摘要
Previous studies have focused on the analysis of single or several function-related genes in oxidative stress; however, little information is available regarding altered expression of oxidative stress-related genes in the process of ischemia-reperfusion injury from microarray experiments. The aim of the present study was to investigate the changes in cell oxidative stress- and toxicity-related gene expression utilizing microarray screening in patients with acute cerebral infarction during cerebral ischemia-reperfusion injury. Of the included 114 genes, expression was significantly upregulated in eight genes, including three heat shock protein-related genes, one oxidative and metabolic stress-related gene, one cell growth arrest/senescence related gene, two apoptosis signal-related genes, and one DNA damage and repair related gene. Expression was significantly downregulated in four genes, including one cell proliferation/cancer related gene, two oxidative and metabolic stress-related genes and one DNA damage and repair related gene. The results demonstrated that cerebral ischemia-reperfusion injury in patients with acute cerebral infarction was affected by many genes including oxidative stress-, heat shock-, DNA damage and repair-, and apoptosis signal-related genes. Therefore, it could be suggested that cerebral ischemia-reperfusion injury may be subjected to complex genetic regulation mechanisms.
Previous studies have focused on the analysis of single or several function-related genes in oxidative stress; however, little information is available regarding altered expression of oxidative stress-related genes in the process of ischemia-reperfusion injury from microarray experiments. The aim of the present study was to investigate the changes in cell oxidative stress- and toxicity-related gene expression utilizing microarray screening in patients with acute cerebral infarction during cerebral ischemia-reperfusion injury. Of the included 114 genes, expression was significantly upregulated in eight genes, including three heat shock protein-related genes, one oxidative and metabolic stress-related gene, one cell growth arrest/senescence related gene, two apoptosis signal-related genes, and one DNA damage and repair related gene. Expression was significantly downregulated in four genes, including one cell proliferation/cancer related gene, two oxidative and metabolic stress-related genes and one DNA damage and repair related gene. The results demonstrated that cerebral ischemia-reperfusion injury in patients with acute cerebral infarction was affected by many genes including oxidative stress-, heat shock-, DNA damage and repair-, and apoptosis signal-related genes. Therefore, it could be suggested that cerebral ischemia-reperfusion injury may be subjected to complex genetic regulation mechanisms.
基金
the National Natural Science Foundation of China,No.30070829
