摘要
目的：研究寒邪、寒湿之邪对大鼠肺组织fractalkine（FKN）mRNA表达的影响及其差异。方法：将24只SPF级Wistar大鼠按随机数字表法分为常温组、寒邪（-10℃,2h;湿度50%～55%）组和寒湿（-10℃,2h;湿度90%～100%）组,每组8只大鼠。第1天将大鼠置于相应环境的调温箱中饲养2h后取出,此后将大鼠置常温下饲养,期间观察大鼠的整体状况,4d后取材。观察各组大鼠肺组织病理改变,放射免疫法检测肺组织匀浆中白细胞介素-6（interleukin-6,IL-6）、肿瘤坏死因子-α（tumor necrosis factor-α,TNF-α）的含量,逆转录-聚合酶链反应（reverse transcription-polymerase chain reaction,RT-PCR）法检测大鼠肺组织FKN mRNA的表达。结果：寒邪组和寒湿组大鼠肺组织都有不同程度的病理改变。寒邪组和寒湿组大鼠肺组织匀浆中IL-6、TNF-α水平均明显高于常温组（P〈0.01）,寒湿组大鼠肺组织匀浆中IL-6、TNF-α水平亦明显高于寒邪组（P〈0.01）。RT-PCR结果显示,FKN在常温组大鼠肺内有较低的表达,随着肺损伤的加重,FKN在肺内的表达亦上调。寒邪组和寒湿组大鼠肺组织FKN mRNA表达水平均明显高于常温组（P〈0.01）;且寒湿组大鼠肺组织FKN mRNA表达水平明显高于寒邪组（P〈0.01）。结论：寒邪对肺脏有不同程度的损害,对肺组织内FKN mRNA的表达有上调作用。一定的湿邪能加重寒邪对肺脏的损害,进而上调肺组织内FKN mRNA的表达。趋化因子FKN与肺脏损伤有极为密切的关系。
Objective： To study the variabilities of the effects of cold pathogen and cold-dampness pathogen on the fractalkine （FKN） mRNA expression in lung tissues of rats. Methods： Twenty-four Wistar rats of SPF grade were randomly divided into 3 groups., normal temperature group, cold pathogen group and cold-dampness pathogen group. There were 8 rats in each group. Rats in normal temperature group were bred at （20±2）℃ and under normal humidity （50%-55%） for 2 h. Rats in cold pathogen group were bred at -10℃ and under normal humidity （50%-55%） for 2 h, and the rats in cold-dampnesspathogen group were bred at -10℃ and under high humidity （90%-100%） for 2 h. Rats inthe three groups were bred in thermostats under the corresponding conditions on the first day of experiment, and then the rats in different groups were all bred at normal temperature. Lung specimens in 3 groups were gathered four days later. The behavior and the pathological changes in the lung tissues of rats in different groups were observed. The content of interleukin-6 （IL-6） and tumor necrosis factor-α （TNF-α） in lung homogenate was detected by radioimmunoassay （RIA） method. Expression of FKN mRNA in lung homogenate was detected by reverse transcription-polymerase chain reaction （RT-PCR）. Results： The lung tissues of rats in both cold pathogen group and cold-dampness pathogen group had various degrees of pathological changes. Compared with normal temperature group, the content of IL-6 and TNF-α was increased obviously in lung homogenate of rats in both cold pathogen group and cold-dampness pathogen group （P〈0.01）. The content of IL-6 and TNF-α in lung homogenate of rats in cold-dampness pathogen group was obviously higher than that in cold pathogen group （P〈0.01）. The RT-PCR results showed a low expression of FKN mRNA in lung tissues of rats in normal temperature group. If the injured lung tissues were aggravated, the expression of FKN mRNA in the lung tissues was elevated. Compared with normal temperature group, FKN mRNA expressions in both cold pathogen group and cold-dampness pathogen group were increased obviously （P〈0.0]）. FKN mRNA expression in lung homogenate of rats in cold-dampness pathogen group was also obviously higher than that in cold pathogen group （P〈0.01）. Conclusion： Cold pathogen can induce lung injury and up-regulate the FKN mRNA expression in lung tissue. Dampness pathogen can up-regulate the FKN mRNA expression through aggravating the injury of lung tissues caused by cold pathogen. FKN has a close relationship with the lung injury.
出处
《中西医结合学报》
CAS
2008年第2期171-175,共5页
Journal of Chinese Integrative Medicine
基金
山东省卫生厅计划课题(No.2005-215)
山东省卫生系统高层次人才1020工程资助课题
关键词
寒邪
湿邪
肺
CX3C趋化因子
大鼠
pathogenic cold
pathogenic dampness
lung
CX3C chemokines
rats
