Huang Wei, Huang Yong, Huang Ren-Qiang, Huang Cheng-Guang, Wang Wen-Hao, Gu Jin-Mao, Dong Yan
Department of Neurosurgery, The 175th Hospital of PLA, Affiliated Southeast Hospital of Xiamen University, Center of Traumatic Neurosurgery in Nanjing Military Command, 269 Middle Zhanghua Road, Zhangzhou 363000, China; Department of Neurosurgery, Changzheng Hospital, Second Affiliated Hospital of Second Military Medical University, 415 Feng Yang Road, Shanghai 200003, China.
Department of Neurosurgery, Changzheng Hospital, Second Affiliated Hospital of Second Military Medical University, 415 Feng Yang Road, Shanghai 200003, China.
Biomed Res Int. 2016;2016:8263926. doi: 10.1155/2016/8263926. Epub 2016 Dec 8.
Sirtuin3 (SIRT3) is an important protein deacetylase which predominantly presents in mitochondria and exhibits broad bioactivities including regulating energy metabolism and counteracting inflammatory effect. Since inflammatory cascade was proved to be critical for pathological damage following subarachnoid hemorrhage (SAH), we investigated the overall expression and cell-specific distribution of SIRT3 in the cerebral cortex of Sprague-Dawley rats with experimental SAH induced by internal carotid perforation. Results suggested that SIRT3 was expressed abundantly in neurons and endothelia but rarely in gliocytes in normal cerebral cortex. After experimental SAH, mRNA and protein expressions of SIRT3 decreased significantly as early as 8 hours and dropped to the minimum value at 24 h after SAH. By contrast, SOD2 expression increased slowly as early as 12 hours after experimental SAH, rose up sharply at the following 12 hours, and then was maintained at a higher level. In conclusion, attenuated SIRT3 expression in cortical neurons was associated closely with enhanced reactive oxygen species generation and cellular apoptosis, implying that SIRT3 might play an important neuroprotective role during early brain injury following SAH.
沉默调节蛋白3（SIRT3）是一种重要的蛋白质脱乙酰酶，主要存在于线粒体中，并具有广泛的生物活性，包括调节能量代谢和对抗炎症作用。由于炎症级联反应被证明在蛛网膜下腔出血（SAH）后的病理损伤中起关键作用，我们研究了通过颈内动脉穿刺诱导实验性SAH的Sprague-Dawley大鼠大脑皮质中SIRT3的整体表达和细胞特异性分布。结果表明，在正常大脑皮质中，SIRT3在神经元和内皮细胞中大量表达，而在神经胶质细胞中很少表达。实验性SAH后，SIRT3的mRNA和蛋白质表达早在8小时就显著下降，并在SAH后24小时降至最低值。相比之下，超氧化物歧化酶2（SOD2）的表达早在实验性SAH后12小时就开始缓慢增加，在接下来的12小时内急剧上升，然后维持在较高水平。总之，皮质神经元中SIRT3表达减弱与活性氧生成增加和细胞凋亡密切相关，这意味着SIRT3可能在SAH后的早期脑损伤中发挥重要的神经保护作用。
