2010.20
Publisher:liyzbs Publish Time:Thursday, December 02, 2010 Source:NRR |
| Research and Reports |
| Neurodegenerative Diseases and Neuroregeneration |
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Two potentially specific but relevant patterns of proteomic change: response of SH-SY5Y cells to differentiation with retinoic acid followed by phorbol ester 12-O-tetradecanoyl-phorbol-13-acetate, and susceptibility of differentiated cells to dopamine Neural Regeneration Research 2010;5(20): 1525 Mingxiu Tian, Xing'an Li, Ming Chang, Yingjiu Zhang, Danping Wang, Hongrong Xie, Linsen Hu Supported by:the Science and Technology Development Program of Jilin Province, No. 200505200*; the Distinguished Professor Foundation of Jilin University, No. 450011011204* |
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BACKGROUND: 1. Pharmacological model of Parkinson’s disease in SH-SY5Y differentiated cells was established, and dopamine neurotoxicity-induced protein expression changes were analyzed using differential proteome. 2. Influence of cell differentiation on protein expression was investigated at proteome level, and the effect of oxidative stress on protein expression was explored. 3. Based on influence of cell differentiation on protein expression and the effect of oxidative stress on protein expression, dopamine neurotoxicity was investigated. | | |
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Endoplasmic reticulum stress is involved in okadaic acid-induced tau phosphorylation and neurotoxic effects of okadaic acid Neural Regeneration Research 2010;5(20): 1534 Lijie Feng, Yuxian Shen, Aimin Sun, Yujun Shen, Shengyun Fang, Jun Li Supported by:he National Natural Science Foundation of China, No. 30772557*; 30870881* |
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BACKGROUND: 1. Present studies have found that ER stress participated in the pathological process of many nerve degenerative diseases. However, few studies have addressed ER stress and tau abnormal phosphorylation-induced neurotoxicity. 2. This study used immunofluorescence staining, RT-PCR and Western blot assay to determine relative protein mRNA and protein levels and cellular localization, and directly verified that OA can induce SH-SY5Y cell tau protein hyperphosphorylation and cytotoxicity. Moreover, ER stress may participate in this pathological process. | | |
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| Traditional Chinese Medicine and Neuroregeneration |
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Tanshinone IIa antagonizes spinal ischemia/reperfusion injury by interfering with upstream glutamic acid factor Neural Regeneration Research 2010;5(20): 1573 Li Zhang, Xiang Lin, Weinan Liu, Jianhua Lin Supported by:the National Natural Science Foundation of China, No.30572401*, No.30973765*; the Natural Science Foundation of Fujian Province, No.2008J0094*; the Science and Technology Activity of Abroad Scholars, Ministry of Personnel, No. [2006]164*; Scientific Research Foundation for Talents of Fujian Province, No. 1401* |
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BACKGROUND:1Previous studies focus on neuroprotective effect of tanshinone in rats. This study observed Glu transporter function and determined Na+-K+-ATPase activity in rats following ischemia/reperfusion injury to provide experimental data and evidence for tanshinone clinical application. 2This study utilized vascular casting and digital imaging techniques for the first time to establish and identify the model of spinal ischemia/reperfusion injury to investigate the effect of tanshinone, a Chinese drug that activates blood circulation to dissipate blood stasis, on spinal ischemia/reperfusion injury | | |
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