Objetive:To investigate the nerve protective effect and mechanism of baicalin on newborn rats with hypoxic ischemic brain damage(HIBD).Methods:A total of 64 SD newborn rats were randomlu divided into control group.mod...Objetive:To investigate the nerve protective effect and mechanism of baicalin on newborn rats with hypoxic ischemic brain damage(HIBD).Methods:A total of 64 SD newborn rats were randomlu divided into control group.model group.nerve growth factor group and baicalin group.with 16 in each group.Left carotid artery ligation method was adopted to establish the HIBD model except fou in control group,which was treatde with intraperitoneal injection of salin e10mL/kg for 3 d.After oxygen recovery on hypoxia ischemia rats.intraperitoneal injectionof salin 10mL/kg was adopted in model group for 3 d.Intraperitoneal injection of nerve growth factor injection50μg/kg per day was adopted in nerve growth factor group for 3 d:intraperitoneal injection of radix scutellariae 16mg/kg per day was adopted in baicalin group for 3 d after modeeling.Four rats of each group were sacrificed at Day 1,2,3,7 for microscopic observation of pathological morphological changes in brain tissus aften HE staining,S-P immunohistochemical method was used for observation of Fas and FasL expression in brain cells.Results:Neat structure of cells was observed in control group;edema cells in disordered arrangement was observed in model group,with some cells necrosis and cavity change;tissue injury in nerve growth factor group and baicalin group was significantly lighter than that in model group;Fas and FasL expression in model group,nerve growth factor group and baicalin group were significantiy higher than that in control group at different time points(P<0.05):Fas and FasL expression in nerve growth factor group and baicalin group were significantly lower than that in model group at different time points(P<0.05):There was no statistical diggerence of Fas,FasL expression at each time point between nerve growth factor group and baicalin group(P>0.05).Conclusions:Baicalin can reduce expression of Fas and FasL in HIBD rats,inhibit apoptosis of nerve cells,thus achieve the protective effect on HIBD rat nerves.展开更多
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展开更多
基金supported by Yantai Science and Technology Projects(GrantNo:2004221)
文摘Objetive:To investigate the nerve protective effect and mechanism of baicalin on newborn rats with hypoxic ischemic brain damage(HIBD).Methods:A total of 64 SD newborn rats were randomlu divided into control group.model group.nerve growth factor group and baicalin group.with 16 in each group.Left carotid artery ligation method was adopted to establish the HIBD model except fou in control group,which was treatde with intraperitoneal injection of salin e10mL/kg for 3 d.After oxygen recovery on hypoxia ischemia rats.intraperitoneal injectionof salin 10mL/kg was adopted in model group for 3 d.Intraperitoneal injection of nerve growth factor injection50μg/kg per day was adopted in nerve growth factor group for 3 d:intraperitoneal injection of radix scutellariae 16mg/kg per day was adopted in baicalin group for 3 d after modeeling.Four rats of each group were sacrificed at Day 1,2,3,7 for microscopic observation of pathological morphological changes in brain tissus aften HE staining,S-P immunohistochemical method was used for observation of Fas and FasL expression in brain cells.Results:Neat structure of cells was observed in control group;edema cells in disordered arrangement was observed in model group,with some cells necrosis and cavity change;tissue injury in nerve growth factor group and baicalin group was significantly lighter than that in model group;Fas and FasL expression in model group,nerve growth factor group and baicalin group were significantiy higher than that in control group at different time points(P<0.05):Fas and FasL expression in nerve growth factor group and baicalin group were significantly lower than that in model group at different time points(P<0.05):There was no statistical diggerence of Fas,FasL expression at each time point between nerve growth factor group and baicalin group(P>0.05).Conclusions:Baicalin can reduce expression of Fas and FasL in HIBD rats,inhibit apoptosis of nerve cells,thus achieve the protective effect on HIBD rat nerves.
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
