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The biological characteristics of colorectal adenomas with CSM were different from those of colorectal adenomas without CSM. Colorectal adenomas with CSM exhibited active cell proliferation and inhibition of apoptotic pathways, suggesting an increased risk of carcinogenesis in these adenomas.

The aim of the present study was to successfully construct a recombinant adeno-associated virus (rAAV) vector containing the human thioredoxin (hTRX)-PR39 chimeric gene (rAAV/hTRX-PR39), and verify that the vector was able to maintain a sustained, stable and efficient expression to achieve protein production in the cell. In the present study, a chicken embryo model was utilized to analyze the therapeutical effect of rAAV/hTRX-PR39 in cerebral ischemia diseases. ECV304 cells were transfected with rAAV/hTRX-PR39 and incubated under conditions of 20, 5 and 1% O. Subsequently, the expression levels of vascular endothelial growth factor (VEGF), vascular endothelial growth factor receptor (VEGFR)-1, VEGFR-2, fibroblast growth factor receptor (FGFR)-1 and syndecan-4 were detected by reverse transcription-quantitative polymerase chain reaction. Under hypoxic conditions, the mRNA expression levels of VEGF, VEGFR-1, VEGFR-2, FGFR-1 and syndecan-4 were found to increase in the PR39-transfected group when compared with the control group, while no statistically significant difference was observed between the PR39-transfected group and the control group under conditions of 20% O. In addition, hTRX-PR39 was shown to increase the density of the vasculature and the survival rate of the chick embryos. Under hypoxic conditions, it was hypothesized that rAAV/hTRX-PR39 was capable of promoting angiogenesis, which may subsequently protect the cells from impairment by hypoxia. In conclusion, rAAV/hTRX-PR39 was demonstrated to promote vascularization and cell survival in hypoxia; thus, rAAV/hTRX-PR39 may have potential for use in therapy targeting cerebral ischemia.

The recombinant adeno-associated virus human thioredoxin-PR39 (rAAV/hTRX-PR39) has been demonstrated to have a protective effect on hypoxic cells. The present study aimed to explore the potential effect of rAAV/hTRX-PR39 on acute cerebral infarction in rats. Middle cerebral artery occlusion (MCAO) model rats were produced and divided into three groups: Normal saline group, empty virus group (rAAV, without hTRX-PR39 cDNA) and rAAV/hTRX-PR39 group. Hematoxylin and eosin staining and electron microscopy observation were used to assess the morphological changes of ischemic brain tissue during different periods. Immunohistochemistry was employed to detect the expression of CD34 to reflect angiogenesis of ischemic brain tissue. Rats treated with rAAV/hTRX-PR39 showed an alleviated degree of ischemic brain edema relative to that in control groups, suggesting PR39 can ameliorate brain damage after cerebral ischemia. In the rAAV/hTRX-PR39 group, CD34-positive cells were significantly increased in ischemic brain tissues compared to control groups. Furthermore, CD34-positive cells were primarily observed around the perivascular in ischemic brain, indicating the angiogenesis role of PR39 in ischemic brain. The present findings suggest that PR39 could effectively ameliorate ischemic brain damage and promote angiogenesis, which may contribute to the treatment of acute cerebral infarction.