The Current Status and Research Progress of Antiviral Therapy in HCV-Associated Lymphoma --Review / 中国实验血液学杂志

Hepatitis C virus (HCV) is one of the leading causes of chronic liver disease. HCV is not only related to hepatic malignancies but may also promote lymphoid neoplasms. Currently, research has confirmed HCV-related lymphoma, including marginal zone lymphoma (MZL), lymphoplasmacytic lymphoma (LPL), follicular lymphoma (FL), diffuse large B-cell lymphoma (DLBCL), and Burkitt lymphoma (BL). Many types of research have shown that antiviral therapy can improve or even remission several HCV-related lymphomas. The direct-acting antiviral agents (DAAs) (such as NS5A protease inhibitors, NS4/4A protease inhibitors and viral polymerase inhibitors) have shown clinical advantages of high efficacy and low side effects for both virus elimination and tumor regression in several HCV-related lymphomas, which may make the selected HCV-related lymphoma patients treated without chemotherapy. In this review the research progress and development direction of antiviral therapy in treating HCV-related lymphoma has summarized briefly.

Effect of butylphthalide on the expression of GFAP and VEGF in the hippocampus of rats with (Alzheimer's) disease / 中南大学学报(医学版)

Objective To determine the expression of glial fibrillary acidic protein(GFAP) and vascular endothelial growth factor(VEGF) in the hippocampus of rats with Alzheimer's disease(AD), and to determine the effect of butylphthalide on them and its significance. Methods Sixty male adult rats were randomly divided into a model group, a Butylphthalide group, and a control group. AD models were established by injecting β-amyloid protein 1-42 into the hippocampus of rats. Sixty days later,the rats were sacrificed and both sides of the hippocampus were sectioned for immunohistochemistry. Results Positive cells of GFAP in the hippocampus of the model group increased and the expression of VEGF decreased statistically, compared with the control group(P<0.01). The positive cells of GFAP in the hippocampus of the butylphthalide group decreased and the expression of VEGF increased significantly, compared with the model group(P<0.05). Conclusion Butylphthalide may protect the neuron-vascular unit of the hippocampus of Alzheimer model rats by inhibiting the expression of GFAP and increasing the expression of VEGF.

Butylphthalide improves learning and memory abilities of rats with Alzheimer's disease possibly by inhibiting P38 mitogen-activated protein kinase and enhancing extra-cellular signal regulated kinase expressions / 南方医科大学学报

<p><b>OBJECTIVE</b>To determine the effect of butylphthalide on the expressions of p38 mitogen-activated protein kinase and extra-cellular signal regulated kinases (ERKs) in the brain tissue of rats with Alzheimer's disease (AD).</p><p><b>METHODS</b>Sixty male adult rats were randomly divided to AD model group, butylphthalide group, and control group (n=20). AD models were established by injecting beta-amyloid protein 1-42 into the hippocampus of rats. Sixty days later, the learning and memory abilities of the rats were evaluated using Y-maze test, and the expressions of p38 and ERKs in the brain tissue of the rats were measured by immunohistochemistry. RESULTS Compared with the control group, the rats in AD model group exhibited significantly reduced learning and memory abilities, increased expressions of P38 in the hippocampus and lowered expression of ERK in the cortex (P<0.01). In comparison with the model group, the rats in the butylphthalide group showed significantly decreased P38-positive cells in the hippocampus and increased expression of ERK in the cortex (P<0.01).</p><p><b>CONCLUSIONS</b>Butylphthalide improves the learning and memory abilities of rats with experimental AD, the mechanism of which may involve inhibition of P38 expression and enhancement of ERK expression in the brain tissues.</p>

Effect of butylphthalide on the expression of S100 and glial fibrillary acidic protein in a rat model of Alzheimer disease / 南方医科大学学报

<p><b>OBJECTIVE</b>To determine the expression of S100-beta protein and glial fibrillary acidic protein (GFAP) in hippocampal astrocytes of rats with Alzheimer disease (AD) model rats, and observe the effect of butylphthalide on their expression.</p><p><b>METHODS</b>Sixty male adult rats were randomized equally into model group, butylphthalide group, and control group, and in the former two groups, AD models were established by injecting beta-amyloid protein 1-40 into the hippocampus. Sixty days later, the rats were sacrificed and the bilateral hippocampuses were taken for immunohistochemistry.</p><p><b>RESULTS</b>The number of cells positive for S100 and GFAP in the hippocampus in butylphthalide group were significantly higher than that in the control group (P/0.01), but lower than that in the model group (P/0.05).</p><p><b>CONCLUSION</b>The expression of S100 protein and glial fibrillary acidic protein increased significantly in the hippocampal astrocytes of rats with AD, and butylphthalide can inhibit the increase of their expression.</p>