摘要
目的探讨细菌脂多糖（LPS）、高体积分数氧（高氧）单独或联合应用对新生大鼠脑发育的影响及其相关机制。方法2日龄（P2）新生sD大鼠120只随机分为4组：空气组、LPS组、高氧组、LPS＋高氧组，分别观察各组大鼠的一般情况，记录其每日体质量。7日龄（P7）时，免疫组织化学法检测各组大鼠脑组织中半胱氨酸天冬氨酸蛋白酶3（Caspase-3）、核转录因子P65（NF—KBP65）的表达情况，ELISA法检测各组大鼠脑组织中IL-6、8-异．前列腺素F2a（8-iso．PGF20L）水平；12日龄（P12）时，免疫组织化学法检测各组大鼠脑组织碱性髓鞘蛋白（MBP）的表达。结果不同处理组中Caspase一3及NF—KBP65表达水平高低依次为LPS＋高氧组、LPS组／高氧组、空气组，前3组与空气组相比差异均有统计学意义（P均〈0．05），且LPS＋高氧组与高氧组、LPS组相比差异亦均有统计学意义（P均〈0．01）；MBP的表达水平高低依次为空气组、高氧组、LPS组、LPS＋高氧组，后3组与空气组相比差异均有统计学意义（P均〈0，05），且LPS＋高氧组与高氧组、LPS组相比差异亦均有统计学意义（P均〈0．01）。各组新生大鼠IL．6表达水平高低依次为LPS＋高氧组、LPS组、高氧组、空气组；8-iso-PGF20L表达水平高低依次为LPS＋高氧组、高氧组、LPS组、空气组，而且各组之间比较差异均有统计学意义（P均〈0．05）。结论感染及高氧均可致新生大鼠脑损伤，导致神经细胞凋亡和MBP表达减少，且感染与高氧同时存在时能加重二者单独作用时脑损伤的程度。其机制可能为炎性反应及氧化应激通过Toll样受体后发生协同作用，激活核转录因子NF-κB P65，并通过Caspase-3介导神经细胞凋亡及脑白质损伤。
Objective To investigate the effects of lipopolysaccharide （LPS） and / or normobaric hyperoxia on brain development of neonatal rat and the possible mechanisms. Methods One hundred and twenty postnatal day 2 （P2） SD rats were randomly assigned into 4 groups ： air group, LPS group, hyperoxia group, LPS ＋ hyperoxia group. General condition and body weight of the rats in each group were observed and recorded every day. The expression of active Caspase-3 and nuclear faetor-KappaB P65 （ NF-KB P65 ） in the brain were detected by immunohistochemistry staining on P7, and the level of IL-6 and 8-iso-PGF2ot in the brain homogenate were measured by enzyme-linked immunosorbent assay（ELISA）. The expression of myelin basic protein （MBP） in the brain was detected by immunohistochemistry staining on P12. Results The expressions of Caspase-3 and NF-KB P65 had the same trends：the number of positive cells from high to low was in LPS ＋ hyperoxia group, LPS group/hyperoxia group, air group. There were significant differences between the first three groups and air group（ all P 〈 0.05 ）. There were also significant differences between LPS ＋ hyperoxia group and LPS group or hyperoxia group（ all P 〈 0. 01 ）. MBP in the brain had the completely reverse expression ： from high to low order was in air group, hyperoxia group, LPS group, LPS ＋ hyperoxia group. There were significant differences between the last three groups and air group （ all P 〈 0.05 ）. There were also significant differences between LPS ＋ hyperoxia group and LPS group or hyperoxia group（ all P 〈0.01 ）. The level of IL-6 in the brain from high to low order respectively was in LPS ＋ hyperoxia group, LPS group, hyperoxia group, air group ; and 8- iso-PGF2α was also in LPS ＋ hyperoxia group, hyperoxia group, LPS group, air group, Significant differences were found among the four groups （ all P 〈 0.05 ）. Conclusions Both postnatal infection and normobarie hyperoxia may induce premature rat brain injury, and i
出处
《中华实用儿科临床杂志》
CAS
CSCD
北大核心
2013年第2期110-114,共5页
Chinese Journal of Applied Clinical Pediatrics
