Hydrogen sulfide prevents formaldehyde-induced neurotoxicity to PC12 cells by attenuation of mitochondrial dysfunction and pro-apoptotic potential
| Autor: | Heng-Rong Fang, Xiao-Qing Tang, Hong-Feng Gu, Chun-Yan Wang, Chun-Tao Yang, Rong-Qian Chen, Cheng-Fang Zhou, Yuan-Yuan Zhuang, Jian-Qin He, Yan-Kai Ren |
|---|---|
| Rok vydání: | 2011 |
| Předmět: |
Blotting
Western Sodium hydrosulfide Apoptosis Mitochondrion medicine.disease_cause Neuroprotection PC12 Cells Cellular and Molecular Neuroscience chemistry.chemical_compound Formaldehyde medicine Animals Hydrogen Sulfide chemistry.chemical_classification Neurons Reactive oxygen species biology Caspase 3 Cytochrome c Neurotoxicity Cytochromes c Cell Biology medicine.disease Flow Cytometry Cell biology Mitochondria Rats Enzyme Activation Oxidative Stress chemistry biology.protein Reactive Oxygen Species Oxidative stress |
| Zdroj: | Neurochemistry international. 61(1) |
| ISSN: | 1872-9754 |
| Popis: | Hydrogen sulfide (H(2)S) has been shown to act as a neuroprotectant and antioxidant. Numerous studies have demonstrated that exposure to formaldehyde (FA) causes neuronal damage and that oxidative stress is one of the most critical effects of FA exposure. Accumulation of FA is involved in the pathogenesis of Alzheimer's disease (AD). The aim of present study is to explore the inhibitory effects of H(2)S on FA-induced cytotoxicity and apoptosis and the molecular mechanisms underlying in PC12 cells. We show that sodium hydrosulfide (NaHS), a H(2)S donor, protects PC12 cells against FA-mediated cytotoxicity and apoptosis and that NaHS preserves the function of mitochondria by preventing FA-induced loss of mitochondrial membrane potential and release of cytochrome c in PC12 cells. Furthermore, NaHS blocks FA-exerted accumulation of intracellular reactive oxygen species (ROS), down-regulation of Bcl-2 expression, and up-regulation of Bax expression. These results indicate that H(2)S protects neuronal cells against neurotoxicity of FA by preserving mitochondrial function through attenuation of ROS accumulation, up-regulation of Bcl-2 level, and down-regulation of Bax expression. Our study suggests a promising future of H(2)S-based preventions and therapies for neuronal damage after FA exposure. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full Text from ScienceDirect