摘要
目的研究神经生长因子(NGF)、白血病抑制因子(LIF)调控支气管哮喘(简称哮喘)大鼠气道神经源性炎症的机制,寻求治疗哮喘的新靶点。方法成年清洁级雄性SD大鼠36只,按随机数字表法分为对照组、哮喘组和抗NGF组,每组12只。采用免疫组织化学和原位杂交技术观察哮喘大鼠肺组织、C7～T5背根神经节内NGF、LIF、P物质(SP)的表达状态及抗NGF干预对其表达的影响。结果(1)哮喘组大鼠肺组织NGF、LIF蛋白及其mRNA的平均灰度值分别为157±7、138±8、156±6、141±10,对照组分别为183±7、190±7、187±7、181±8,抗NGF干预组分别为177±6、169±9、178±7、172±9,三组比较差异有统计学意义(t分别=19.40、15.80、0.38、14.79,P均<0.01);(2)哮喘组大鼠C7～T5背根神经节NGF、LIF、SP蛋白及SPmRNA的灰度值分别为136±8、148±6、140±8、128±8,对照组分别为185±7、187±8、174±7、180±8,抗NGF干预组分别为164±6、170±8、163±9、157±7,三组比较差异有统计学意义(t分别=29.50、22.65、23.12、28.71,P均<0.01)。结论促进背根神经节细胞合成和释放SP可能是NGF、LIF参与哮喘气道神经源性炎症形成的机制之一,抗NGF干预能够有效地将其抑制。
Objective To study the mechanisms of regulating airway neurogenic inflammation in asthma by never growth factor （NGF） and leukemia inhibitory factor （LIF） , and then to explore new targets in treating asthma. Methods Adult male SD rats （ n 36） were divided into the normal group, the asthmatic group and the anti-NGF group at random. There were 12 rats in each group. The asthma models were established by sensitization and challenge with ovalbumin, and the asthma model was treated with anti-NGF. The expression of NGF, LIF and substance P （SP） in lung tissue or in doral root ganglion of each rat were detected by immunohiscbemistry and hybridisation in situ. Results （ 1 ） The gray-levels of NGF protein/ NGF mRNA, LIF protein/LIF mRNA in the lungs were 157±7, 138±8, 156 ± 6, 141± 10 for the asthmatic group respectively, 183±7, 190±7, 187±7, 181±8 for the normal control group respectively, and 177±6, 169±9, 178±7, 172±9 for the asthmatic group with anti-NGF treatment. There were significant differences in gray-level of NGF protein/NGF mRNA, LIF protein/LIF mRNA among those three groups （t = 19.40±15. 80,0. 38±14. 79, all P 〈0.01 ）. （2） The gray-levels of NGF protein/LIF protein, SP protein/SP mRNA in the doral root ganglions were 136±8, 148 ±6, 140 ±8, 128±8 for the asthmatic group respectively, 185 ±7, 187±8, 174±7, 180 ±8 for the normal control group respectively, and 164±6, 170±8, 163±9, 157±7 for the asthmatic group with anti-NGF treatment. There were also significant differences in gray-level of NGF protein/LIF protein, SP protein/SP mRNA among those three groups （t = 29.50±22. 65,23.12±28.71, all P 〈0. 01 ）. Conclusion Enhancing the synthesis and release of SP in doral root ganglion may be one of the mechanisms by which NGF and LIF regulate airway neurogenic inflammation in asthmatic rats, and this mechanism can be depressed by the intervention of anti-NGF.
出处
《中华结核和呼吸杂志》
CAS
CSCD
北大核心
2006年第6期376-380,共5页
Chinese Journal of Tuberculosis and Respiratory Diseases
基金
国家自然科学基金资助项目(30300146)
关键词
哮喘
神经生长因子
白血病抑制因子
神经源性炎症
Asthma
Never grown factor
Leukemia inhibitory factor
Neurogenic inflammation
