| Objective: To observe the regulatory role of actins microfilament on inflammation in lung tissue of rat with acute lung injury (ALI). Methods: Thirty-six SD rats were injected lipopolysaccharide (LPS) to form ALI or saline intravenously, then were divided randomly into six groups: (1) Control (Normal) group; (2) Acute lung injury (LPS) group; (3) Cytochalasin D (CD) group; (4) Phalloidin (P) group; (5) LPS+ Cytochalasin D (CD+LPS) group; (6) LPS+ Phalloidin (P+LPS) group. All rats were killed after 6 hours. Polarized light microscope, Electron microscope and confocal microscope were used to observe the change of actins microfilament. RT-PCR and immunohistochemistry were used to observe the change of TNF-αmRNA and TNF-α. The phosphorylated extracellular signal-regulated kinase (ERK) 1/2 in rat lung tissues were measured by Western immunoblot. Results: (1) The length of actin was decreased in CD and CD+LPS group compared Normal group, there is an decrease in CD+LPS group and increase in group P+LPS compared in LPS group (P <0.05). Three groups (P, P+LPS and N) had the similar results (P>0.05). (2) TNF-αmRNA was increased in CD, CD+LPS and LPS group compared with Normal group (P <0.05). But there is no difference between thegroup CD and CD+LPS, P and P+LPS. Also there is no difference between group CD and CD+LPS as well as group P and P+LPS (P >0.05). (3) The expression of ERK1/2 in lung tissue. To compare with Normal group, there is a significantly decrease in CD and LPS group (P <0.05). To compare with LPS group, the expression of P+LPS group was significantly decrease (P <0.05). Also, there is no difference between CD and CD+LPS group. Conclusions: Disrupion of actin may promote the synthesis and expression of TNF-αin rat with acute lung injury lung tissue via activation of ERK1/2 to enhance pulmonary inflammatory.
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