Zhu Jin-qi, Feng Jun-tao, Hu Cheng-ping, Tang Yu-ling, Lin Min-juan, Luo Bai-ling
Department of Respiratory Medicine, Xiangya Hospital of Central South University, Changsha 410008, China.
Zhonghua Jie He He Hu Xi Za Zhi. 2006 Jun;29(6):376-80.
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.
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 immunohistochemistry and hybridisation in situ.
(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, 20.38, [corrected] 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).
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.
研究神经生长因子（NGF）和白血病抑制因子（LIF）对哮喘气道神经源性炎症的调节机制，进而探索哮喘治疗的新靶点。
将36只成年雄性SD大鼠随机分为正常组、哮喘组和抗NGF组，每组12只。采用卵白蛋白致敏和激发建立哮喘模型，并给予抗NGF治疗哮喘模型。通过免疫组织化学和原位杂交检测每组大鼠肺组织或背根神经节中NGF、LIF和P物质（SP）的表达。
（1）哮喘组肺组织中NGF蛋白/NGF mRNA、LIF蛋白/LIF mRNA的灰度值分别为157±7、138±8、156±6、141±10，正常对照组分别为183±7、190±7、187±7、181±8，抗NGF治疗的哮喘组分别为177±6、169±9、178±7、172±9。三组间NGF蛋白/NGF mRNA、LIF蛋白/LIF mRNA灰度值差异有统计学意义（t = 19.40、15.80、20.38、[校正后]14.79，均P < 0.01）。（2）哮喘组背根神经节中NGF蛋白/LIF蛋白、SP蛋白/SP mRNA的灰度值分别为136±8、148±6、140±8、128±8，正常对照组分别为185±7、187±8、174±7、180±8，抗NGF治疗的哮喘组分别为164±6、170±8、163±9、157±7。三组间NGF蛋白/LIF蛋白、SP蛋白/SP mRNA灰度值差异也有统计学意义（t = 29.50、22.65、23.12、28.71，均P < 0.01）。
增强背根神经节中SP的合成与释放可能是NGF和LIF调节哮喘大鼠气道神经源性炎症的机制之一，抗NGF干预可抑制该机制。
