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Increased leucine-rich repeats and immunoglobulin- like domains 1 expression enhances chemosensitivity in glioma 被引量:1
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作者 Baohui Liu Qianxue Chen +12 位作者 Daofeng Tian Licluan Wu Junmin Wang Qiang Cai Heng Shen Baowei Ji Long Wang Shenqi Zhang Dong Ruan Xiaonan Zhu Zhentao Guo Huimin Dong mingmin yan 《Neural Regeneration Research》 SCIE CAS CSCD 2011年第32期2516-2520,共5页
Leucine-rich repeats and immunoglobulin-like domains 1 (LRIG1) is an anti-oncogene. LRIG1 is correlated with Bcl-2 in ependymomas. Decreased Bcl-2 and manganese superoxide dismutase expression can improve the chemos... Leucine-rich repeats and immunoglobulin-like domains 1 (LRIG1) is an anti-oncogene. LRIG1 is correlated with Bcl-2 in ependymomas. Decreased Bcl-2 and manganese superoxide dismutase expression can improve the chemosensitivity of glioma. In the present study, a tissue microarray of human brain astrocytomas was constructed. To investigate the relationship of LRIG1 with Bcl-2 and manganese superoxide dismutase, LRIG1, Bcl-2 and manganese superoxide dismutase expression in our tissue microarray was determined using immunohistochemistry. In addition, we constructed the LRIG1-U251 cell line, and its responses to doxorubicin and temozolomide were detected using the MTT assay. Results showed that LRIG1 expression was significantly negatively correlated with Bcl-2 and manganese superoxide dismutase expression in glioma. Also, proliferation of LRIG1-U251 cells exposed to doxorubicin or temozolomide was significantly inhibited, i.e. in the LRIG1-U251 cell line, the chemosensitivity to doxorubicin and temozolomide was increased. This indicates that increased LRIG1 expression produces a chemosensitivity in glioma. 展开更多
关键词 Leucine-rich repeats and immunoglobulin-like domains 1 astrocytoma CHEMOSENSITIVITY
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Schisandrin B protects PC12 cells by decreasing the expression of amyloid precursor protein and vacuolar protein sorting 35
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作者 mingmin yan Shanping Mao +4 位作者 Huimin Dong Baohui Liu Qian Zhang Gaofeng Pan Zhiping Fu 《Neural Regeneration Research》 SCIE CAS CSCD 2012年第9期652-658,共7页
PC12 cell injury was induced using 20 μM amyloid β-protein 25-35 to establish a model of Alzheimer's disease. The cells were then treated with 5, 10, and 25 μM Schisandrin B. Methylthiazolyldiphenyl-tetrazolium br... PC12 cell injury was induced using 20 μM amyloid β-protein 25-35 to establish a model of Alzheimer's disease. The cells were then treated with 5, 10, and 25 μM Schisandrin B. Methylthiazolyldiphenyl-tetrazolium bromide assays and Hoechst 33342 staining results showed that with increasing Schisandrin B concentration, the survival rate of PC12 cells injured by amyloid β-protein 25-35 gradually increased and the rate of apoptosis gradually decreased. Reverse transcription-PCR, immunocytochemical staining and western blot results showed that with increasing Schisandrin B concentration, the mRNA and protein expression of vacuolar protein sorting 35 and amyloid precursor protein were gradually decreased. Vacuolar protein sorting 35 and amyloid precursor protein showed a consistent trend for change. These findings suggest that 5, 10, and 25 μM Schisandrin B antagonizes the cellular injury induced by amyloid β-protein 25-35 in a dose-dependent manner. This may be caused by decreasing the expression of vacuolar protein sorting 35 and amyloid precursor protein. 展开更多
关键词 Schisandrin B PC12 cells amyloid β-protein 25-35 amyloid precursor protein vacuolar protein sorting 35 neural protection
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