc对DVDP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(6只/组):对照组,单独使用DVDP(8毫克。kg-day-lar),DVDP提供Hes-7-RGlc(50和100mg。kg-天-)或参考药物阿托品(0.2mg。kg-day-lar),和单独的Hes-7-RGlc(50和10毫克。kg-1天-1)是被调查的七个组。DVDP口服给药7天,随后14天的Hes-7-RGlc治疗。然后对大鼠实施安乐死,他们的血和心脏都被切除了.Hes-7-RGlc化疗基本上(p<0.05)恢复了DVDP引起的血浆和心脏/心肌肌酸激酶同工酶(CK-MB)动力学,主要脂质(胆固醇,三酰基甘油,和磷脂),电解质(钠,K,Ca²,Mg²,Cl),和总蛋白质。Hes-7-RGlc补救措施(p<0.05)消除了DDVP刺激的心脏浓度中的H2O2,NO和丙二醛;心脏GSH水平的环状DVDP消除降低,GST的活动,SOD,过氧化氢酶,和谷胱甘肽过氧化物酶,离子转运体(Na²/K²-ATP酶和Ca²/Mg²-ATP酶),ALT,AST,ALP,和LDH-1。总的来说,Hes-7-RGlc可以被提倡为DVDP引起的心脏缺陷的天然补充候选者和阻断剂,通过其逆转电解质破坏的能力,离子泵,氧化还原状态,和脂质稳态。
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.