Phthalates are common plasticizers present in medical-grade plastics and other everyday products. Di-ethylhexyl phthalate (DEHP) has been noted as a causative risk factor for the initiation and augmentation of cardiovascular functional disorders. G-CSF is a glycoprotein found in numerous tissues throughout the body and is currently applied in clinical practice and has been tested in congestive heart failure. We aimed to examine in depth the effect of DEHP on the histological and biochemical structure of the cardiac muscle in adult male albino rats and the mechanisms underlying the possible ameliorative effect of G-CSF. Forty-eight adult male albino rats were divided into control group, DEHP group, DEHP+ G-CSF group and DEHP-recovery group. We measured serum levels of aspartate aminotransferase (AST), creatine kinase MB isoenzyme (CK-MB) and lactate dehydrogenase (LDH). Left ventricular sections were processed for light and electron microscope examination, and immunohistochemical staining of Desmin, activated Caspase-3 and CD34. DEHP significantly increased enzyme levels, markedly distorted the normal architecture of cardiac muscle fibers, downregulated Desmin protein levels and enhanced fibrosis, and apoptosis. G-CSF treatment significantly decreased the enzyme levels compared to DEHP group. It enhanced CD34 positive stem cells recruitment to injured cardiac muscle, therefore improved the ultrastructural features of most cardiac muscle fibers via anti-fibrotic and anti-apoptotic effects in addition to increased Desmin protein expression levels. The recovery group showed partial improvement due to persistent DEHP effect. In conclusion, administration of G-CSF effectively corrected the histopathological, immunohistochemical and biochemical alterations in the cardiac muscle after DEHP administration by stem cells recruitment, Desmin protein regulation, antifibrotic and antiapoptotic mechanisms.

邻苯二甲酸盐是医用级塑料和其他日常产品中常见的增塑剂。邻苯二甲酸二乙基己酯 (DEHP) 已被认为是引发和加剧心血管功能障碍的致病危险因素。G-CSF是一种在全身许多组织中发现的糖蛋白，目前应用于临床实践，并已在充血性心力衰竭中进行了测试。我们的目的是深入研究 DEHP 对成年雄性白化大鼠心肌组织学和生化结构的影响，以及 G-CSF 可能改善作用的机制。48只成年雄性白化大鼠分为对照组、DEHP组、DEHP+G-CSF组和DEHP-恢复组。我们测量了天冬氨酸转氨酶 (AST)、肌酸激酶 MB 同工酶 (CK-MB) 和乳酸脱氢酶 (LDH) 的血清水平。对左心室切片进行光学和电子显微镜检查，以及结蛋白、活化的Caspase-3和CD34的免疫组织化学染色。DEHP 显着增加酶水平，显着扭曲心肌纤维的正常结构，下调结蛋白水平并增强纤维化和细胞凋亡。与 DEHP 组相比，G-CSF 处理显着降低了酶水平。它增强了 CD34 阳性干细胞向受损心肌的募集，因此除了增加 Desmin 蛋白表达水平外，还通过抗纤维化和抗凋亡作用改善了大多数心肌纤维的超微结构特征。由于 DEHP 的持续作用，恢复组表现出部分改善。总之，G-CSF的施用通过干细胞募集、Desmin蛋白调节、抗纤维化和抗凋亡机制有效地纠正了DEHP施用后心肌的组织病理学、免疫组织化学和生化改变。