| 摘要: |
| 【目的】 探讨在慢性缺氧和炎性刺激影响下，大鼠十二指肠粘膜层酪氨酸羟化酶(TH)和尿皮质素(Urocortin，Ucn)的表达变化，为阐明慢性缺氧和炎性刺激影响十二指肠功能活动和应激反应机制提供形态学依据。【方法】建立慢性缺氧和促炎性细胞因子rmIL-1β刺激的大鼠模型，采集供试大鼠十二指肠，制备切片，用荧光免疫组织化学方法观察TH和Ucn的表达变化。【结果】慢性缺氧引起十二指肠粘膜固有层中的TH阳性细胞数显著减少，这种作用与缺氧的时间呈负相关（P＜0.01）；而炎性细胞因子刺激后，十二指肠粘膜固有层中的Ucn阳性细胞数增加（P＜0.05）。【结论】慢性缺氧刺激可能通过十二指肠中TH的表达减少而使其生理功能减弱;炎性细胞因子刺激引起Ucn表达增加，可能是因为其参与了肠对缺氧的应激反应。 |
| 关键词: 慢性缺氧 促炎性细胞因子 十二指肠 酪氨酸羟化酶 尿皮质素 |
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| 基金项目:陕西省自然科学基金项目（SJ08C105） |
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| Effects of chronic hypoxia and pro-inflammatory cytokine stimulation on the expression of TH and urocortin in the duodenum of the rat |
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| Abstract: |
| 【Objective】The study observed the alteration of tyrosine hydroxylase (TH) and urocortin (Ucn) expressions in the rat duodenum to provide morphological basis for understanding the mechanism underlying the effect of chronic hypoxia and proinflammatory cytokine stimulation on the intestinal function.【Method】Chronic hypoxia and IL-1β stimulation model was established in the rat.The expressions of TH and Ucn were studied by using immunohistochemistry and image analysis.【Result】 The number of TH immunoreactive cells decreased time dependently following chronic hypoxia (P＜0.01),while the number of Ucn positive cells in duodenum increased following the pro inflammatory cytokine stimulation (P＜0.05).【Conclusion】Chronic hypoxia might inhibit the physiological function by attenuate the expression of TH in the duodenum, and pro inflammatory cytokine stimulation might be involved the mechanisms of stress response of intestine through increase of the Ucn expression. |
| Key words: chronic hypoxia pro-inflammatory cytokine duodenum tyrosine hydroxylase urocortin |
