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Purpose To clarify the effect of adenosine on brain metastasis of lung cancer and the possible mechanism of adenosine promoting brain metastasis of lung cancer. Methods Western blot was used to dynamically detect the expression level of hypoxia inducible factor-1 (HIF-1) in lung cancer cells and tight junction protein ZO-1 in brain microvascular endothelial cells on blood-brain barrier. The content of adenosine in lung cancer cell culture was determined by ELISA. Fluorescence analysis was used to detect the changes of permeability of the blood-brain barrier model in vitro. Hemocytometer counts the number of A549 lung cancer cells in Transwell's lower chamber. Results The expression level of HIF-1 in lung cancer cells and the content of adenosine in lung cancer cell culture reached the highest level when lung cancer cells were deprived of oxygen for 12 hours. At the same time, the expression level of ZO-1 protein in the blood-brain barrier was the lowest, the blood-brain barrier permeability was the highest (7.11), and the number of lung cancer cells passing through the blood-brain barrier model was the highest (84.6). The permeability of the blood-brain barrier model increased after the action of adenosine, and its change trend was consistent with the effect of hypoxic lung cancer cell culture solution. Conclusion Hypoxia can induce the lung cancer cell to release adenosine, the increased adenosine can reduce the expression of tight junction protein ZO-1 in blood brain barrier, which leads to the increase of permeability of blood-brain barrier and eventually lead to brain metastasis of lung cancer.
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<p><b>AIM</b>To study the protective mechanism of HSP70 induced by the heat stress pretreatment on the hepatic ischemia/ reperfusion (I/R) injury.</p><p><b>METHODS</b>To establish the models of the hepatic ischemia/ reperfusion injury using pringle's maneuver with or without heat stress pretreatment. The rats were randomly divided into pretreatment group (HP + I/R) and non-pretreatment group (I/R), in which the expression of HSP70, the MDA contents and SOD activity in liver, the activities of serum AST and ALT, and the pathological changes in liver were detected at 0, 4, 8, 12 and 24 h after I/R.</p><p><b>RESULTS</b>At any time point set after I/R, the SOD activity in the liver in HP + I/R group were higher than those in IR group, HSP70 expression maximum was attained at 12 h after heat pre-treatment. While in HP+ I/R group the levels of liver enzymes and the production of MDA significantly reduced and the pathological changes improved compared with those in I/R group.</p><p><b>CONCLUSION</b>HSP70 induced by heat pretreated protecting liver against I/R injury may be through increasing the SOD content and then reducing the insults of oxygen free radicals in the liver.</p>