Background To confirm the proliferation of vascular smooth muscle cell （VSMC） lead by advanced glycation end products （AGEs） and investigate weather the mechanism is work through MAPK pathway. To investigate weath...Background To confirm the proliferation of vascular smooth muscle cell （VSMC） lead by advanced glycation end products （AGEs） and investigate weather the mechanism is work through MAPK pathway. To investigate weather the prolification of VSMC lead by AGEs can be inhibited by reduced glutathione（GSH） and what the mechanisam is. Methods VSMC of rats were isolated and cultivated, separated in 8 groups, each group contained 12 samples. Density of cell was 1×105 /mL in each sample, cultivated with AGEs at different concentrations and intervened with GSH at different concentrations. In order to determine the mechanism and interventional factors of VSMCs, sandwich ELISA method was used to test the concentration of P-P38 and MTT colorimetry was adopted to evaluate the amount of VSMC. Results 1.Effect of AGEs to the OD value of MTT in VSMC： with stimulation of AGEs, OD valued of P-P38 in VSMC increased simultaneously （P0.01）, their value were 0.43±0.15, 0.49±0.16, 0.48±0.19 [L/（g·cm）]. With the increase of the dose of AGEs, there were no difference between groups B, C of MTT OD value（P0.05）. 2.Effect of GSH to the OD value of MTT in VSMC stimulated by AGEs： OD value of MTT decreased with the increase of GSH concentration, their value were 0.347±0.102, 0.333±0.108, 0.285±0.080 [L/（g·cm）] respectively, decreased by 45%, 56%, 60%（P0.01）compared with value of AGEs control group. With the increasing of the dose of GSH, the MTT OD value had no difference between groups F, G and H （P0.05）. 3.Effect of AGEs to the OD value of P-P38 in VSMC： with stimulation of AGEs, OD valued of P-P38 in VSMC increased obviously （P0.01）, their value were 0.65±0.17, 0.85±0.26, 0.94±0.17 [L/（g·cm）]. With the increasing of the dose of AGEs, the P-P38 OD value increase simultaneously（P0.05）. 4.Effect of GSH on the OD value of P-P38 in VSMC stimulated by AGEs： OD value of P-P38 decreased with the increasing of GSH concentration, their value were 0.356±0.090, 0.281±0.070, 0.256±0.072 [L/（g·cm）] respectively, decreased by 45%, 56%, 60%（P0.01）compared with the value of control group. With the increasing of the dose of GSH, the P-P38 OD value between groups F, G and H were decreased gradually （P0.01）. Conclusions 1.AGEs has the function of inducing the proliferation of vascular SMC, the activation of the P-P38 MAPK signal pathway may be the mechanism of the proliferation of VSMC. 2.GSH can inhibit the proliferation of VSMC lead by AGEs, The P-P38-MAPK pathway is being blocked by GSH, which is the mechanism of inhibiting the proliferation of VSMC lead by AGEs.展开更多
目的探讨七氟醚后处理对犬体外循环肺缺血/再灌注损伤的效果及晚期糖基化终末产物受体(receptor for ad-vanced glycosylation end products,RAGE)在此过程中的作用。方法 12只健康犬依据主动脉开放后是否吸入七氟醚随机分为两组:对照组...目的探讨七氟醚后处理对犬体外循环肺缺血/再灌注损伤的效果及晚期糖基化终末产物受体(receptor for ad-vanced glycosylation end products,RAGE)在此过程中的作用。方法 12只健康犬依据主动脉开放后是否吸入七氟醚随机分为两组:对照组(control,n=6)在主动脉开放后常规机械通气和实验组(test,n=6)在主动脉开放后吸入1MAC七氟醚,持续10min。在开胸后即刻(T1)、主动脉开放90min实验结束前(T2)留取肺组织标本和肺静脉血标本。标检测肺组织湿干重比(wet/dry weight,W/D);比色法检测肺组织髓过氧化物酶活性(myeloperoxidase activity,MPO);光镜观察并盲法评分比较肺组织病理学变化;分别采取RT-PCR方法、Western blot检测肺组织RAGE的表达;酶联免疫吸附法检测血清白介素6(IL-6)和肿瘤坏死因子α(TNF-α)含量。结果两组相比,实验组肺组织W/D、MPO、肺损伤评分、RAGE基因表达和蛋白表达、IL-6和TNF-α含量在T2时较对照组降低(P<0.05);组内比较,所有指标实验结束时均较基础值明显升高(P<0.05)。结论七氟醚后处理对体外循环缺血/再灌注导致的肺损伤具有一定的保护作用,可能与其抑制RAGE合成与激活有关。展开更多
目的观察大豆异黄酮(soybean isoflavones)对阿尔茨海默病(Alzheimer's disease,AD)大鼠高级糖化终产物受体(receptor for advanced glycation end products,RAGE)介导的信号转导系统的影响。方法采用β淀粉样蛋白25-35片段(amyloid...目的观察大豆异黄酮(soybean isoflavones)对阿尔茨海默病(Alzheimer's disease,AD)大鼠高级糖化终产物受体(receptor for advanced glycation end products,RAGE)介导的信号转导系统的影响。方法采用β淀粉样蛋白25-35片段(amyloidβ25-35,Aβ25-35)双侧海马注射建立AD大鼠模型,60只大鼠随机分为模型组、大豆异黄酮高剂量组[30mg/(kg·d)]、大豆异黄酮低剂量组[10mg/(kg·d)]、雌激素组[0.4mg/(kg·d)]及假手术组,每组12只。大豆异黄酮高、低剂量组和雌激素组造模后3天灌胃给药(2mL/只),模型组与假手术组给予等体积的0.5%羧甲基纤维素钠(CMC-Na)灌胃,连续21天。酶联免疫吸附法观察各组大鼠海马组织RAGE、白细胞介素-6(interleukin-6,IL-6)的含量。分光光度法检测大鼠海马组织天冬氨酸特异性半胱氨酸蛋白酶-3(cysteine-containing aspartate-specific protease-3,Caspase-3)活性。免疫组织化学法观察大鼠海马组织磷酸化细胞外信号调节激酶1/2(phosphorylation extracellular signal-regulatedkinase1/2,P-ERK1/2)的表达。结果与模型组比较,大豆异黄酮可显著降低AD大鼠海马RAGE蛋白、IL-6含量、Caspase-3活性及ERK1/2蛋白磷酸化水平(P<0.01)。结论大豆异黄酮对AD大鼠海马组织RAGE介导的炎症信号通路具有下调作用,减弱炎症反应,降低Aβ的神经毒性,抵抗海马神经元凋亡。展开更多
文摘Background To confirm the proliferation of vascular smooth muscle cell （VSMC） lead by advanced glycation end products （AGEs） and investigate weather the mechanism is work through MAPK pathway. To investigate weather the prolification of VSMC lead by AGEs can be inhibited by reduced glutathione（GSH） and what the mechanisam is. Methods VSMC of rats were isolated and cultivated, separated in 8 groups, each group contained 12 samples. Density of cell was 1×105 /mL in each sample, cultivated with AGEs at different concentrations and intervened with GSH at different concentrations. In order to determine the mechanism and interventional factors of VSMCs, sandwich ELISA method was used to test the concentration of P-P38 and MTT colorimetry was adopted to evaluate the amount of VSMC. Results 1.Effect of AGEs to the OD value of MTT in VSMC： with stimulation of AGEs, OD valued of P-P38 in VSMC increased simultaneously （P0.01）, their value were 0.43±0.15, 0.49±0.16, 0.48±0.19 [L/（g·cm）]. With the increase of the dose of AGEs, there were no difference between groups B, C of MTT OD value（P0.05）. 2.Effect of GSH to the OD value of MTT in VSMC stimulated by AGEs： OD value of MTT decreased with the increase of GSH concentration, their value were 0.347±0.102, 0.333±0.108, 0.285±0.080 [L/（g·cm）] respectively, decreased by 45%, 56%, 60%（P0.01）compared with value of AGEs control group. With the increasing of the dose of GSH, the MTT OD value had no difference between groups F, G and H （P0.05）. 3.Effect of AGEs to the OD value of P-P38 in VSMC： with stimulation of AGEs, OD valued of P-P38 in VSMC increased obviously （P0.01）, their value were 0.65±0.17, 0.85±0.26, 0.94±0.17 [L/（g·cm）]. With the increasing of the dose of AGEs, the P-P38 OD value increase simultaneously（P0.05）. 4.Effect of GSH on the OD value of P-P38 in VSMC stimulated by AGEs： OD value of P-P38 decreased with the increasing of GSH concentration, their value were 0.356±0.090, 0.281±0.070, 0.256±0.072 [L/（g·cm）] respectively, decreased by 45%, 56%, 60%（P0.01）compared with the value of control group. With the increasing of the dose of GSH, the P-P38 OD value between groups F, G and H were decreased gradually （P0.01）. Conclusions 1.AGEs has the function of inducing the proliferation of vascular SMC, the activation of the P-P38 MAPK signal pathway may be the mechanism of the proliferation of VSMC. 2.GSH can inhibit the proliferation of VSMC lead by AGEs, The P-P38-MAPK pathway is being blocked by GSH, which is the mechanism of inhibiting the proliferation of VSMC lead by AGEs.
文摘目的探讨七氟醚后处理对犬体外循环肺缺血/再灌注损伤的效果及晚期糖基化终末产物受体(receptor for ad-vanced glycosylation end products,RAGE)在此过程中的作用。方法 12只健康犬依据主动脉开放后是否吸入七氟醚随机分为两组:对照组(control,n=6)在主动脉开放后常规机械通气和实验组(test,n=6)在主动脉开放后吸入1MAC七氟醚,持续10min。在开胸后即刻(T1)、主动脉开放90min实验结束前(T2)留取肺组织标本和肺静脉血标本。标检测肺组织湿干重比(wet/dry weight,W/D);比色法检测肺组织髓过氧化物酶活性(myeloperoxidase activity,MPO);光镜观察并盲法评分比较肺组织病理学变化;分别采取RT-PCR方法、Western blot检测肺组织RAGE的表达;酶联免疫吸附法检测血清白介素6(IL-6)和肿瘤坏死因子α(TNF-α)含量。结果两组相比,实验组肺组织W/D、MPO、肺损伤评分、RAGE基因表达和蛋白表达、IL-6和TNF-α含量在T2时较对照组降低(P<0.05);组内比较,所有指标实验结束时均较基础值明显升高(P<0.05)。结论七氟醚后处理对体外循环缺血/再灌注导致的肺损伤具有一定的保护作用,可能与其抑制RAGE合成与激活有关。
