Background: Apelin-13 is an endogenous adipocytokine known for its antioxidant, antiinflammatory, and antiapoptotic properties. Objective: We aimed to investigate the possible protective effects of exogenous Apelin-13 administration on oxidative stress, inflammation, and apoptosis induced by the cytotoxic agent cyclophosphamide (CP) in the lungs. Methods: Twenty-four male Wistar albino rats were divided into four groups: Control (saline), CP (200 mg/kg), Apelin-13 (10 µg/kg/day), and CP+Apelin-13. CP was administered as a single dose on the fifth day, and apelin-13 was administered intraperitoneally for five days. Total oxidant status (TOS), total antioxidant status (TAS), and lipid peroxidation were determined with spectrophotometry, TNFα and IL1β were determined with ELISA, APJ, Sirt1, NF-κB, and p53 mRNA expressions were determined with qRT-PCR, cytochrome (Cyt) C and caspase-3 protein expressions were studied with western blotting in lung tissues. The oxidative stress index (OSI) was also calculated. Furthermore, serum surfactant protein-D (SP-D) and Krebs von den Lungen-6 (KL-6) levels were measured with ELISA. Results: Compared to the control group, TOS, OSI, lipid peroxidation, TNFα, IL1β, cyt C, caspase-3, APJ, NF-κB, and p53 were higher, and Sirt1 was lower in the lung tissue of rats in the CP group. Serum KL-6 and SP-D levels were higher in the CP group. Co-administration of CP with Apelin-13 completely reversed the changes induced by CP administration. Conclusion: Exogenous Apelin-13 treatment protected lung tissue against injury by inhibiting cyclophosphamide-induced oxidative stress, inflammation, and apoptosis. This protective effect of apelin-13 was accompanied by upregulation of the Sirt1 and downregulation of NF-κB/p53 in the lungs.

中文翻译：

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外源性 Apelin-13 给药可改善环磷酰胺诱导的大鼠肺氧化应激、炎症和细胞凋亡

背景：Apelin-13 是一种内源性脂肪细胞因子，以其抗氧化、抗炎和抗凋亡特性而闻名。目的：我们旨在探讨外源性 Apelin-13 给药对细胞毒剂环磷酰胺（CP）诱导的肺部氧化应激、炎症和细胞凋亡的可能保护作用。方法：24 只雄性 Wistar 白化大鼠分为四组：对照组（盐水）、CP（200 mg/kg）、Apelin-13（10 µg/kg/天）和 CP+Apelin-13。CP在第五天以单剂量施用，apelin-13腹腔内施用五天。用分光光度法测定总氧化状态（TOS）、总抗氧化状态（TAS）和脂质过氧化，用ELISA测定TNFα和IL1β，用qRT-PCR、细胞色素测定APJ、Sirt1、NF-κB和p53 mRNA表达通过免疫印迹法研究肺组织中 (Cyt) C 和 caspase-3 蛋白的表达。还计算了氧化应激指数（OSI）。此外，使用 ELISA 测量血清表面活性蛋白-D (SP-D) 和 Krebs von den Lungen-6 (KL-6) 水平。结果：与对照组相比，CP组大鼠肺组织中TOS、OSI、脂质过氧化、TNFα、IL1β、cyt C、caspase-3、APJ、NF-κB、p53升高，Sirt1降低团体。CP组血清KL-6和SP-D水平较高。CP 与 Apelin-13 共同给药完全逆转了 CP 给药引起的变化。结论：外源性 Apelin-13 治疗通过抑制环磷酰胺诱导的氧化应激、炎症和细胞凋亡来保护肺组织免受损伤。apelin-13 的这种保护作用伴随着肺部 Sirt1 的上调和 NF-κB/p53 的下调。