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出 处:《国际呼吸杂志》2015年第5期321-324,共4页International Journal of Respiration
摘 要:目的观察BCG-CpG-DNA干预对支气管哮喘(简称哮喘)小鼠信号转导和转录激活因子4(sTAT4)、STAT6的影响,探讨其对小鼠哮喘的作用机制。方法将30只BALB/c小鼠随机分为3组:正常对照组(A组)、哮喘模型组(B组)、BCG-CpG-DNA治疗组(C组)。其中B、C组小鼠于第0天、第13天分别给予卵清白蛋白(OVA)和佐剂液态铝混悬液致敏,于第25天至第30天每天给予雾化OVA建立哮喘模型,C组于致敏后以BCG-CpG-DNA腹腔注射,A组以生理盐水代替OVA致敏和激发。所有动物于第31天处死,采用Westernblot技术检测小鼠肺组织中STAT4、STAT6的蛋白表达水平。结果与A组比较,B组STAT4、pSTAT4表达降低(P值均〈0.01),STAT6、pSTAT6的表达升高(P值均〈O.01);与B组比较,BCG-CpG-DNA治疗后小鼠哮喘症状和肺组织的炎症病理变化减轻,STAT4、pSTAT4表达增加,STAT6、pSTAT6表达降低,差异具有统计学意义(P值均〈0.01)。结论BCG-CpG-DNA可能通过抑制STAT6、促进STAT4的表达,调节Th1/Th2细胞因子平衡,从而起到抑制气道炎症的作用。Objective To observe the influence of BCG-CpG-DNA on expression of signal transducers and activators of transcription 4 (STAT4), STAT6 in asthmatic mice lung,in order to discuss the potential mechanism of BCG-CpG-DNA in treating bronchial asthma (asthma). Methods Thirty BALB/c mice were randomly divided into three groups: normal control group (group A) and asthma model group (group B), BCG-CpG-DNA treated group (group C). Asthma model was established by OVA. Mice in group B and C were treated with mixed suspension of OVA and liquid aluminum ad]uvant at day 0 and 13 respectively,and given aerosolized OVA from day 25 to 30,once every day. Mice in group C were intraperitoneal injected BCG-CpG-DNA after sensitization by OVA. OVA was replaced by physiological saline in group A. All the animals were killed at day 31. Western blot was performed to detect the protein expression level of STAT4 and STAT6 in the lung tissues of different group mice. Results The expression of STAT4 and pSTAT4 in group B were lower than group A ( P 〈0.01). The expression of STAT6 and pSTAT6 in group B were higher than group A ( P 〈0.01). BCG-CpG-DNA relieved the symptoms of asthma, increased the expression level of STAT4 and pSTAT4, depressed the the expression level of STAT6 and pSTAT6 when compared with group B. Differences are statistically significant ( P 〈0.01). Conclusions BCG-CpG-DNA may regulate the eytokines balance of Thl and Th2 bv inhibiting STAT6 and promoting STAT4 to adjust the airway allergic inflammation.
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