Han Ying, Yi Wenxia, Qin Jiong, Zhao Yang, Zhang Jing, Chang Xingzhi
Department of Pediatrics, Peking University First Hospital, Beijing 100034, China.
Department of Pediatrics, Peking University First Hospital, Beijing 100034, China.
Neurosci Lett. 2014 Mar 20;563:149-54. doi: 10.1016/j.neulet.2013.12.042. Epub 2013 Dec 25.
Sulfur dioxide (SO2) regulates many physiological processes. Little is known about its roles in neurological disorders. In this study, we investigated the role of endogenous SO2 in the development of febrile seizures (FS) and related brain damages. In the rat model of recurrent FS, we found that endogenous SO2 in the plasma and hippocampus was increased, accompanied by upregulation of aspartate amino-transferase 1 (AAT1) and AAT2, and neuronal apoptosis and mossy fiber sprouting (MFS) in the hippocampus. Preconditioning with low concentration of SO2 (1-10 μmol/kg) alleviated the neuronal damage, and attenuated neuronal apoptosis and MFS, whereas preconditioning with high concentration of SO2 (100 μmol/kg) or inhibition of AAT aggravated the neuronal damage, and promoted neuronal apoptosis and MFS in hippocampus of rats with recurrent FS. These data indicate that endogenous SO2 is involved in the development of FS and related brain damage. Preconditioning with low concentration of SO2 may protect neurons from toxicity caused by FS.
二氧化硫（SO₂）调节多种生理过程。其在神经系统疾病中的作用鲜为人知。在本研究中，我们探究了内源性SO₂在热性惊厥（FS）发生发展及相关脑损伤中的作用。在复发性FS大鼠模型中，我们发现血浆和海马中的内源性SO₂增加，同时伴有天冬氨酸氨基转移酶1（AAT1）和AAT2上调，以及海马神经元凋亡和苔藓纤维出芽（MFS）。低浓度SO₂（1 - 10 μmol/kg）预处理可减轻神经元损伤，减弱神经元凋亡和MFS，而高浓度SO₂（100 μmol/kg）预处理或抑制AAT则加重复发性FS大鼠海马神经元损伤，促进神经元凋亡和MFS。这些数据表明内源性SO₂参与FS的发生发展及相关脑损伤。低浓度SO₂预处理可能保护神经元免受FS所致毒性作用。
