Aim: Renin-angiotensin system (RAS) is thought to have a noticeable effect in the pathophysiological injury in multiple organs by inducing different cellular and molecular reactions. The objective of the current study is to investigate the possible protective effects of perindopril against lipopolysaccharide (LPS)-induced cardiopulmonary oxidative and inflammatory damage in rats. Methods: To achieve this goal, animals were randomly divided into six groups: normal group, LPS group (3 mg/kg, i.p., single dose), perindopril-LPS treated group (1 mg/kg/day, i.p.), perindopril-LPS treated group (2 mg/kg/day, i.p.), and two perindopril negative groups (perindopril 1 or 2 mg/kg/day, i.p.) alone for seven days. Lungs and hearts tissue angiotensin II (Ang-II), angiotensin-1-7 (Ang-1-7), and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase were assessed using ELISA. Nuclear factor kappa-B-p65 (NF-κB-p65) was assessed using real time PCR, while protein kinase B (Akt) was evaluated by Western blot analysis. Furthermore, oxidative stress biomarkers and myeloperoxidase (MPO) enzyme were evaluated spectrophotometrically. Tissues inducible and endothelial nitric oxide synthases (iNOS and eNOS) were assessed immunohistochemically. Histopathological study was carried out to confirm our results. Results: LPS-intoxicated rats significantly elevated Ang-II, NF-κB-p65, Akt, and iNOS levels, coupled with significant down-regulation of Ang-1-7 and eNOS levels and corrected the oxidative stress biomarkers. Perindopril administration significantly attenuated the disturbances induced by LPS in a dose-dependent manner. Conclusion: Perindopril mitigates LPS-induced heart and lung damage through modulation of RAS, iNOS/eNOS, Akt, and NF-κB-p65 signaling pathways.

中文翻译：

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培哚普利通过抑制肾素血管紧张素系统，炎症和氧化应激减轻LPS诱导的心肺氧化和炎症损害。

目的：肾素-血管紧张素系统（RAS）被认为通过诱导不同的细胞和分子反应，在多个器官的病理生理损伤中具有明显的作用。本研究的目的是研究培哚普利对脂多糖（LPS）诱导的大鼠心肺氧化和炎性损伤的可能的保护作用。方法：为实现这一目标，将动物随机分为六组：正常组，LPS组（3 mg / kg，腹膜内，单剂量），培哚普利-LPS治疗组（1 mg / kg /天，腹膜内），培哚普利- LPS治疗组（2 mg / kg /天，腹膜内）和两个培哚普利阴性组（培哚普利1或2 mg / kg /天，腹膜内）连续7天。肺和心脏组织血管紧张素II（Ang-II），血管紧张素-1-7（Ang-1-7），使用ELISA评估烟酰胺和烟酰胺腺嘌呤二核苷酸磷酸（NADPH）氧化酶。使用实时PCR评估核因子κB-p65（NF-κB-p65），而蛋白激酶B（Akt）通过Western印迹分析评估。此外，通过分光光度法评估了氧化应激生物标志物和髓过氧化物酶（MPO）酶。免疫组织化学方法评估了组织诱导型和内皮型一氧化氮合酶（iNOS和eNOS）。进行了组织病理学研究以证实我们的结果。结果：LPS中毒的大鼠可显着升高Ang-II，NF-κB-p65，Akt和iNOS水平，并显着下调Ang-1-7和eNOS水平并纠正氧化应激生物标志物。培哚普利的给药以剂量依赖的方式显着减轻了LPS引起的干扰。结论：