王彦青
痛和针刺镇痛机理研究
个性化签名
- 姓名:王彦青
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学术头衔:
博士生导师,
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学科领域:
中西医结合医学
- 研究兴趣:痛和针刺镇痛机理研究
王彦青,女,副教授,1970年出生于山东省。1992年毕业于上海医科大学药学院药理专业,1995毕业于上海医科大学医学神经生物学国家重点实验室获得硕士学位并留校任教,1996年起读在职博士研究生,于2000年毕业获得博士学位。2000-2002年获得日本科学技术振兴会特别研究员计划资助(STA Fellowship),在日本千叶癌症中心研究所做博士后研究。2002-2003年在复旦大学上海医学院中西医结合系针灸神经生物学实验室任教。研究生期间起长期从事痛和针刺镇痛机理研究,发表多篇论文。在日本进修期间,研究化学趋化因子Mig及新发现的白细胞介素23(IL-23)的抗肿瘤作用及其免疫学机理等,发表多篇论文并申请中国专利两项。回国后建立转移性骨癌痛和皮肤癌痛模型,研究癌痛和针刺镇痛机理,取得初步进展。先后获得复旦大学“世纪之星”称号(2003)、教育部新世纪优秀人才支持计划资助(2004),负责国家自然科学基金资助项目一项。参加国家自然科学基金重点项目(2004)和973计划各一项(2005)。
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成果数
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王彦青, WANG Yan-Qing, CAO Xiao-Ding, LI Kuan-Yan, WU Gen-Cheng
中国药理学报,1997 Nov; 18 (6): 494-496,-0001,():
-1年11月30日
研究多巴胺受体拮抗剂左旋四氢巴马汀(l2THP)加强电针镇痛(EAA)的原理,阐明中枢神经系统内多巴胺(DA) 系统在EAA中的作用。方法:分别将D1受体激动剂SK&F-38393和D2受体激动剂quinpirole hydrochloride(Qui)注射入大鼠伏膈核,观察对EAA及ι-THP加强EAA的作用。结果:SK&F-38393(5μg,10μg)明显对抗了ι-THP加强EAA的作用,10μgSK&F-38393则减弱EAA;Qui(10μg,20μg)对EAA及ι-THP加强EAA的作用没有显著影响。结论:伏膈核内D1受体活动在EAA及ι-THP加强EAA中起重要作用,D2受体没有显著作用。
电针镇痛, 伏膈核, SK&, F-38393, 喹吡罗, 左旋四氢巴马汀, 多巴胺D1 受体, 多巴胺D2受体
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王彦青, YANQING WANG, , MIKA SEIMIYA, KIYOKO KAWAMURA, LING YU, TOMOO OGI, KEIZO TAKENAGA, TOMOTANE SHISHIKURA, AKIRA NAKAGAWARA, SHIGERU SAKIYAMA, MASATOSHI TAGAWA and JIYANG O-WANG
INTERNATIONAL JOURNAL OF ONCOLOGY 25: 161-165, 2004,-0001,():
-1年11月30日
DNA polymerase κ (POLκ) is a low fidelity translesional DNA polymerase implicated in spontaneous and DNA damage-induced mutagenesis. We have previously shown that POLκ was frequently overexpressed in human lung cancer tissues as compared with their matched nontumorous tissue counterpart. In the present study, we found a close correlation between elevated POLκ expression and p53 inactivation in lung cancer tissues. To investigate whether POLK expression might be regulated by p53, we have determined the transcriptional initiation site of POLK gene and examined its promoter activity in A549, H358-129, and PC-3 human lung cancer cell lines. Wild-type p53, but not a mutant p53 (R273H) devoid of the DNA-binding activity, strongly inhibited POLK promoter activity in these cells. In addition, POLK promoter exhibited a significantly higher activity in p53-/- murine embryo fibroblasts (MEF) than in p53+√- and p53+√+ MEF. These results link p53 status with POLκ expression and suggest that loss of p53 function may in part contribute to the observed POLκ upregulation in human lung cancers.
DNA polymerase κ,, p53,, trans, c, r, i, p, t, ion,, lung cancer
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【期刊论文】INDUCTION OF SYSTEMIC IMMUNITY BY EXPRESSION OF INTERLEUKIN-23IN MURINE COLON CARCINOMA CELLS
王彦青
,-0001,():
-1年11月30日
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【期刊论文】INDUCTION OF SYSTEMIC IMMUNITY BY EXPRESSION OF INTERLEUKIN-23 IN MURINE COLON CARCINOMA CELLS
王彦青, Yan-Qing WANG, , Shin-ichi UGAI, Osamu SHIMOZATO, Ling YU, Kiyoko KAWAMURA, Hiroshi YAMAMOTO, Taketo YAMAGUCHI, Hiromitsu SAISHO and Masatoshi TAGAWA*
Int. J. Cancer: 105, 820-824 (2003),-0001,():
-1年11月30日
Interleukin-23 (IL-23), a novel cytokine composed of a newly identified p19 molecule and the p40 subunit of IL-12, can stimulate the proliferation in vitro of memory T cells. We examined whether Colon 26 murine colon carcinoma cells that were retrovirally transduced with the p19-linked p40 gene (Colon 26/IL-23) could produce antitumor effects in inoculated mice. The growth of Colon 26/IL-23 tumors developed in immunocompetent mice was significantly retarded and the tumors disappeared thereafter. Spleen cells from the mice that received Colon 26/IL-23 cells produced significant amounts of interferon-γ, when they were cultured with irradiated Colon 26 but not irrelevant cells. Depletion of CD8+T cells suppressed the production of interferon-γ. The mice that had rejected Colon 26/IL-23 tumors were resistant to subsequent challenge of parent but not irrelevant tumor cells. Colon 26/IL-23 tumors were not rejected in nude mice but the growth was retarded compared to parent tumors. Treatment of nude mice with anti-asialo GM1 antibody did not influence the growth of Colon 26/IL-23 tumors. These data suggest that expression of IL-23 in tumors produces T cell-dependent antitumor effects and induces systemic immunity.
IL-23, gene therapy, protective immunity, colon carcinoma, IFN-γ
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王彦青, YAN-QING WANG, , AKIHIKO WADA, SHIN-ICHI UGAI, and MASATOSHI TAGAWA
ONCOLOGY REPORTS 10: 909-913, 2003,-0001,():
-1年11月30日
We examined whether expression of monokine induced by IFN-γ(Mig, CXCL9) in tumors could produce antitumor effects. Murine lung carcinoma cells (A11) were retrovirally transduced with the murine Mig gene (A11/Mig) and were inoculated into syngeneic mice. Although proliferation in vitro of A11/Mig cells was not different from that of parent cells, the growth in vivo of A11/Mig tumors was significantly retarded compared with that of parent tumors. The antitumor effect was dependent on the amount of Mig produced. We compared the expression level of marker genes of lymphocytes and endothelial cells between parent and A11/Mig tumor masses with reverse transcription-polymerase chain reaction. Expression of CD4, CD8α, CD40, CD86, CD28, CD31 and vascular endothelial growth factor was not different between the two tumor groups but expression of CD40 ligand, CD80, NK1.1 and CXCR3 was relatively lower in A11/Mig tumors. Although Mig is a chemotactic factor for activated T and NK cells and an inhibitor for angiogenesis, the present data suggested that production of Mig in tumors did not recruit activated T and NK cells efficiently or suppress angiogenesis. The antitumor effects by Mig could be independent of anti-angiogenesis and recruitment of T and NK cells.
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王彦青, Yan-Qing Wang, Jin-Lan Wang, Chong-Bin Zhu, Xiao-Ding Cao, Gen-Cheng Wu*
Neuroscience Letters 290(2000)193-196,-0001,():
-1年11月30日
Opioid receptor like 1 (ORL1) receptor is a novel member of the opioid receptor family, which was not bound by any of the typical opioid receptor ligands but bound by the recently discovered nociceptin (also termed orphanin FQ) with high af
ORL1 receptor, mRNA, Nociceptin, Autoreceptor, Rat brain
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王彦青, Yan-Qing Wang, Chong-Bin Zhu, Xiao-Ding Cao, Gen-Cheng Wu*
European Journal of Pharmacology 376(1999)R1-R3,-0001,():
-1年11月30日
[Phe1ψ(CH2-NH) Gly2 nociceptin-(1-13)-NH2, a pseudopeptide analog of nociceptin, was originally seen as an antagonist of nociceptin receptors. In the present study, it was observed that intracerebroventricular (i. c. v.) injection of this pseudopeptide (1, 5, 10μg) significantly decreased the tail-flick latency of rats, indicating a hyperalgesic effect, while intrathecal (i. t.) injection of it (1, 2.5, 10μg) dramatically increased the tail-flick latency, indicating an analgesic effect. This strengthened the in vivo evidence that [Phe1ψ(CH2-NH) Gly2] nociceptin-1-13-NH might be an agonist of nociceptin receptors.
Nociceptin pseudopeptide analog, Hyperalgesia, Analgesia
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【期刊论文】Effects of orphanin FQ on endomorphin-1 induced analgesia
王彦青, Yan-Qing Wanga, Chong-Bin Zhua, Gen-Cheng Wua, *, Xiao-Ding Caoa, Yan Wangb, Da-Fu Cuib
Brain Research 835(1999)241-246,-0001,():
-1年11月30日
Orphanin FQ (also known as nociceptin) is a 17-amino-acid peptide which acts as a potent endogenous agonist of the orphan opioid receptor-like (ORL1) receptor. Endomorphin-1, a 4-amino-acid peptide discovered recently, is a potent and selective endogenous agonist for the m-opiate receptor. In the present study, the effect of OFQ orrand endomorphin-1 on the response to noxious thermal stimuli was observed using the tail-flick test in rats. Intracerebroventricular (i. c. v.) administration of OFQ (1,5μg) could shorten tail-flick latency; In contrast, intrathecal (i. t.) administration of OFQ (1, 2 or 10μg) could increase the latency; i. c. v. (1, 2, 5μg) or i. t. (0.2, 2, 5μg) administration of endomorphin-1 dose-dependently increased the latency, indicating an analgesic effect. Furthermore, OFQ (0.1-5μg) when intraventricularly injected together with endomorphin-1 (5μg), could dose-dependently reverse the analgesia induced by the latter. On the contrary, OFQ (1μg) intrathecally injected together with endomorphin-1 (0.2μg) could further increase the tail-flick latency. The results showed that OFQ at the supraspinal level produces hyperalgesia and is antagonistic to endomorphin-1, while at the spinal level it produces analgesia and is synergic with endomorphin-1. Different interaction mechanism between OFQ and endomorphin-1 in the brain and the spinal cord is thus suggested. © 1999 Elsevier Science B. V. All rights reserved.
Hyperalgesia, Analgesia, Endomorphin-1, m-opiate receptor, Orphanin FQ, ORL1 receptor
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