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生物合成的金纳米粒子通过下调 iNOX、LCN2 和 IL-1β 基因减轻氯化铝诱导的肾毒性。

Biologically Synthesized Gold Nanoparticles Mitigate Aluminum Chloride-Induced Nephrotoxicity via Downregulation of iNOX, LCN2 and IL-1β Genes.

机构信息

Nanomedicine, Drug Metabolism and Toxicology Research Laboratory, Biochemistry Program, Department of Chemical Sciences, Afe Babalola University, P.M.B 5454, Ado-Ekiti, Nigeria.

Department of Internal Medicine, Afe Babalola University Teaching Hospital, P.M.B 5454, Ado-Ekiti, Nigeria.

出版信息

Cell Biochem Biophys. 2024 Sep;82(3):2493-2502. doi: 10.1007/s12013-024-01360-3. Epub 2024 Jun 22.

DOI:10.1007/s12013-024-01360-3
PMID:38907938
Abstract

Humans are constantly exposed to aluminum (Al), an environmental toxicant, and its accumulation in the glomerular could lead to acute kidney disease. Biologically synthesized gold nanoparticles (AuNPs) have been employed in the management of kidney disorders. This study assessed the modulatory effect of AuNPs mediated by Hibiscus sabdariffa (HS) on aluminum chloride (AlCl)-induced nephrotoxicity in rats. Experimental rats were randomly distributed into six groups of seven animals each. Aluminum chloride (100 mg/kg bw) was orally given to the rats for 42 days to induce nephrotoxicity. Treatment with silymarin and HS-AuNPs lasted for 14 days. Serum kidney function, tissue arginase level and oxidative stress biomarkers, as well as tissue gene expression of inducible nitric oxide synthase (iNOS), lipocalin 2 (LCN2) and interleukin-1 beta (IL-1β) were evaluated. Exposure of AlCl to the rats produced a marked (p < 0.05) increase in the levels of serum urea and creatinine in comparison with the control. Similarly, tissue arginase and malondialdehyde (MDA) levels were also increased while a reduction in the activity of superoxide dismutase (SOD) and the levels of reduced glutathione (GSH) and nitric oxide (NO) were noted in the AlCl-induced rats. Aluminum chloride also upregulated the mRNA expression of iNOS, LCN2 and IL-1β in the rats. These biochemical alterations were, however, attenuated by the administration of HS-AuNPs but the 5 mg/kg HS-AuNPs exhibited better anti-nephrotoxic activity than the 10 mg/kg dose, and could, thus serve as a potential dose for managing renal diseases.

摘要

人类不断暴露于环境毒物铝(Al)中,其在肾小球中的积累可导致急性肾病。生物合成的金纳米粒子(AuNPs)已被用于治疗肾脏疾病。本研究评估了由 Hibiscus sabdariffa(HS)介导的 AuNPs 对氯化铝(AlCl)诱导的大鼠肾毒性的调节作用。实验大鼠随机分为六组,每组 7 只。大鼠口服给予氯化铝(100mg/kg bw)42 天以诱导肾毒性。给予水飞蓟素和 HS-AuNPs 治疗 14 天。评估血清肾功能、组织精氨酸酶水平和氧化应激生物标志物,以及诱导型一氧化氮合酶(iNOS)、脂联素 2(LCN2)和白细胞介素-1β(IL-1β)的组织基因表达。与对照组相比,暴露于 AlCl 的大鼠血清尿素和肌酐水平显著升高(p<0.05)。同样,组织精氨酸酶和丙二醛(MDA)水平也升高,而超氧化物歧化酶(SOD)活性和还原型谷胱甘肽(GSH)和一氧化氮(NO)水平降低在 AlCl 诱导的大鼠中观察到。铝还上调了大鼠中 iNOS、LCN2 和 IL-1β 的 mRNA 表达。然而,这些生化变化通过给予 HS-AuNPs 得到了减弱,但 5mg/kg 的 HS-AuNPs 表现出比 10mg/kg 剂量更好的抗肾毒性活性,因此可以作为治疗肾脏疾病的潜在剂量。

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本文引用的文献

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Hesperidin protects against aluminum-induced renal injury in rats via modulating MMP-9 and apoptosis: biochemical, histological, and ultrastructural study.橙皮苷通过调节 MMP-9 和细胞凋亡来保护大鼠免受铝诱导的肾损伤:生化、组织学和超微结构研究。
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