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The Effect Of Sevoflurane On The Expression Of TLR4of Lung Tissue In Mouse Model Of ARDS Induced By Lipopolysaccharide

Posted on:2015-03-25Degree:MasterType:Thesis
Country:ChinaCandidate:H Y CuiFull Text:PDF
GTID:2284330431475572Subject:Anesthesia
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Objective:To study the effect of inhalation anesthetic sevoflurane on the expression of TLR4of the lung tissue in the mouse with ARDS and to explore its mechanism of action.Methods:The mouse model of sepsis-injured ARDS was set up by infusing LPS5μg/g into tail vein.40healthy male BALB/c mice, weighting18(±2) g, were randomly divided into4groups(n=10each):normal control group(CON group); LPS group (LPS group), received LPS5μg/g intravenously;1%sevoflurane+LPS group (SP1group);2%sevoflurane+LPS group (SP2group). After the SP1group and SP2group were infused LPS5μg/g30minutes later, the two groups were treated with sevoflurane1%and2%respectively delivered by100%oxygen1hour and were cleaned10minutes. After LPS or physiological saline instillation six hours later,the mice were killed and the left hilar and the right hilar were ligated. And then the right lung tissue was weighted to calculate lung wet/dry weight ratio(W/D); the left lung tissue was used to observe the gene expression of TLR4mRNA by RT-PCR, and then the expression intensity of TLR4mRNA of all the groups were compared by the grey value.Results:1.The W/D in every group respectively:CON group (3.45±0.41), LPS group (5.12±0.17), SP1group (4.96±0.27),SP2group (4.91±0.15).Compared with CON group, lung W/D was increased clearly in LPS group,SP1group and SP2group (P<0.05); compared with LPS group, W/D was declined in SP1and SP2group (P<0.05); compared with SP1group, W/D was declined in SP2group further (P<0.05).2.The grey value in every group respectively:CON group (0.81±0.13), LPS group (1.53±0.13), SP1group (1.31±0.12), SP2group (1.17±0.13).Compared with CON group, the gene expression intensity of TLR4mRNA was strengthen all in LPS group,SP1group and SP2group (P<0.05); compared with LPS group, the gene expression intensity of TLR4mRNA was declined all in SP1group and SP2group (P<0.05); compared with SP1group, the gene expression intensity of TLR4mRNA was declined in SP2group further (P<0.05). Conclusions:Inhalating low concentrations of sevoflurane can reduce inflammatory response of ARDS stimulated by LPS, the mechanism of which may be associated with the down-regulated expression of TLR4in injured lung.
Keywords/Search Tags:acute respiratory distress syndrome, Toll-like receptor4, lipopolysaccharide, sevoflurane
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