摘要
目的研究神经生长因子(NGF)介导哮喘大鼠神经源性气道炎症肿瘤坏死因子α(TNF-α)mRNA的表达机制,探讨防治哮喘的新方法。方法采用放射免疫分析方法检测卵清蛋白致敏哮喘大鼠下呼吸道肺组织NGF、TNF-α的表达及抗NGF干预对其表达的影响。结果 (1)哮喘组大鼠肺组织NGF蛋白、NGF mRNA的平均灰度值分别为145±7、128±7;对照组分别为189±7、191±6;抗NGF干预组分别为156±6、139±8;3组比较差异均有统计学意义(P<0.01);(2)哮喘组大鼠TNF-α蛋白及TNF-αmRNA的灰度值分别为141±7、127±7;对照组分别为175±8、179±9;抗NGF干预组分别为164±8、155±6;3组比较差异均有统计学意义(P<0.01)。结论 NGF促进合成和释放TNF-α可能是NGF参与哮喘气道神经源性炎性反应的机制之一,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 nerve growth factor(NGF) on TNF-α mRNA expression,and to explore new ideas for prevention and treatment of asthma.Methods The asthma models were established by sensitization and challenge with ovalbumin,and the asthma model was treated with anti-NGF.The expression of NGF and TNF-α in lung tissue of each rat was detected by immunohischemistry and hybridisation in situ1.Results(1) The gray-levels of NGF protein /NGF mRNA,in the lungs were 145±7,128±7 for the asthmatic group respectively;189±7,191±6 for the normal control group respectively,and 156±6,139±8 for the asthmatic group with anti-NGF treatment.There were significant differences in gray-level of NGF protein /NGF mRNA among those three groups(P0.01).(2) The gray-levels of TNF-α protein /TNF-α mRNA,in the lungs were 141±7,127±7 for the asthmatic group respectively;175±8,179±9 for the normal control group respectively,and 164±8,155±6 for the asthmatic group with anti-NGF treatment.There were also significant differences in gray-level of TNF-α protein / TNF-α mRNA among those three groups(P0.01).Conclusion In this experimental,enhancing the synthesis and release of TNF-α may be one of the mechanisms by which NGF regulate airway neurogenic inflammation in asthmatic rats,and this mechanism can be depressed by the intervention of anti-NGF.
出处
《重庆医学》
CAS
CSCD
北大核心
2011年第2期108-110,F0002,共4页
Chongqing medicine
基金
广西卫生厅科学基金资助项目(Z2009353)