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作 者:王广雷[1] 黄国伟[1] 张绪梅[1] 丛革新[1] 姬长珍[1] 田志红[1]
出 处:《中国公共卫生》2008年第4期462-464,共3页Chinese Journal of Public Health
基 金:国家自然科学基金项目(30571563)
摘 要:目的研究叶酸对胎鼠大噙神经干细胞(NSCs)增殖的影响及其作用机制。方法采用孕14~16dSD胎鼠,进行NSCs原代培养。将NSCs分为4组:对照组、叶酸缺乏组、叶酸低剂量组、叶酸高剂量组。收集培养6d的细胞,采用5-溴脱氧尿苷(BrdU)掺入法和免疫组化双标记检测NSCs的增殖情况,采用蛋白印迹法(Westernblot)检测胎鼠增殖期NSCs活化的细咆外信号调节激酶1/2(pERKl/2)的表达含量。结果叶酸低剂量组、高剂量组BrdU+巢蛋白(Nestin)阳性细胞占总细胞(70.5±2.7),(78.8±6.9)%与对照组(64.2±8.9)%比较,差异均有统计学意义,且高剂量组明显高于低剂量组(P〈0.05);叶酸低剂量组、高剂量组pERKl蛋白的表达(0.407±0.018),(0.443±0.019)与对照组(0.388±0.011)比较,差异均有统计学意义(P〈0.05)。叶酸低剂量组、高剂量组pERK2蛋白的表达(0.547±0.044),(0.563±0.041)与对照组(0.507±0.018)比较,差异均有统计学意义(P〈0.05)。结论叶酸能够促进胎鼠NSCs的增值。其作用机制可能是通过丝裂原活化蛋白激酶信号通路调节NsCs的增殖。Objective To study the effect of folate on neural stem cells(NSCs) proliferation via MARK signal pathway in fetal rats in vitro. Methods NSCs of fetal Sprague - Dawley rat from E14d to E16d were cultured, divided into four groups which were control group, folate - deficiency group, folate - low group and folate - high group. NSCs were collected af- ter being cultrured 6 d. The proliferation of NSCs was detected by BrdU in corporating method and immunohistochemistry method. The level of pERK1/2 expression were detected by western blot method. Results The percentage of Nestin and BrdU positive cells in total cells(x ± s ) in folate - low group(70.5 ± 2.7) and folate - high group (78.8 ± 6.9) was significantly higher than that in control group [ (64.2 ± 8.9), P 〈 0. 053 . The levels of pERK1 (x ± s ) in folatelow group(0. 407 ± 0.018) and folate- high group (0.443 ± 0.019) were higher than those in control group((0.388 ± 0.011), P〈0.05), and the levels of pERK2 in folate- low group (0. 547 ± 0. 044) and folate - high group (0. 563 ± 0. 041 ) were higher than those in control group (( 0. 507 ± 0. 018 ), P 〈 0.05 ). Conclusion Folate could promote proliferation of fetal NSCs via MAPK signal pathway.
关 键 词:叶酸 神经干细胞 增殖 丝裂原活化蛋白激酶(MAPK)信号通路
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