Betanin mitigates vancomycin-induced acute kidney injury in mice and molecular docking indicated inhibition of STAT3 phosphorylation

IF 2.5 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell Pub Date : 2025-09-25 DOI:10.1016/j.tice.2025.103159

Haifa Alrshedi , Sawsan A. Zaitone , Reem Alshaman , Mohamed A. Helal , Abdullah Alattar , Sarah A. Alshammari , Hibah S. Bedaiwi , Ghiadaa K. Sroor , Ibtisam R. Alnasser , Abduallh J. Ghabban , Eman Serry Zayed , Roba Alatawy , Dina M. Khodeer

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Abstract

Acute kidney injury (AKI) is a common, complicated disorder affecting hospitalized and critically ill patients. The signal transducer and activator of transcription-3 (STAT3) is associated with the progress of AKI. Betanin is a natural betacyanin with multiple biological activities. The contribution of STAT3 in vancomycin-induced AKI and possible protection by betanin were investigated in this study. Molecular docking and molecular dynamics simulation (MDS) studies were done to test the probability of inhibition of STAT3 phosphorylation by betanin. Further, the experiment included eighteen male albino mice were assigned as (i) saline group, (ii) AKI control group (received vancomycin 200 mg/kg) by intraperitoneal injection for 14 doses, and (iii) vancomycin + betanin (50 mg/kg) group. Serum urea and creatinine were measured. Frozen kidneys were used for measuring inflammatory markers, whereas formalin-fixed kidneys were cut into sections to prepare specimens stained with hematoxylin and eosin. Molecular docking showed that betanin can hinder STAT3 phosphorylation. Serum urea and creatinine were found elevated in the AKI group versus the saline group; but reduced in the vancomycin + betanin group. Further, histopathological examination indicated tubular degeneration and interstitial inflammation that was mitigated by betanin. Betanin attenuated vancomycin-induced AKI, enhanced kidney function parameters, and retained the integrity of renal histological structures. These effects were, at least partly, facilitated via inhibiting the phosphorylation of the upregulated STAT3. These results open an avenue to fully test the effect and mechanism of betanin in various models of kidney injuries.

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甜菜素减轻万古霉素诱导的小鼠急性肾损伤，分子对接显示抑制STAT3磷酸化。

急性肾损伤（AKI）是一种常见的复杂疾病，影响住院和危重患者。信号转导和转录激活因子-3 （STAT3）与AKI的进展有关。甜菜素是一种具有多种生物活性的天然甜菜青素。本研究探讨STAT3在万古霉素诱导AKI中的作用及甜菜素可能的保护作用。通过分子对接和分子动力学模拟（MDS）研究，验证甜菜素抑制STAT3磷酸化的可能性。将18只雄性白化小鼠分为生理盐水组、AKI对照组（万古霉素200 mg/kg）腹腔注射14次、万古霉素+ β素（50 mg/kg）组。测定血清尿素和肌酐。冷冻肾脏用于测量炎症标志物，而福尔马林固定肾脏切成切片，制备苏木精和伊红染色标本。分子对接表明，甜菜素可以抑制STAT3磷酸化。与生理盐水组相比，AKI组血清尿素和肌酐升高；但万古霉素+甜菜素组降低。此外，组织病理学检查显示小管变性和间质炎症被甜菜素减轻。甜菜素减轻万古霉素引起的AKI，增强肾功能参数，并保持肾脏组织结构的完整性。这些作用至少部分是通过抑制上调的STAT3的磷酸化来促进的。这些结果为充分检验甜菜素在各种肾损伤模型中的作用和机制开辟了途径。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Tissue & cell 医学-解剖学与形态学

CiteScore

3.90

自引率

0.00%

发文量

234

期刊介绍： Tissue and Cell is devoted to original research on the organization of cells, subcellular and extracellular components at all levels, including the grouping and interrelations of cells in tissues and organs. The journal encourages submission of ultrastructural studies that provide novel insights into structure, function and physiology of cells and tissues, in health and disease. Bioengineering and stem cells studies focused on the description of morphological and/or histological data are also welcomed. Studies investigating the effect of compounds and/or substances on structure of cells and tissues are generally outside the scope of this journal. For consideration, studies should contain a clear rationale on the use of (a) given substance(s), have a compelling morphological and structural focus and present novel incremental findings from previous literature.