Mitchell Charles L, Matveyenka Mikhail, Kurouski Dmitry
Interdisciplinary Program in Genetics and Genomics, Texas A&M University, College Station, Texas, USA; Department of Biochemistry and Biophysics, Texas A&M University, College Station, Texas, USA.
Department of Biochemistry and Biophysics, Texas A&M University, College Station, Texas, USA.
J Biol Chem. 2025 May;301(5):108498. doi: 10.1016/j.jbc.2025.108498. Epub 2025 Apr 9.
Mitochondrial dysfunction is an expected cause of etiology and progression in numerous human neurological pathologies, including stroke, Alzheimer's, and Parkinson's diseases. Therefore, a neuroprotective treatment is an urgent and unmet need. Transition metal dichalcogenide nanoflowers (TMD NFs) exhibit unique biological properties. However, neuroprotective properties of these nanomaterials remain poorly understood. In the current study, the biological effect of molybdenum disulfide and molybdenum diselenide TMD NFs on neurons and astrocytes was investigated. It was found that both nanomaterials lowered reactive oxygen species levels, reduced mitochondrial impairment, and increased mitochondrial biogenesis. Neuroprotective effects of both TMD NFs resulted from upregulation of the peroxisome proliferator-activated receptor gamma coactivator 1 alpha pathway, the biological system responsible for mitochondrial biogenesis. Furthermore, administration of TMD NFs to Caenorhabditis elegans extended lifespan of the nematodes. These results indicate that TMD NFs can be used as novel neuroprotective therapeutic agents against acute and chronic neurological condition linked to mitochondrial dysfunction.
线粒体功能障碍是包括中风、阿尔茨海默病和帕金森病在内的众多人类神经病理学病因和进展的预期原因。因此，神经保护治疗是一项迫切且未得到满足的需求。过渡金属二硫属化物纳米花（TMD NFs）具有独特的生物学特性。然而，这些纳米材料的神经保护特性仍知之甚少。在当前研究中，研究了二硫化钼和二硒化钼TMD NFs对神经元和星形胶质细胞的生物学效应。发现这两种纳米材料均降低了活性氧水平，减少了线粒体损伤，并增加了线粒体生物发生。两种TMD NFs的神经保护作用均源于过氧化物酶体增殖物激活受体γ共激活因子1α途径的上调，该生物学系统负责线粒体生物发生。此外，将TMD NFs施用于秀丽隐杆线虫可延长线虫的寿命。这些结果表明，TMD NFs可作为针对与线粒体功能障碍相关的急性和慢性神经疾病的新型神经保护治疗剂。
