沈玉先
个性化签名
- 姓名:沈玉先
- 目前身份:
- 担任导师情况:
- 学位:
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学术头衔:
教育部“新世纪优秀人才支持计划”入选者, 博士生导师
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学科领域:
药物化学
- 研究兴趣:
沈玉先,1989毕业于安徽医科大学医学系,1992年获药理学硕士学位,2000年获药理学博士学位。2003~2004在美国马利兰大学生物技术研究所做博士后。现为安徽医科大学教授,博士生导师。2000年获第四届中国药理学会Servier青年药理学工作者奖,2003年被评为安徽省拔尖人才,2004年入选教育部“新世纪优秀人才支持计划”。主要学术兼职:中国药理学会抗炎免疫专业委员会委员、Journal Pharmacological Science编委、中国药理学通报编辑、Free Radical Bio Med, Neurosci Res,J Pharm Pharmacol, Arch Med Res, Acta Pharmacol Sin, Medical Science Monitor等期刊的审稿人。发表专业论文80余篇,其中SCI源论文30余篇。目前承担的课题有国家自然科学基金、教育部人才基金、教育部重点项目、安徽省科技攻关、安徽省优秀人才基金等。作为主要研究人员参与国家973项目的研究。参编大型参考书4部如《药理实验方法学》、《中华临床药物学》(编委)、《治疗学的药理学基础》等。
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成果数
13
【期刊论文】The ubiquitin ligase Hrd1 promotes degradation of the Z variant
沈玉先, Haiping Wang, Qi Li, Yujun Shen
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-1年11月30日
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【期刊论文】Induction profile of MANF/ARMET by cerebral
沈玉先, Yong-Qiang Yu, Lian-Cheng Liu, Fa-Cai Wang, Yan Liang, Da-Qin Cha
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-1年11月30日
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沈玉先, Yong-Qiu Zheng, Wei Wei, Yu-Xian Shen, Min Dai, Li-Hua Liu
Copyright ,-0001,():
-1年11月30日
To investigate the curative effects of oral and nasal administration of chicken type II collagen (CII) on adjuvant arthritis (AA) in rats with meloxicam-induced intestinal lesions.
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沈玉先, Hua Wang, Wei Wei, Yu-Xian Shen, Chen Dong, Ling-Ling Zhang, Ni-Ping Wang, Li Yue, Shu-Yun Xu
Copyright ,-0001,():
-1年11月30日
To investigate the effects and mechanisms of melatonin on immunological liver injury in mice.
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沈玉先, Xiaoyan Zhong‡, Yuxian Shen‡, Petek Ballar‡, Andria Apostolou‡, Reuven Agami§, and Shengyun Fang‡¶
Vol. 279, No. 44, Issue of October 29, pp. 45676-45684, 2004,-0001,():
-1年11月30日
Endoplasmic reticulum-associated degradation (ERAD)is a protein quality control mechanism that eliminates unwanted proteins from the endoplasmic reticulum (ER) through a ubiquitin-dependent proteasomal degradation pathway. gp78 is a previously described ER membrane-anchored ubiquitin ligase (E3) involved in ubiquitination of ER proteins. AAA ATPase (ATPase associated with various cellular activities) p97/valosincontaining protein (VCP) subsequently dislodges the ubiquitinated proteins from the ER and chaperones them to the cytosol, where they undergo proteasomal degradation. We now report that gp78 physically interacts with p97/VCP and enhances p97/VCP-polyubiquitin association. The enhanced association correlates with decreases in ER stress-induced accumulation of olyubiquitinated proteins. This effect is abolished when the p97/VCP-interacting domain of gp78 is removed. Further, using ERAD substrate CD3, gp78 consistently enhances p97/VCP-CD3 binding and facilitates CD3 degradation. Moreover, inhibition of endogenous gp78 expression by RNA interference markedly increases the levels of total polyubiquitinated proteins, including CD3, and abrogates VCP-CD3 interactions. The gp78 mutant with deletion of its p97/VCP-interacting domain fails to increase CD3 degradation and leads to accumulation of polyubiquitinated CD3, suggesting a failure in delivering ubiquitinated CD3 for degradation. These data suggest that gp78-p97/VCP interaction may represent one way of coupling ubiquitination with retrotranslocation and degradation of ERAD substrates.
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沈玉先, Li YUE, Hua WANG, Li-hua LIU, Yu-xian SHEN, Wei WEI
Yue Let al/Acta Pharmacol Sin 2004 Sep; 25(9):1182-1185,-0001,():
-1年11月30日
To investigate the profile of endostatin on adjuvant arthritis (AA) and angiogenesis blockade in synovitis. METHODS: The model of rat AA was induced by injection of intradermal complete Freund's adjuvant (CFA). Hind paw volume of rat was measured by volume meter and the activities of interleukin-1 (IL-1) and IL-2 were measured by the assay of thymocytes proliferation. IL-1β and tumor necrosis factor-α (TNF-α) produced by synoviocytes was estimated with radioimmunoassay. The number of new blood vessels in knee joint synovium was counted under microscope by hematoxylin and eosin (HE) staining. RESULTS: The secondary inflammation of AA rats appeared on the 10th day after injection of CFA. The therapeutic administration of endostatin (0.1, 0.5, and 2.5mg·kg-1·d-1, sc, ×7d) was given from that time (d 10). It was found that endostatin significantly inhibited the secondary paw swelling and the number of new blood vessels in the synovium of AA rats. Endostatin significantly decreased the production of IL-1 derived from both peritoneal macrophages and synoviocytes and IL-2 from splenocytes, especially at the dose of 2.5mg/kg. This effect of endostatin also was seen on TNF-α produced by synoviocytes. CONCLUSION: The recombinant human endostatin had an inhibitory effect on rat AA, which was related to its anti-angiogenesis and inhibition of proinflammatory cytokines.
rats, experimental arthritis, endostatin, angiogenesis inhibitors, cytokines
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沈玉先, DAI Min, WEI Wei, SHEN Yu-Xian, ZHENG Yong-Qiu
Dai Met al/Acta Pharmacol Sin 2003 Nov; 24(11):1161-1166,-0001,():
-1年11月30日
To investigate the effects of Glucosides of Chaenomeles speciosa (GCS) on rat adjuvant arthritis (AA) and to clarify the role of synoviocytes in this process. METHODS: Complete Freund's adjuvant was used to induce AA in rats. Secondary paw swelling of AA rats was measured with MK-550 volume meter. The pain response and polyarthritis index were scored. Synoviocytes were separated by incubation of collagenase and trypsin, and morphological changes of synoviocytes were observed by transmission electron microscope. Interleukin-1 (IL-1) production was measured by thymocyte proliferation assay. Tumor necrosis factor (TNFα) and prostaglandin E2 (PGE2) production were determined by radioimmunoassay. RESULTS: There were significant secondary inflammatory reactions in AA rats. The morphology of synoviocytes from AA rats was changed, companying the elevation of the level of IL-1,TNFα, and PGE2 produced by synoviocytes from AA rats. GCS (60 and 120 mg/kg, ig, 8d) suppressed secondary inflammatory paw swelling, pain response, and polyarthritis index. It also improved ultrastructural changes of synoviocytes and inhibited IL-1,TNFα, and PGE2 production in AA rats. The inhibitory effect of GCS 120mg/kg was more evident than that of Actarit 60 mg/kg. CONCLUSION: GCS reduced the secondary inflammatory in AA rats, which is associated with prevention of ultrastructural changes of synoviocytes and inhibition of secretion of proimflammatory cytokines.
Chaenomeles speciosa, glucosides, immunologic adjuvants, experimental arthritis, synovial membrane, interleukin-1, tumor necrosis factor, prostaglandins E
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【期刊论文】Effects and mechanisms of melatonin on immune responses in mice of different months
沈玉先, WEI Wei, SHEN Yu-Xian, DAI Min, CHEN Qun
Wei Wet al/Acta Pharmacol Sin 2003 Jul; 24(7):719-723,-0001,():
-1年11月30日
To study the effects and mechanisms of melatonin (MT) on immune responses in mice of different months. METHODS: Thymocyte proliferation and IL-2 activity were assayed by 3-(4,5-dimethylthiazol-2-yl) 2,5-diphenyltetrazolium bromide (MTT) and activated mouse splenocyte proliferation methods, respectively; cAMP and methionine-enkephalin (met-Enk) level was determined by competitive protein binding assay and radioimmunoassay, respectively. RESULTS: The function of lymphocytes, obtained from BALB/c mice aged 6 and 11 months were decreased, which was restored by melatonin at the dose of 5 mg/kg or 30 mg/kg. In vitro, proliferation of lymphocytes in 11-month-old mice was decreased and cAMP level was increased. Melatonin (0.1nmol/L or 1mmol/L) had negative regulation to this. Forskolin (10 mmol/L) enhanced the cAMP level of lymphocytes in 2-and 11-month-old mice (P<0.01), which was antagonized partially by melatonin and this effect of melatonin was also abolished by pertussis toxin (1mg/L) completely. Melatonin (1mmol/L and 0.1nmol/L) increased the content of met-Enk of lymphocytes in 2-and 11-month-old mice, respectively (P<0.01), which was blocked by nifedipine (1 mmol/L). CONCLUSION: Melatonin exerted an effect on immune responses in mice of different months, which might be mediated by G protein-AC-cAMP signal transduction pathway and regulation of met-Enk level.
melatonin, immunity, GTP-binding proteins, cyclic AMP, enkephalins
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【期刊论文】Melatonin reduces memory changes and neural oxidative damage in mice treated with D-galactose
沈玉先, Yu-Xian Shen, Shu-Yun Xu, Wei Wei, Xiu-Xia Sun, Jun Yang, Li-Hua Liu and Chen Dong
J. Pineal Res. 2002; 32: 173-178,-0001,():
-1年11月30日
To investigate the role of melatonin in D-galactose-induced amnesic mice, the avoidance/escape and water maze tests were performed to evaluate their learning and memory function. Spectrophotometry was employed to determine the content of thiobarbituric acid-reactive substances (TBARS) and the activities of antioxidative enzymes in the brain. The present results demonstrate that D-galactose-induced amnesic mice had signir cantly decreased learning and memory function. The reduced activities of superoxide dismutase and glutathione peroxidase and increased levels of TBARS were found in brain tissue of the amnesic mice. Melatonin, administered (ig) at doses of 0.1, 1, or 10mg/kg to the D-galactose-treated mice for 3 months, was su
antioxidative enzymes,, D-galactose,, free radicals,, learning and memory,, melatonin
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沈玉先, SHEN Yu-Xian, WEI Wei, XU Shu-Yun
2002 Jam 23(1):71-76,-0001,():
-1年11月30日
To study the effects of melatonin on primary rat cortico-hippocampal neurotoxicity induced by amyloid beta-peptide 25-35. METHODS: The neuronal mor-phology was observed by phase-contrast microscopy. The iw.urotoxieity was quantitatively estimated by measur-ing laclate duhydrogenase (LDH) released into the culture medium from the damaged neurons. The neuronal metabolic state was quantified by the reduction of 3-[4,5-dimethylthiazol-2-yl]-2, 5-diphenyltetrazo1ium bromide (MTr). RESULTS: Treatment ofprimary rat cortico-hipocampal neuonns with amyloid beta-peptide 25-35 (20 μmol/L) for 24h caused a significant decrease in neurocyte viability (P<0.01, compared with control). Melatonin (1 or 10 μmol/L) reduced the neurotoxicity induced by amyloid beta-peptidu 25-35. CONCLU-SION: Amyloid beta-peptide 25-35 could exert direct cytotoxicity on rat cortico-hippocampal neurocytes and melatonin concerdration-dependently rescued cultured neurons from exposure to amyloid beta-peptide 25-35 induced injury.
melatonin, neurons, amyloid beta-protein, lactate dehydrogenase
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