补肾活血对大鼠慢性高眼压模型初级视皮质损害的干预及作用机制研究
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摘要
目的：观察补肾活血对大鼠慢性高眼压(elevated intraocular pressure, EIOP)模型初级视皮质损害的干预作用,并对其作用机理进行初步探讨。
方法：采用烙闭上巩膜静脉法,烙闭大鼠3支上巩膜静脉,制作大鼠慢性EIOP模型,随机分为3组：模型组,给药组,空白组。连续灌胃8周,并于8周末处死大鼠,观察其对EIOP大鼠眼压(intraocular pressure, IOP),初级视皮质(primary visual cortex, PVC)尼氏小体(nissl bodies)含量、神经元细胞超微结构及脑源性神经营养因子(brain-derived neurotrophic factor, BDNF)表达的影响。
结果：本实验采用的烙闭上巩膜静脉的造模方法使大鼠IOP明显升高,在造模后8周(实验结束)IOP仍为造模前的大约3倍；补肾活血对大鼠慢性EIOP模型初级视皮质损害的干预作用如下：轻度降低IOP,提高初级视皮质尼氏小体(nissl bodies)含量、增强脑源性神经营养因子(brain-derived neurotrophic factor, BDNF)的表达及改善神经元细胞超微结构。
结论：采用烙闭上巩膜静脉的方法建立的慢性EIOP大鼠模型操作简单、效果稳定,可获得不少于两个月的中等度EIOP;补肾活血可以有效的保护慢性EIOP大鼠模型视功能,其作用主要表现在轻度降低IOP,提高初级视皮质尼氏小体含量、增强BDNF表达、改善神经元细胞超微结构。
Objective:To observe the effect traditional Chinese medicine(TCM) of BuShenHuoXue on primary visual cortex damage in rat model of chronic, elevated intraocular pressure, and explore the mechanism of it initially.
Methods:By unilaterally cauterizing 3 episcleral vessels,the rat model of chronic, moderately elevated intraocular pressure was gotten.30 rats were divided into 3 groups randomly:model group, treatment group,and normal control group.After given drugs or normal saline for 8 weeks,the rats were put to death. To observe the effection by intraocular pressure(IOP), content of nissl bodies,expression of brain-derived neurotrophic factor,ultrastructure of neuron cell in the primary visual cortex (PVC)
Results:Chronic elevated intraocular pressre was gotten and there was an approximately 3-fold increase in IOP for 2 months comparing to pre-models building. The Intervention:BuShenHuoXue of TCM can lower IOP slightly, and increase content of nissl bodies,enhance expression of brain-derived neurotrophic factor, and improve ultrastructure of neuron cell.
Conclusion: This model is simple and stable, and moderately elevated IOP can last at least 2 months. BuShenHuoXue of TCM can protect the visual function from elevating intraocular pressre,by increasing content of nissl bodies,enhancing expression of brain-derived neurotrophic factor,improving ultrastructure of neuron cell.
方法：采用烙闭上巩膜静脉法,烙闭大鼠3支上巩膜静脉,制作大鼠慢性EIOP模型,随机分为3组：模型组,给药组,空白组。连续灌胃8周,并于8周末处死大鼠,观察其对EIOP大鼠眼压(intraocular pressure, IOP),初级视皮质(primary visual cortex, PVC)尼氏小体(nissl bodies)含量、神经元细胞超微结构及脑源性神经营养因子(brain-derived neurotrophic factor, BDNF)表达的影响。
结果：本实验采用的烙闭上巩膜静脉的造模方法使大鼠IOP明显升高,在造模后8周(实验结束)IOP仍为造模前的大约3倍；补肾活血对大鼠慢性EIOP模型初级视皮质损害的干预作用如下：轻度降低IOP,提高初级视皮质尼氏小体(nissl bodies)含量、增强脑源性神经营养因子(brain-derived neurotrophic factor, BDNF)的表达及改善神经元细胞超微结构。
结论：采用烙闭上巩膜静脉的方法建立的慢性EIOP大鼠模型操作简单、效果稳定,可获得不少于两个月的中等度EIOP;补肾活血可以有效的保护慢性EIOP大鼠模型视功能,其作用主要表现在轻度降低IOP,提高初级视皮质尼氏小体含量、增强BDNF表达、改善神经元细胞超微结构。
Objective:To observe the effect traditional Chinese medicine(TCM) of BuShenHuoXue on primary visual cortex damage in rat model of chronic, elevated intraocular pressure, and explore the mechanism of it initially.
Methods:By unilaterally cauterizing 3 episcleral vessels,the rat model of chronic, moderately elevated intraocular pressure was gotten.30 rats were divided into 3 groups randomly:model group, treatment group,and normal control group.After given drugs or normal saline for 8 weeks,the rats were put to death. To observe the effection by intraocular pressure(IOP), content of nissl bodies,expression of brain-derived neurotrophic factor,ultrastructure of neuron cell in the primary visual cortex (PVC)
Results:Chronic elevated intraocular pressre was gotten and there was an approximately 3-fold increase in IOP for 2 months comparing to pre-models building. The Intervention:BuShenHuoXue of TCM can lower IOP slightly, and increase content of nissl bodies,enhance expression of brain-derived neurotrophic factor, and improve ultrastructure of neuron cell.
Conclusion: This model is simple and stable, and moderately elevated IOP can last at least 2 months. BuShenHuoXue of TCM can protect the visual function from elevating intraocular pressre,by increasing content of nissl bodies,enhancing expression of brain-derived neurotrophic factor,improving ultrastructure of neuron cell.
引文
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