| Objective To explore the influence and possible mechanism of the expression ofClaudin-4and ZO-1brought by Colquhounia Root through observing the expression ofClaudin-4and ZO-1and the relationship among W/D,LPI and LIS on rats of ALI induced byoleic acid.It will provide a treatment strategy and theoretical evidence for the use ofColquhounia Root on clinical treatment of ALI/ARDS.Methods45healthy SD rats were randomly divided into three groups: the contr-ol group,the ALI group and the colquhounia root treated group so that there were15rats in each group. In control group, sodium chloride2ml were instilled into the sto-mach of each rat for ten consecutive days before intravenous injection of sodium chl-oride0.04ml/kg. In ALI group, sodium chloride2ml were instilled into the stomachof each rat for ten consecutive days until oleic acid0.04ml/kg was injected into trailvein to establish ALI models, and in colquhounia root treated group,colquhounia roottalet with600mg/kg·day were instilled into the stomach of each rat for ten consecutiv-e days before intravenous injection of same dose oleic acid with ALI group. After4hof establishing model, all animals were sacrificed to collect lung tissue of rats to testlungtissue wet/dry weight ratio(W/D); collect rat blood serum, bronchoalveolar lavagefluid to test lung permeability index(LPI). Lung tissue was fixed-embedded to do he-matoxylin-eosin(HE)staining to test lung injury score(LIS). Immunohistochemical staini-ng was completed to detect the expression and localization of Claudin-4and ZO-1.Results Through general observation, the lung tissue was normal in control gro- up. In ALI group, the lung tissue was swelled, and there were widespread bleeding p-oints on the surface. In colquhounia root treated group, lung tissue was swelled slight-ly.Under the microscope, alveolar epithelium was integrity, and there was no significa-nt pathological change in alveolar spaces and pulmonary interstitium in control group.In ALI group, the alveolar wall was not complete. There were lots of inflammatory c-ells infiltration, redblood cell exudation and alveolar interstitial edema. Change in col-quhounia root treated group was not serious. The LIS of ALI group was significantlyincreased than that of control group (P<0.01).The LIS of colquhounia root treated gro-up was significantly lower than that of ALI group (P<0.01), but still higher than thatof control group (P<0.05).In ALI group, W/D and LPI were respectively significantlyincreased than that of the control group and colquhounia root treated group (P<0.05).In colquhounia root treated group, W/D was higher than that of control group (P<0.01), but there was no significant difference between that of colquhounia root treated gr-oup and control group.In control group, Claudin-4was expressed in the cell membraneof alveolar epithelium,and there was a small amount of expression in the cytoplasm.IOD of ALI group wassignificantly lower than those of control group and colquhouniaroot treatedgroup(P<0.01). IOD of colquhounia root treated group was higher than thatof controlgroup(P<0.05). In control group, ZO-1was expressed in the cytoplasm of ratalveolar epithelial cells. IOD of ALI group was significantly lower than those of nor-mal control group and colquhounia root treated group(P<0.01), IOD of colquhounia ro-ot treatedgroup wasincreased than that of control group(P<0.05).Conclusion Colquhounia root pretreatment can effectively protect the rats from oleicacid induced ALI. The permeability barrier of the lung was destroyed in acute lung injury.Themain structure of permeability barrier was tight junction protein as Claudin-4and ZO-1. Theexpression of them was decreased in the early age of ALI but was increased in theColquhounia root pretreatment group.The protective effect of Colquhounia root may be associated with the expression of tight junction protein. |
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