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评估牛血清白蛋白还原的贻贝衍生硒纳米颗粒在斑马鱼模型中减轻硫酸铜诱导的肝损伤和神经退行性变的治疗潜力。

Evaluating the therapeutic potential of BSA-reduced mussel-derived selenium nanoparticles to mitigate copper sulfate-induced hepatic damage and neurodegeneration in a zebrafish model.

作者信息

Umapathy Suganiya, Pan Ieshita

机构信息

Department of Medical Biotechnology, Institute of Biotechnology, Saveetha School of Engineering, Saveetha Institute of Medical and Technical Sciences, Chennai, Tamil Nadu, India.

出版信息

Front Genet. 2025 May 19;16:1522370. doi: 10.3389/fgene.2025.1522370. eCollection 2025.

DOI:10.3389/fgene.2025.1522370
PMID:40458560
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12127314/
Abstract

INTRODUCTION

Liver fibrosis is the abnormal accumulation of extracellular matrix and eventual formation of fibrous scar in response to chronic liver injury, which can be triggered by increased levels of reactive oxygen species. The brain-liver axis is a crucial communication pathway that significantly influences the intricate interactions between hepatic function and brain health. Selenium, as a source of selenoproteins, plays a vital role in antioxidant defense systems. The extraction of selenium from mussels leverages their natural bioaccumulation, providing a biocompatible source. Selenium nanoparticles are known for their potential antioxidant activity and can be employed to regulate ROS levels to overcome hepatic damage.

METHODS

Selenium nanoparticles were synthesized from mussel-extracted selenium and stabilized with bovine serum albumin. The zebrafish models exposed to copper sulfate were treated with selenium nanoparticles (5-25 μg/ml). This study evaluated their potential role as antioxidants against hepatic damage induced by copper sulfate in the zebrafish model.

RESULTS

The bovine serum albumin stabilized selenium nanoparticles reduced for 30 minutes and 1 hour were spherical with a size of 19 and 16 nm. Stabilized selenium nanoparticles reduced for 30 minutes (25 μg/ml) showed significant reactive oxygen species scavenging activity and improved antioxidant enzyme levels by decreasing lipid peroxidation and nitric oxide levels. Histopathological examination revealed a delay in the progression of copper sulfate-induced hepatic damage, and upregulated the expression of antioxidants, while the hepatic and mitochondrial damage markers were downregulated.

CONCLUSION

In conclusion, bovine serum albumin-reduced selenium nanoparticles can be a promising therapeutic antioxidant for protecting against reactive oxygen species-induced hepatic damage and neurodegeneration.

摘要

引言

肝纤维化是细胞外基质的异常积聚以及对慢性肝损伤的反应中最终形成纤维瘢痕,这可能由活性氧水平升高引发。脑-肝轴是一条关键的通讯途径,对肝功能和脑健康之间的复杂相互作用有重大影响。硒作为硒蛋白的来源,在抗氧化防御系统中发挥着至关重要的作用。从贻贝中提取硒利用了它们的天然生物积累特性,提供了一种生物相容性来源。硒纳米颗粒以其潜在的抗氧化活性而闻名,可用于调节活性氧水平以克服肝损伤。

方法

从贻贝提取的硒合成硒纳米颗粒,并用牛血清白蛋白进行稳定化处理。用硒纳米颗粒(5-25微克/毫升)处理暴露于硫酸铜的斑马鱼模型。本研究评估了它们在斑马鱼模型中作为抗氧化剂对抗硫酸铜诱导的肝损伤的潜在作用。

结果

经30分钟和1小时还原的牛血清白蛋白稳定化硒纳米颗粒呈球形,尺寸分别为19纳米和16纳米。经30分钟还原的稳定化硒纳米颗粒(25微克/毫升)表现出显著的活性氧清除活性,并通过降低脂质过氧化和一氧化氮水平提高了抗氧化酶水平。组织病理学检查显示硫酸铜诱导的肝损伤进展延迟,抗氧化剂表达上调,而肝和线粒体损伤标志物下调。

结论

总之,牛血清白蛋白还原的硒纳米颗粒可能是一种有前景的治疗性抗氧化剂,用于预防活性氧诱导的肝损伤和神经退行性变。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8764/12127314/5d5723d7db26/fgene-16-1522370-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8764/12127314/3dbd1b25ee3e/fgene-16-1522370-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8764/12127314/89d049347f35/fgene-16-1522370-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8764/12127314/6715f0774fc1/fgene-16-1522370-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8764/12127314/4f2a07e2c210/fgene-16-1522370-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8764/12127314/1bd47da7ac6a/fgene-16-1522370-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8764/12127314/5d5723d7db26/fgene-16-1522370-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8764/12127314/3dbd1b25ee3e/fgene-16-1522370-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8764/12127314/89d049347f35/fgene-16-1522370-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8764/12127314/6715f0774fc1/fgene-16-1522370-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8764/12127314/4f2a07e2c210/fgene-16-1522370-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8764/12127314/1bd47da7ac6a/fgene-16-1522370-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8764/12127314/5d5723d7db26/fgene-16-1522370-g006.jpg

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