AIM:To evaluate effects of endogenous dopamine induced by low concentration atropine eye drops on choroidal neovascularization(CNV)in high myopia mice.METHODS:The C57BL/6J mice were deprived of the right eye for 4wk,a...AIM:To evaluate effects of endogenous dopamine induced by low concentration atropine eye drops on choroidal neovascularization(CNV)in high myopia mice.METHODS:The C57BL/6J mice were deprived of the right eye for 4wk,and the high myopia was diagnosed by optometry,the diopter was less than-6.00 D,and CNV was induced by 532 nm laser.The changes of dopamine D1 receptor(DRD1),dopamine D2 receptor(DRD2),and vascular endothelial growth factor A(VEGFA)were detected by Western blot technology at 0.5,1,2h,and 7d after 0.01%,0.05%,and 0.1%atropine eye drops,respectively,the area of CNV was measured.RESULTS:Significant increases were observed on the expression of DRD2 in mouse high myopia model at 0.5,1,2h,7d with 0.05%and 0.1%atropine eye drops(P<0.05).Significant decreases were observed on the expression of DRD1 and VEGFA in mouse high myopia model at 0.5,1,2h,7d with 0.05%and 0.1%atropine eye drops(P<0.05).The area of CNV induced by laser in the drug-treated group was significantly smaller than that in the control group,and the higher the concentration,the more significant the inhibitory effect(P<0.05).CONCLUSION:The 0.01%,0.05%,0.1%atropine eye drops can decrease the level of VEGFA and inhibit high myopia CNV indirectly by up-regulating the level of DRD2 and down-regulating the level of DRD1,and the effect of 0.05%and 0.1%atropine eye drops is more significant.展开更多
目的通过建立大鼠肺缺血再灌注损伤(IRI)模型,进行低强度脉冲超声(LIPUS)预处理治疗,探讨IRI后高迁移率蛋白1(HMGB1)在肺组织的表达和LIPUS预处理的保护作用。方法雄性SD大鼠32只,体质量250~300 g,随机分为4组,每组8只。对照组(A组),开...目的通过建立大鼠肺缺血再灌注损伤(IRI)模型,进行低强度脉冲超声(LIPUS)预处理治疗,探讨IRI后高迁移率蛋白1(HMGB1)在肺组织的表达和LIPUS预处理的保护作用。方法雄性SD大鼠32只,体质量250~300 g,随机分为4组,每组8只。对照组(A组),开胸游离左肺门,未行阻断;缺血再灌注组(B组),阻断左肺门45 min后再灌注180 min;预处理组(C组)低强度超声波治疗仪超声定位辐照30 min,然后同B组处理;预处理加α7-烟碱型胆碱能受体(α7n ACh R)拮抗剂组(D组),LIPUS预处理前30 min腹腔注射α7n ACh R拮抗剂甲基牛扁亭2 mg/Kg,然后同预处理组处理。测量肺组织湿干重比值(W/D)和肺通透指数(LPI),大鼠肺组织病理学观察及评分,ELISA法测定肺组织IL1和IL6的浓度,免疫荧光和Western blot检测HMGB1蛋白表达。结果与A组比较,其他三组IR后肺组织W/D值(5.75±0.47)和LPI(2.77±0.18)明显升高(P<0.05),病理学评分(13.31±2.82)明显升高(P<0.05),肺组织IL1(69.13±9.11)和IL6(62.77±8.14)水平明显升高(P<0.05),免疫荧光检测平均IOD值(0.046±0.019)和Western blot检测显示HMGB1表达明显增加(P<0.05)。给于LIPUS预处理后,C组IR后肺组织W/D值(5.07±0.28)和LPI(1.85±0.17)比B组明显降低(P<0.05),病理学评分(8.13±1.76)比B组明显降低(P<0.05),同时肺组织IL1和IL6水平以及HMGB1表达也明显降低,给于α7n ACh R拮抗剂后该作用明显被抑制。结论 LIPUS预处理能够减轻IRI后肺损伤,其机制可能是通过激活依赖α7n ACh R的胆碱能抗炎通路,从而降低肺组织HMGB1的表达。展开更多
文摘AIM:To evaluate effects of endogenous dopamine induced by low concentration atropine eye drops on choroidal neovascularization(CNV)in high myopia mice.METHODS:The C57BL/6J mice were deprived of the right eye for 4wk,and the high myopia was diagnosed by optometry,the diopter was less than-6.00 D,and CNV was induced by 532 nm laser.The changes of dopamine D1 receptor(DRD1),dopamine D2 receptor(DRD2),and vascular endothelial growth factor A(VEGFA)were detected by Western blot technology at 0.5,1,2h,and 7d after 0.01%,0.05%,and 0.1%atropine eye drops,respectively,the area of CNV was measured.RESULTS:Significant increases were observed on the expression of DRD2 in mouse high myopia model at 0.5,1,2h,7d with 0.05%and 0.1%atropine eye drops(P<0.05).Significant decreases were observed on the expression of DRD1 and VEGFA in mouse high myopia model at 0.5,1,2h,7d with 0.05%and 0.1%atropine eye drops(P<0.05).The area of CNV induced by laser in the drug-treated group was significantly smaller than that in the control group,and the higher the concentration,the more significant the inhibitory effect(P<0.05).CONCLUSION:The 0.01%,0.05%,0.1%atropine eye drops can decrease the level of VEGFA and inhibit high myopia CNV indirectly by up-regulating the level of DRD2 and down-regulating the level of DRD1,and the effect of 0.05%and 0.1%atropine eye drops is more significant.
文摘目的通过建立大鼠肺缺血再灌注损伤(IRI)模型,进行低强度脉冲超声(LIPUS)预处理治疗,探讨IRI后高迁移率蛋白1(HMGB1)在肺组织的表达和LIPUS预处理的保护作用。方法雄性SD大鼠32只,体质量250~300 g,随机分为4组,每组8只。对照组(A组),开胸游离左肺门,未行阻断;缺血再灌注组(B组),阻断左肺门45 min后再灌注180 min;预处理组(C组)低强度超声波治疗仪超声定位辐照30 min,然后同B组处理;预处理加α7-烟碱型胆碱能受体(α7n ACh R)拮抗剂组(D组),LIPUS预处理前30 min腹腔注射α7n ACh R拮抗剂甲基牛扁亭2 mg/Kg,然后同预处理组处理。测量肺组织湿干重比值(W/D)和肺通透指数(LPI),大鼠肺组织病理学观察及评分,ELISA法测定肺组织IL1和IL6的浓度,免疫荧光和Western blot检测HMGB1蛋白表达。结果与A组比较,其他三组IR后肺组织W/D值(5.75±0.47)和LPI(2.77±0.18)明显升高(P<0.05),病理学评分(13.31±2.82)明显升高(P<0.05),肺组织IL1(69.13±9.11)和IL6(62.77±8.14)水平明显升高(P<0.05),免疫荧光检测平均IOD值(0.046±0.019)和Western blot检测显示HMGB1表达明显增加(P<0.05)。给于LIPUS预处理后,C组IR后肺组织W/D值(5.07±0.28)和LPI(1.85±0.17)比B组明显降低(P<0.05),病理学评分(8.13±1.76)比B组明显降低(P<0.05),同时肺组织IL1和IL6水平以及HMGB1表达也明显降低,给于α7n ACh R拮抗剂后该作用明显被抑制。结论 LIPUS预处理能够减轻IRI后肺损伤,其机制可能是通过激活依赖α7n ACh R的胆碱能抗炎通路,从而降低肺组织HMGB1的表达。
