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目的探讨羟考酮依赖引起大鼠海马CA1区和中脑腹侧被盖区(VTA)内神经元的损伤情况,以及l-四氢巴马汀(l-THP)对羟考酮依赖大鼠神经元损伤的保护作用。方法采用连续递增给羟考酮建立依赖模型:大鼠连续给药22 d,每天2次,从第1天到第8天,从开始剂量2 mg.kg–1,每日递增1 mg至第8天固定为9 mg.kg–1,直到第22天。l-THP伴随给药,l-THP灌胃给药40 min后给羟考酮。末次给药24 h后,取脑,石蜡切片,采用ABC法测海马CA1区和VTA内GFAP的免疫组织化学反应,以其阳性神经元的平均吸光度值表示其含量。结果羟考酮引起大鼠海马CA1区和VTA内GFAP含量明显升高,提示羟考酮能造成神经元损伤。l-THP(15,30 mg.kg–1)抑制海马CA1区和VTA内GFAP含量的升高。结论长期大剂量给予羟考酮能造成大鼠神经元损伤,l-THP对羟考酮依赖大鼠神经元损伤有保护作用。
Objective To investigate the neuronal damage induced by oxycodone-induced hippocampal CA1 and ventral tegular area (VTA) in rats and the effect of l-tetrahydropalmatine (l-THP) on oxycodone-dependent rats Protection of neuronal injury. Methods Continuous oxycodone was used to establish the dependent model. The rats were given continuous administration for 22 days twice daily from the first day to the eighth day, starting from the initial dose of 2 mg.kg-1 and increasing from 1 mg daily to 8 days fixed at 9 mg.kg-1, until the first 22 days. l-THP accompanied by administration, l-THP intragastric administration of oxycodone 40 minutes after. Twenty-four hours after the last administration, brain and paraffin sections were taken for immunohistochemical analysis of GFAP in hippocampal CA1 region and VTA by ABC method, and the average value of the positive neurons was used to express the content. Results Oxycodone significantly increased the level of GFAP in hippocampal CA1 region and VTA, suggesting that oxycodone can cause neuronal damage. l-THP (15, 30 mg.kg-1) inhibited the increase of GFAP level in hippocampal CA1 area and VTA. Conclusion Long-term high-dose oxycodone can cause neuronal damage in rats, and l-THP has a protective effect on neuronal damage in oxycodone-dependent rats.