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1.
Chinese Journal of Information on Traditional Chinese Medicine ; (12)2006.
Article in Chinese | WPRIM | ID: wpr-580203

ABSTRACT

Objective To investigate airway inflammation,number of eosinophils in blood and BALF,the expression of inhibitor protein ?(I ?B ?) and nuclear factor-?B(NF-?B) activity in lung of rat with spleen deficiency asthma,and the effect of herbs of reinforcing spleen to replenishing Qi.Method Thirty rats were randomly divided into three groups:control group(group A),spleen deficiency asthma group(group B),decoction group(group C).The pathological changes of lung was detected by HE staining,and the expression of I ?B ? and activity of nuclear factor ?B p65(NF-?B p65) was assessed in lung by immunohistochemistry.Results Compared with group A,the expression of I ?B ? significantly reduced(P

2.
Medical Journal of Chinese People's Liberation Army ; (12)2001.
Article in Chinese | WPRIM | ID: wpr-554090

ABSTRACT

Objective To investigate changes in NF ?B signal pathway in PAM stimulated by lipopolysaccharide(LPS) in vitro , and to explore the molecular pathological mechanism of acute lung injury(ALI). Methods After PAM were stimulated by LPS, the changes in expression of IKK mRNA, activation of NF ?B, degradation of I?B, and secretion of TNF ? in PAM were measured at 0, 15min, 30min, 1h, 2h, and 4h by in situ hybridization, electrophoretic mobility shift assay (EMSA), and enzyme linked immune absorbing analysis (ELISA), respectively. Results The expression of IKK ? mRNA was increased 15min after LPS stimulation and reached the peak at 30 min, then returned to the base line after 1 hour. The changes in I?B ? mRNA were opposite. The activity of NF ?B was increased 15min after LPS stimulation, peaking at 1 hours, and returned to the pre stimulation level after 2 hours. The content of TNF ? was increased initially at 30min, reached the peak at 1 hour, and gradually returned to the pre stimulation level in 2~4 hour. Conclusion The transduction pathway of activation of IKK ? degradation of I?B/activation of NF ?B/synthesization of TNF ? might play a critical role in the molecular pathological mechanism of LPS induced ALI.

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