目的观察3种神经细胞保护措施对缺氧缺血性脑损伤新生大鼠脑组织凋亡相关因子及其配体(Fas和FasL)基因表达的影响。方法选择120只7日龄Wistar大鼠,按随机数字表法将大鼠分为神经干细胞组、促红细胞生成素(EPO)组、ω-3不饱和脂肪酸组、...目的观察3种神经细胞保护措施对缺氧缺血性脑损伤新生大鼠脑组织凋亡相关因子及其配体(Fas和FasL)基因表达的影响。方法选择120只7日龄Wistar大鼠,按随机数字表法将大鼠分为神经干细胞组、促红细胞生成素(EPO)组、ω-3不饱和脂肪酸组、缺氧缺血性脑损伤模型组,每组30只。神经干细胞组、EPO组、ω-3不饱和脂肪酸组于制模后经尾静脉注射5 mL神经干细胞、EPO、ω-3不饱和脂肪酸.缺氧缺血性脑损伤模型组给予等量生理盐水给药后6.12、24、48、72 h 5个时间点各组处死6只大鼠取海马组织.测定大脑海马组织Fas/FasL的基因表达,以及Toll样受体4(TLR4)、核转录因子-κB(NF-κB)、肿瘤坏死因子-α(TNF-α)、白细胞介素(IL-1β、IL-6)的蛋白表达水平和细胞凋亡率。结果①mRNA表达:3个实验组给药后Fas和FasL的mRNA表达均较缺氧缺血性脑损伤模型组显著降低,以给药后24h降低最为显著,且神经干细胞组VEPO组<ω-3不饱和脂肪酸组<缺氧缺血性脑损伤模型组〔FasmRNA表达(2^-△△Ct):140.5±2.9、156.4±2.5.165.2±2.7比173.7±2.8,FasL mRNA表达(2^-△△Ct):143.1±4.3、154.6±1.5,160.7±1.4比174.7±2.8],各组间比较差异均有统计学意义(均P<0.05)。②蛋白表达:3个实验组给药后海马组织TLR4、NF-κB、TNF-α、IL-1β、IL-6的蛋白表达水平均较缺氧缺血性脑损伤模型组显著降低(TLR4/GAPDH:0.7±0.2,0.6±0.1、0.2±0.1比1.4±0.1;NF-κB/GAPDH:6.7±0.4,5.3±0.1、1.1±0.2比11.2±0.3;TNF-α/GAPDH:14.3±1.4、11.2±1.2、3.2±2.1比23.2±0.5;IL-1β/GAPDH:9.4±0.2,7.4±0.3,2.2±0.3比13.4±0.1;IL-6/GAPDH:36.2±4.4.39.3±1.5、26.2±2.1比51.4±1.4,均P<0.05).神经干细胞组上述指标的蛋白表达水平VEPO组<ω-3不饱和脂肪酸组<缺氧缺血性脑损伤模型组:③细胞凋亡率:ω-3不饱和脂肪酸组、EPO组、神经干细胞组给药后海马组织细胞凋亡率均明显低于缺氧缺血性脑损伤模型组〔(3.7±0.3)%、(3.4±0.2)%、(2.5±0.1)%比(5.5±0.4)%,均P<0.05〕。结论缺氧缺血性脑损伤新生大鼠脑组织Fas和FasLmRNA呈高表达;而给予神经干细胞、EPO及ω-3不饱和脂肪酸处理均能减少脑组织Fas和FasL的mRNA表达.展开更多
Objective： Recent evidence indicates that the increased expression of FOXG1 is associated with tumor genesis. This study was designed to explore the expression and role which FOXG1 plays in human glioma. Methods： We...Objective： Recent evidence indicates that the increased expression of FOXG1 is associated with tumor genesis. This study was designed to explore the expression and role which FOXG1 plays in human glioma. Methods： We detected the expression of FOXG1 by immunohistochemistry in glioma tissue samples. Following the down-regulation of FOXG1 in glioma cell lines by a specific short hairpin RNA, the function of FOXG1 in proliferation and apoptosis was assessed. Results： Glioma tissues exhibited notably higher expression of FOXG1 compared with control brain tissues and was positively corre- lated with histological malignancy. The down-regulation of FOXG1 in glioma cells led to a cell apoptosis in vitro. Cenclusion： The overexpression of FOXG1 is a novel glioma malignancy marker, and FOXG1 may be used as a new target in therapeutic strategies for human glioma.展开更多
Objective To observe the influence of hypotherrnic circulatory arrest （HCA） on the apoptotic processes of neurons in the hippocampus and the expression of the related genes Bcl-2 and Bax, and compare to the intermit...Objective To observe the influence of hypotherrnic circulatory arrest （HCA） on the apoptotic processes of neurons in the hippocampus and the expression of the related genes Bcl-2 and Bax, and compare to the intermittent antegrade cerebral perfusion. Methods Eighteen dogs were randomly divided into three groups： control group （6 animals, underwent normal temperature cardiopulmonary bypass, NCPB）, HCA group （6 animals, underwent HCA for 1 h）, and HCA ＋ IACP group （6 animals, underwent HCA for 1 h, combined with intermittent antegrade cerebral perfusion （IACP） every 15 min）. The hippocampus tissue was retrieved 2h after the CPB discontinued The expression of Bcl-2 and Bax were examined with immunohistochemistry method. The cytomorphologic changes of the hippocampus tissue were investigated with transmission electron microscopy （TEM）. Results The immunohistochemical staining showed that Bax protein levels were significantly higher in HCA group than in the other two groups （P〈0.01）, while Bcl-2 protein levels were significantly higher in HCA ＋ IACP group than that of the other two groups （P〈0.01）. Meanwhile, the TEM results showed that there was no apoptosis of neurons in control group, but neuronal apoptotic changes could be clearly observed in HCA group, and only a small amount of apoptotic neurons were seen in HCA ＋ IACP group. Conclusions HCA alone can induce neuronal apoptosis in the hippocampus. IACP during the HCA period has a protective effect on the cerebral tissue through suppressing apoptosis by decreasing Bax expression and increasing Bcl-2 expression.展开更多
文摘目的观察3种神经细胞保护措施对缺氧缺血性脑损伤新生大鼠脑组织凋亡相关因子及其配体(Fas和FasL)基因表达的影响。方法选择120只7日龄Wistar大鼠,按随机数字表法将大鼠分为神经干细胞组、促红细胞生成素(EPO)组、ω-3不饱和脂肪酸组、缺氧缺血性脑损伤模型组,每组30只。神经干细胞组、EPO组、ω-3不饱和脂肪酸组于制模后经尾静脉注射5 mL神经干细胞、EPO、ω-3不饱和脂肪酸.缺氧缺血性脑损伤模型组给予等量生理盐水给药后6.12、24、48、72 h 5个时间点各组处死6只大鼠取海马组织.测定大脑海马组织Fas/FasL的基因表达,以及Toll样受体4(TLR4)、核转录因子-κB(NF-κB)、肿瘤坏死因子-α(TNF-α)、白细胞介素(IL-1β、IL-6)的蛋白表达水平和细胞凋亡率。结果①mRNA表达:3个实验组给药后Fas和FasL的mRNA表达均较缺氧缺血性脑损伤模型组显著降低,以给药后24h降低最为显著,且神经干细胞组VEPO组<ω-3不饱和脂肪酸组<缺氧缺血性脑损伤模型组〔FasmRNA表达(2^-△△Ct):140.5±2.9、156.4±2.5.165.2±2.7比173.7±2.8,FasL mRNA表达(2^-△△Ct):143.1±4.3、154.6±1.5,160.7±1.4比174.7±2.8],各组间比较差异均有统计学意义(均P<0.05)。②蛋白表达:3个实验组给药后海马组织TLR4、NF-κB、TNF-α、IL-1β、IL-6的蛋白表达水平均较缺氧缺血性脑损伤模型组显著降低(TLR4/GAPDH:0.7±0.2,0.6±0.1、0.2±0.1比1.4±0.1;NF-κB/GAPDH:6.7±0.4,5.3±0.1、1.1±0.2比11.2±0.3;TNF-α/GAPDH:14.3±1.4、11.2±1.2、3.2±2.1比23.2±0.5;IL-1β/GAPDH:9.4±0.2,7.4±0.3,2.2±0.3比13.4±0.1;IL-6/GAPDH:36.2±4.4.39.3±1.5、26.2±2.1比51.4±1.4,均P<0.05).神经干细胞组上述指标的蛋白表达水平VEPO组<ω-3不饱和脂肪酸组<缺氧缺血性脑损伤模型组:③细胞凋亡率:ω-3不饱和脂肪酸组、EPO组、神经干细胞组给药后海马组织细胞凋亡率均明显低于缺氧缺血性脑损伤模型组〔(3.7±0.3)%、(3.4±0.2)%、(2.5±0.1)%比(5.5±0.4)%,均P<0.05〕。结论缺氧缺血性脑损伤新生大鼠脑组织Fas和FasLmRNA呈高表达;而给予神经干细胞、EPO及ω-3不饱和脂肪酸处理均能减少脑组织Fas和FasL的mRNA表达.
文摘Objective： Recent evidence indicates that the increased expression of FOXG1 is associated with tumor genesis. This study was designed to explore the expression and role which FOXG1 plays in human glioma. Methods： We detected the expression of FOXG1 by immunohistochemistry in glioma tissue samples. Following the down-regulation of FOXG1 in glioma cell lines by a specific short hairpin RNA, the function of FOXG1 in proliferation and apoptosis was assessed. Results： Glioma tissues exhibited notably higher expression of FOXG1 compared with control brain tissues and was positively corre- lated with histological malignancy. The down-regulation of FOXG1 in glioma cells led to a cell apoptosis in vitro. Cenclusion： The overexpression of FOXG1 is a novel glioma malignancy marker, and FOXG1 may be used as a new target in therapeutic strategies for human glioma.
文摘Objective To observe the influence of hypotherrnic circulatory arrest （HCA） on the apoptotic processes of neurons in the hippocampus and the expression of the related genes Bcl-2 and Bax, and compare to the intermittent antegrade cerebral perfusion. Methods Eighteen dogs were randomly divided into three groups： control group （6 animals, underwent normal temperature cardiopulmonary bypass, NCPB）, HCA group （6 animals, underwent HCA for 1 h）, and HCA ＋ IACP group （6 animals, underwent HCA for 1 h, combined with intermittent antegrade cerebral perfusion （IACP） every 15 min）. The hippocampus tissue was retrieved 2h after the CPB discontinued The expression of Bcl-2 and Bax were examined with immunohistochemistry method. The cytomorphologic changes of the hippocampus tissue were investigated with transmission electron microscopy （TEM）. Results The immunohistochemical staining showed that Bax protein levels were significantly higher in HCA group than in the other two groups （P〈0.01）, while Bcl-2 protein levels were significantly higher in HCA ＋ IACP group than that of the other two groups （P〈0.01）. Meanwhile, the TEM results showed that there was no apoptosis of neurons in control group, but neuronal apoptotic changes could be clearly observed in HCA group, and only a small amount of apoptotic neurons were seen in HCA ＋ IACP group. Conclusions HCA alone can induce neuronal apoptosis in the hippocampus. IACP during the HCA period has a protective effect on the cerebral tissue through suppressing apoptosis by decreasing Bax expression and increasing Bcl-2 expression.
