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Protective effects of inosine on urinary bladder function in rats with partial bladder outlet obstruction.

机译:肌苷对部分膀胱出口梗阻大鼠膀胱功能的保护作用。

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OBJECTIVES: To evaluate the protective effects of inosine on bladder dysfunction, nerve density, and oxidative damage after partial bladder outlet obstruction in rats. METHODS: A total of 60 adult male Sprague-Dawley rats were divided into 5 groups. Groups 1-4 underwent bladder outlet obstruction. Groups 1-3 were treated with inosine at 100, 150, or 225 mg/kg/d intraperitoneally and group 4 with saline. Group 5 consisted of sham-operated control rats. At 21 days postoperatively, cystometry were performed in 30 rats (6 per group). In the remaining 30 rats (6 per group), the bladders were excised and used for contractile responses to various stimulations, immunohistochemical examination for protein gene product 9.5 (a neuronal marker) and evaluation of superoxide dismutase activity and thiobarbituric acid reductase substance level. RESULTS: Inosine administration resulted in dose-dependent protective effects on the contractile responses to both field stimulation and carbachol, although the protective responses to KCl was restricted to a greater dose of inosine. A dose-dependent reduction in residual volume was noted in inosine-treated groups at different dosages compared with the saline-treated group. In addition, the protein gene product 9.5-positive nerve density decreased in the saline-treated group but significantly increased in the inosine-treated (225 mg/kg/d) group. Compared with the saline-treated group, significantly enhanced superoxide dismutase activity and a reduced thiobarbituric acid reductase substance level were observed in the inosine-treated group at 150 and 225 mg/kg/d. CONCLUSIONS: These results suggest that inosine has a potential protective effect against partial bladder outlet obstruction-induced bladder dysfunction and oxidative injury in rats.
机译:目的:评价肌苷对大鼠部分膀胱出口梗阻后膀胱功能障碍,神经密度和氧化损伤的保护作用。方法:将60只成年雄性Sprague-Dawley大鼠分为5组。 1-4组经历膀胱出口梗阻。 1-3组分别以100、150或225 mg / kg / d的肌苷腹膜内治疗,第4组则用盐水治疗。第5组由假手术的对照大鼠组成。术后21天,对30只大鼠进行了膀胱测压(每组6只)。在剩下的30只大鼠中(每组6只),切开膀胱并用于对各种刺激的收缩反应,蛋白基因产物9.5(神经元标记)的免疫组织化学检查以及超氧化物歧化酶活性和硫代巴比妥酸还原酶物质水平的评估。结果:肌苷给药对田间刺激和卡巴胆碱的收缩反应具有剂量依赖性的保护作用,尽管对KCl的保护反应仅限于更大剂量的肌苷。与盐水处理组相比,肌苷处理组在不同剂量下残留量的剂量依赖性降低。此外,在盐水处理组中,蛋白质基因产物9.5阳性的神经密度降低,但在肌苷处理组(225 mg / kg / d)中则明显增加。与盐水处理组相比,肌苷处理组在150和225 mg / kg / d时观察到超氧化物歧化酶活性显着增强,硫代巴比妥酸还原酶物质水平降低。结论:这些结果表明,肌苷对大鼠部分膀胱出口梗阻引起的膀胱功能障碍和氧化损伤具有潜在的保护作用。

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