Abstract

Objective To study the effects of triptolide on the expression of STAT-1 and ICAM-1 in asthmatic mice,and to explore the possible therapeutic mechanism of triptolide in asthma.Methods Forty Kunming male mice were randomly divided into 4 groups:control group,asthmatic group,dexamethasone group and triptolide group.The asthmatic model was established by ovalbumin injection and ihalation.And the 4 groups were treated respectively with normal saline (as control),dexamethasone or triptolide.Twenty-four days later,the mice were executed.The numbers of total leukocytes and eosinophils in bronchoalveolar lavage fluid (BALF) were counted by optical microscope.RT-PCR was employed to detect the mRNA of STAT-1 and ICAM-1 in the lung tissue.The protein of STAT-1 and ICAM-1 expression were measured by immunohistochemistry.Results STAT-1 and ICAM-1 mRNA and the protein expression in lung tissue of asthmatic group significantly increased compared with those of control group (P <0.01).The mRNA and protein expression of STAT-1 and ICAM-1 in mice treated with triptolide and dexamethasone were significantly lower than those in asthmatic group (P <0.01).STAT-1 protein expression in lung tissue was correlated with the number of total leukocytes and eosinophils in BALF and protein expression of ICAM-1 (r =0.665,0.735 and 0.677,P <0.01,respectively).ICAM-1 protein expression in lung tissue was correlated with the number of total leukocytes and eosinophils in BALF (r =0.792 and 0.776,P <0.01,respectively).Conclusions The mechanism of triptolide inhibiting asthmatic airway inflammation may be related to its inhibiting activities of STAT-1 and ICAM-1. Key words: Bronchial asthma; Triptolide; Signal transducer and activator of transcription-1; Intercellular adhesion molecule-1

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