Wang Lei, Li Ting-Qian, Xiang Guo-Xia, Wang Gang
Department of Respiratory Medicine, West China Hospital, Sichuan University, Chengdu 610041, China
Sichuan Da Xue Xue Bao Yi Xue Ban. 2006 Mar;37(2):250-3.
To investigate the effect of dexamethasone on the expression of fractalkine (FKN) in lipopolysaccharide (LPS)-induced acute lung injury (ALI).
The rat model of ALI was established by injection of LPS at the dose of 4 mg/kg. 42 Wistar rats were randomly divided into the normal group (n=6), LPS group (n=18), and dexamethasone (DEX) group (n = 18), and then the rats in both LPS and DEX groups were divided into three subgroups (1 h, 2 h and 4 h after injection of LPS), respectively. The pathological condition and the wet/dry ratio (W/D) of the lung were observed, and serum TNF-alpha level, and FKN mRNA of the lung were detected with ELISA and RT-PCR.
The W/D, serum TNF-alpha level, and FKN mRNA of the lung were significantly increased in LPS group, compared with those in normal group (all P < 0.05), but the W/D, serum TNF-alpha level, and FKN mRNA of the lung in the DEX group were much more decreased than those in the LPS group (all P < 0.05). In addition, the expression of FKN mRNA in the lung tissue positively correlated with the concentration of TNF-alpha (r = 0.674, P <0.05).
The findings suggested that pre-treatment with dexamethasone could inhibit the TNF-alpha level and prevent the increase of the expression of FKN mRNA, which may be one of the mechanisms by which DEX serves as a protection against LPS-induced lung injury.
探讨地塞米松对脂多糖(LPS)诱导的急性肺损伤(ALI)中趋化因子(FKN)表达的影响。
通过注射4mg/kg剂量的LPS建立大鼠ALI模型。42只Wistar大鼠随机分为正常组(n=6)、LPS组(n=18)和地塞米松(DEX)组(n=18),然后将LPS组和DEX组大鼠分别分为三个亚组(注射LPS后1小时、2小时和4小时)。观察肺组织病理状况及肺湿/干比(W/D),采用酶联免疫吸附测定(ELISA)和逆转录-聚合酶链反应(RT-PCR)检测血清肿瘤坏死因子-α(TNF-α)水平及肺组织FKN信使核糖核酸(mRNA)。
与正常组相比,LPS组肺组织W/D、血清TNF-α水平及肺组织FKN mRNA均显著升高(均P<0.05),但DEX组肺组织W/D、血清TNF-α水平及肺组织FKN mRNA均较LPS组明显降低(均P<0.05)。此外,肺组织中FKN mRNA表达与TNF-α浓度呈正相关(r=0.674,P<0.05)。
研究结果表明,地塞米松预处理可抑制TNF-α水平,阻止FKN mRNA表达增加,这可能是地塞米松对LPS诱导的肺损伤发挥保护作用的机制之一。