Paintlia Manjeet K, Paintlia Ajaib S, Barbosa Ernest, Singh Inderjit, Singh Avtar K
Department of Pediatrics, Medical University of South Carolina, 96 Jonathan Lucas Street, Charleston, SC 29425, USA.
J Neurosci Res. 2004 Nov 1;78(3):347-61. doi: 10.1002/jnr.20261.
Periventricular leukomalacia (PVL), the dominant form of brain injury in premature infants, is characterized by diffuse white matter injury and is associated with cerebral palsy (CP). Maternal and placental infections are major causes of prematurity and identifiable etiology of PVL and CP. Here we have evaluated the therapeutic efficacy of N-acetylcysteine (NAC), a potent antioxidant and precursor of glutathione, to attenuate lipopolysaccharide (LPS)-induced white matter injury and hypomyelination in the developing rat brain, an animal model of PVL. Intraperitoneal pretreatment of pregnant female rats with NAC (50 mg/kg), 2 hr prior to administration of LPS at embryonic day 18 (E18), attenuated the LPS-induced expression of inflammatory cytokines such as tumor necrosis factor-alpha, interleukin-1beta, and inducible nitric oxide synthase in fetal rat brains. There were significantly reduced numbers of TUNEL(+) nuclei coimmunostained for platelet-derived growth factor-alphaR(+) [a surface marker for oligodendrocyte progenitor cells (OPCs)] at E20 in the subventricular zone of fetal rat brain in the NAC + LPS group compared with the untreated LPS group. Interestingly, immunostaining for O4 and O1 as markers for late OPCs and immature oligodendrocytes demonstrated fewer O4(+) and O1(+) cells in the LPS group compared with the NAC + LPS and control groups. Consistent with O4(+)/O1(+) cell counts, the expression of myelin proteins such as myelin basic protein, proteolipid protein, and 2'3'-cyclic nucleotide phosphodiesterase, including transcription factors such as MyT1 and Gtx, was less in the LPS group at late postnatal days, indicating severe hypomyelination in the developing rat brain when compared with NAC + LPS and control groups. Collectively, these data support the hypothesis that NAC may provide neuroprotection and attenuate the degeneration of OPCs against LPS evoked inflammatory response and white matter injury in developing rat brain. Moreover, these data suggest the possible use of NAC as a treatment for pregnant women with maternal or placental infection as a means of minimizing the risk of PVL and CP.
脑室周围白质软化(PVL)是早产儿脑损伤的主要形式,其特征为弥漫性白质损伤,并与脑瘫(CP)相关。母体和胎盘感染是早产的主要原因,也是PVL和CP可明确的病因。在此,我们评估了N-乙酰半胱氨酸(NAC)的治疗效果,NAC是一种强效抗氧化剂和谷胱甘肽的前体,用于减轻脂多糖(LPS)诱导的发育中大鼠脑白质损伤和髓鞘形成不足,这是PVL的一种动物模型。在胚胎第18天(E18)给予LPS前2小时,对怀孕雌性大鼠进行腹腔内NAC(50mg/kg)预处理,可减轻LPS诱导的胎鼠脑中炎性细胞因子如肿瘤坏死因子-α、白细胞介素-1β和诱导型一氧化氮合酶的表达。与未处理的LPS组相比,NAC + LPS组在E20时胎鼠脑室下区血小板衍生生长因子-αR(+)[少突胶质细胞祖细胞(OPCs)的表面标志物]共免疫染色的TUNEL(+)细胞核数量显著减少。有趣的是,与NAC + LPS组和对照组相比,LPS组中作为晚期OPCs和未成熟少突胶质细胞标志物的O4和O1免疫染色显示O4(+)和O1(+)细胞较少。与O4(+)/O1(+)细胞计数一致,在出生后晚期,LPS组中髓鞘蛋白如髓鞘碱性蛋白、蛋白脂蛋白和2'3'-环核苷酸磷酸二酯酶的表达减少,包括转录因子如MyT1和Gtx,这表明与NAC + LPS组和对照组相比,发育中大鼠脑存在严重的髓鞘形成不足。总体而言,这些数据支持以下假设:NAC可能提供神经保护作用,并减轻发育中大鼠脑内OPCs的变性,以对抗LPS诱发的炎症反应和白质损伤。此外,这些数据表明NAC可能作为一种治疗方法用于患有母体或胎盘感染的孕妇,以降低PVL和CP的风险。