Ahmed Rasha F, Okasha Ahmed M, Hafiz Salwa Hamdy Ibrahim, Abdel-Gaber Seham A, Yousef Rehab K Mohamed, Sedik Wael F
Department of Medical Biochemistry, Faculty of Medicine, Minia University, 61511, Minia, Egypt.
Department of Pharmacology, Faculty of Medicine, Minia University, 61511, Minia, Egypt.
Iran J Basic Med Sci. 2022 Mar;25(3):399-404. doi: 10.22038/ijbms.2022.60579.13428.
Acute Kidney Injury (AKI) is characterized by a rapid and reversible decline in renal function with a rapid decrease in Glomerular Filtration Rate (GFR), which is associated with high mortality. Rhabdomyolysis accounts for 10-40% of AKI, to which the therapeutic approach is limited. is a protein that modulates sodium-phosphate co-transporters, ion channels that have been reported to have a renal protective effect. Guanosine, a purine nucleoside, has already been reported to have a renal protective effect; however, the mechanism of such protection and its relation to modification has not been evaluated yet. This study aims to evaluate the mechanism of the protective effect of guanosine against rhabdomyolysis-induced AKI and its relation to the expression of the gene.
In the current study, rats were divided into three groups: control, glycerol-induced AKI, and guanosine-treated. Serum urea and creatinine levels, renal tissue Total Antioxidant Capacity (TAC), and and genes expression were evaluated. Furthermore, caspase-3 immunostaining and histopathological evaluations were done.
Results showed that guanosine treatment resulted in a significant reduction in serum urea and creatinine, genes expression, and caspase-3 immunoexpression, and an increase in TAC and genes expression. Results also revealed an improvement of renal histopathology when compared with the glycerol-induced AKI group.
Guanosine may be a promising agent in the treatment of rhabdomyolysis-induced AKI. The proposed mechanism for guanosine may be through its ability to enhance gene expression in renal tissue, with subsequent antioxidant and anti-apoptotic activity.
急性肾损伤(AKI)的特征是肾功能迅速且可逆地下降,肾小球滤过率(GFR)快速降低,这与高死亡率相关。横纹肌溶解症占急性肾损伤的10%-40%,其治疗方法有限。[蛋白质名称]是一种调节钠-磷酸盐共转运体的蛋白质,这些离子通道据报道具有肾脏保护作用。鸟苷,一种嘌呤核苷,已被报道具有肾脏保护作用;然而,这种保护机制及其与[蛋白质名称]修饰的关系尚未得到评估。本研究旨在评估鸟苷对横纹肌溶解诱导的急性肾损伤的保护作用机制及其与[蛋白质名称]基因表达的关系。
在本研究中,将大鼠分为三组:对照组、甘油诱导的急性肾损伤组和鸟苷治疗组。评估血清尿素和肌酐水平、肾组织总抗氧化能力(TAC)以及[蛋白质名称]和[基因名称]基因的表达。此外,进行了半胱天冬酶-3免疫染色和组织病理学评估。
结果表明,鸟苷治疗导致血清尿素和肌酐、[蛋白质名称]基因表达以及半胱天冬酶-3免疫表达显著降低,TAC和[基因名称]基因表达增加。与甘油诱导的急性肾损伤组相比,结果还显示肾组织病理学有所改善。
鸟苷可能是治疗横纹肌溶解诱导的急性肾损伤的一种有前景的药物。鸟苷的作用机制可能是通过其增强肾组织中[蛋白质名称]基因表达的能力,随后产生抗氧化和抗凋亡活性。