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哮喘大鼠肺泡巨噬细胞电压依赖性钾通道的活性研究
  • 期刊名称:中国医科大学学报,2008,37(6):721-723.
  • 时间:0
  • 分类:R318.13[医药卫生—生物医学工程;医药卫生—基础医学]
  • 作者机构:[1]中国医科大学药学院药理学教研室,沈阳110001
  • 相关基金:国家自然科学基金资助项目(30570810)
  • 相关项目:巨噬细胞分泌功能变化在哮喘发病中的作用与调控机制研究
中文摘要:

目的探讨哮喘模型大鼠肺泡巨噬细胞(AM)电压依赖性钾通道(Kv)活性的变化及其对巨噬细胞功能的影响。方法利用卵蛋白(OVA)致敏并激发大鼠建立哮喘模型,收集支气管肺泡灌洗液(BALF)培养AM。利用全细胞电压钳模式记录AM细胞膜上的Kv电流,观察比较哮喘模型组和对照组Kv通道活性的变化。结果病理学检测发现哮喘模型组(n=7)炎性细胞浸润明显增加,BALF细胞总数显著增高,与对照组(n=7)比较差异显著(P〈0.01),但AM百分比无明显差异;应用Kv通道特异性阻断剂4-氨基吡啶(4-AP)后电流幅度明显降低,证实检测到的AM细胞膜上的电流为Kv电流;哮喘大鼠AM细胞Kv电流幅度[(243.56±133.56)pA,n=10]较对照组[(656.23±162.34)pA,n=11]明显降低(P〈0.01)。结论哮喘大鼠AM细胞Kv通道活性降低,可能导致AM兴奋性增高,易被激活分泌各种炎性介质和细胞因子,从而参与哮喘炎症的形成。

英文摘要:

Objective To study the change of voltage-dependent potassium channel (Kv) activity in alveolar macrophages (AM) in asthma rats and the effects of Kv channel on AM membrane. Methods Rats were sensitized and challenged with ovalbumin (OVA) to make asthma model. Bronchus alveolar lavage fluid (BALF) were collected and AM were cultured. Kv channel current in AM were recorded using whole-cell voltage-clamp system. Kv status in AM was compared from asthma group and control group. Results There was infiltration of generous inflammatory cells by the detection of pathology in asthma group. Significant increases in total cells in bronchus alveolar lavage fluid (BALF) were found in asthma group (n = 7) compared with control group (n = 7) (P 〈 0.01 ). Compared with control group,there was no significant difference of the percentage of AM in asthma group ;The current altitude which we detected on AM membrane was obviously decreased with the specific blocker of Kv channd (4-AP) confirmed that the current was Kv current. The Kv current altitude in AM in asthma group [(243.56±133.56) pA,n = 10] was significantly lower than that in control gToup [(656.23±162.34) pA,n = 11 ] (P 〈 0.01). Conclusion Reduction of Kv activity may be result in the activation of AM that increase excision from asthma rats and the secretion of cytokine and mediators of inflammation, accordingly, participates the development of inflammation in asthma.

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