Publications (2)0 Total impact
Article: [Effects of polymixin B on I-kappaB kinase mRNA expression in lipopolysaccharide- induced pulmonary alveolar macrophages].[show abstract] [hide abstract]
ABSTRACT: To investigate effects of polymixin B (PMB) on I-kappaB kinase(IKK-beta), inhibitor protein(IkappaB-alpha) and nuclear factor-kappa B(NF-kappaB) in lipopolysaccharide(LPS)-induced pulmonary alveolar macrophages (PAM), and explore the anti-inflammatory mechanism of PMB. PAM from rats collected by bronchoalveolar lavage was cultured and divided into three groups. In the control group, PAM was not stimulated with LPS and not treated with PMB. In the LPS stimulated group, PAM was stimulated with LPS. In the PMB treated group, PAM was pretreated with PMB half an hour prior to LPS stimulation. The expression of IKK-beta mRNA, level of IkappaB-alpha and the activity of NF-kappaB in PAM were measured by in situ hybridization(ISH), enzyme linked immunoadsorbent assay (ELISA) and electrophoretic mobility shift assay(EMSA), respectively. In the LPS stimulated group, the expression of IKK-beta mRNA (0.147+/-0.015) and activity of NF-kappaB (0.828+/-0.019) in PAM significantly increased, whereas levels of IkappaB-alpha (0.228+/-0.021) decreased (all P<0.01) in PMB treated groups. The expression of IKK-beta mRNA (0.112+/-0.022) and activity of NF-kappaB (0.358+/-0.011) were down-regulated while level of IkappaB-alpha (0.477+/-0.016) was up-regulated(P<0.01). LPS might induce expression of IKK-beta mRNA, degradation of IkappaB-alpha and activation of NF-kappaB PMB could inhibit the expression of IKK-beta, degradation of IkappaB-alpha and activation of NF-kappaB, showing marked anti-inflammatory property.Zhongguo wei zhong bing ji jiu yi xue = Chinese critical care medicine = Zhongguo weizhongbing jijiuyixue 08/2003; 15(7):429-31.
Article: [Effects of polymyxin B on LPS-induced activation of NF-kappaB in pulmonary alveolar macrophages].[show abstract] [hide abstract]
ABSTRACT: To observe effects of polymyxin B (PMB) on LPS-induced activation of NF-kappaB of pulmonary alveolar macrophages(PAMs) and explore the possible anti-inflammation efficiency of PMB. Rat PAMs were isolated and cultured. The PAMs were divided into 3 groups, namely, normal control group (PAMs+normal solution), LPS stimulation group (PAMs+10 mg/L LPS) and PMB interference group(after PMB treatment for 30 min, using LPS stimulation). The PAMs were fixed respectively at 0,15,30,60,120 and 240 min after stimulation. Nucleoprotein was extracted from cultured PAMs and culture supernatant of the PAMs was collected. The expression of IKK-beta mRNA in the PAMs, NF-kappaB activity in PMB nucleoprotein extractive, TNF-alpha content in culture supernatant of the PAMs were detected by in situ hybridization (ISN), electrophoretic mobility shift assay (EMSA) and ELISA, respectively. IKK-beta mRNA level in LPS group increased at 15 min, reached the peak at 30 min, while IkappaB-alpha level turned out contrary to IKK-beta mRNA level. The peak of NF-kappaB activity appeared at 60-120 min after stimulation was significantly higher than those of pre-stimulation and normal control group (P<0.01). In PMA interference group, NF-kappaB activity and TNF-alpha level were markedly lower than those in LPS stimulation group (P<0.01). The lowest level of IkappaB-alpha was notably higher than that in LPS stimulation group, while the peak of IKK-beta mRNA was obviously lower than that in LPS stimulation group (P<0.01). LPS can induce IKK-beta and NF-kappaB activation, IkappaB-alpha degradation, accelerate TNF-alpha release, but PMB can counteract those effects induced by LPS stimulation.Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology 06/2003; 19(3):235-8.