Abstract：
Lipopolysaccharide (LPS) has been associated with myocardial inflammation, oxidative stress, apoptosis, and cardiac dysfunction, as well as death by causing sepsis. In this study, we investigated the effect of irbesartan (IRB), an angiotensin receptor antagonist, on cardiotoxicity caused by LPS.
The experiment involved 24 Wistar albino rats divided into three groups of eight: control, LPS (5 mg/kg), and LPS (5 mg/kg)+IRB (3 mg/kg). Parameters including total oxidative status, total antioxidant status, oxidative stress index, and ischemia-modified albumin were measured to assess oxidative stress in heart tissues and serum. Serum CK, CK-MB, and LDH levels were measured spectrophotometrically. RT-qPCR was used to detect the mRNA expression levels of Bcl-2, BAX, p53, caspase-3, and sirtuin 1. Tissues taken from the heart and aorta were examined by immunohistochemistry and histopathology.
While there was an increase in the parameters indicating heart damage, oxidative stress, and apoptosis in the group given LPS, there was an improvement in all parameters and heart damage in the group treated with IRB.
As a result of our study, we determined that IRB has an ameliorating effect on myocardial damage caused by oxidative stress and apoptosis developed by the LPS-induced sepsis model.
The experiment involved 24 Wistar albino rats divided into three groups of eight: control, LPS (5 mg/kg), and LPS (5 mg/kg)+IRB (3 mg/kg). Parameters including total oxidative status, total antioxidant status, oxidative stress index, and ischemia-modified albumin were measured to assess oxidative stress in heart tissues and serum. Serum CK, CK-MB, and LDH levels were measured spectrophotometrically. RT-qPCR was used to detect the mRNA expression levels of Bcl-2, BAX, p53, caspase-3, and sirtuin 1. Tissues taken from the heart and aorta were examined by immunohistochemistry and histopathology.
While there was an increase in the parameters indicating heart damage, oxidative stress, and apoptosis in the group given LPS, there was an improvement in all parameters and heart damage in the group treated with IRB.
As a result of our study, we determined that IRB has an ameliorating effect on myocardial damage caused by oxidative stress and apoptosis developed by the LPS-induced sepsis model.
摘要：
目的：脂多糖（LPS）与心肌炎症有关，氧化应激，凋亡，和心脏功能障碍，以及导致败血症的死亡。在这项研究中,我们研究了厄贝沙坦（IRB）的作用，血管紧张素受体拮抗剂，关于LPS引起的心脏毒性。
方法：该实验涉及24只Wistar白化病大鼠，分为三组，每组八只：对照组，LPS（5mg/kg），和LPS(5mg/kg)+IRB(3mg/kg)。参数包括总氧化状态，总抗氧化剂状态，氧化应激指数，测量缺血修饰的白蛋白以评估心脏组织和血清中的氧化应激。血清CK,CK-MB,用分光光度法测定LDH水平。RT-qPCR检测Bcl-2、BAX、p53、caspase-3和沉默酶1。通过免疫组织化学和组织病理学检查取自心脏和主动脉的组织。
结果：虽然表明心脏损伤的参数有所增加，氧化应激，在给予LPS的组中，细胞凋亡，IRB治疗组的所有参数和心脏损伤均有改善.
结论：作为我们研究的结果，我们确定IRB对LPS诱导的脓毒症模型建立的氧化应激和细胞凋亡引起的心肌损伤有改善作用。
方法：该实验涉及24只Wistar白化病大鼠，分为三组，每组八只：对照组，LPS（5mg/kg），和LPS(5mg/kg)+IRB(3mg/kg)。参数包括总氧化状态，总抗氧化剂状态，氧化应激指数，测量缺血修饰的白蛋白以评估心脏组织和血清中的氧化应激。血清CK,CK-MB,用分光光度法测定LDH水平。RT-qPCR检测Bcl-2、BAX、p53、caspase-3和沉默酶1。通过免疫组织化学和组织病理学检查取自心脏和主动脉的组织。
结果：虽然表明心脏损伤的参数有所增加，氧化应激，在给予LPS的组中，细胞凋亡，IRB治疗组的所有参数和心脏损伤均有改善.
结论：作为我们研究的结果，我们确定IRB对LPS诱导的脓毒症模型建立的氧化应激和细胞凋亡引起的心肌损伤有改善作用。
