郭青龙
一直从事肿瘤药理学的研究工作
个性化签名
- 姓名:郭青龙
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学术头衔:
博士生导师,
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学科领域:
药物化学
- 研究兴趣:一直从事肿瘤药理学的研究工作
郭青龙,中国药科大学生理教研室主任、硕士生导师,多年来一直从事肿瘤药理学的研究工作,所领导的抗肿瘤药物研发实验室已经建立一套较为完善的抗肿瘤药物研究平台,由用于初步筛选的荷瘤小鼠药效学平台,到机理研究用的细胞学平台和含有基因到蛋白至蛋白活性研究的分子生物学研究平台。经过十多年积累,与相关同仁通力合作,研究开发出国家一类抗肿瘤新药藤黄酸,并对其抗肿瘤作用机理进行深入、全面而广泛的研究,发表数篇SCI相关论文。
近几年进行了大量肿瘤相关科研工作,承担多项重大科研项目,包括国家科技部“863计划”3项,国家自然科学基金1项,国家教育部重大专项1项,国家中药管理局基金项目2项,江苏省科技厅重点基金1项,江苏省科技厅三药基金2项及抗肿瘤药物的制药企业委托项目16项,申请多项专利。
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11
郭青龙, GUO Qing-Long*, ZHAO Li, WU Zhao-Qiu, YOU Qi-Dong, YU Gang, ZHANG Qing
中国天然药物,2003,1(4):229~332,-0001,():
-1年11月30日
目的:研究藤黄酸(THS)对实验性动物造血及免疫功能的影响,以验证该药的主要毒副作用。方法:以荷瘤小鼠外周血中白细胞数,正常大鼠体重增长、胸腺及脾脏系数、外周血中白细胞数和骨髓有核细胞数,正常小鼠的血清半数溶血值(HC50)及吞噬指数 等为指标,观察药物的毒副作用。结果:THS iv(8,4,2 ms/kg)对荷瘤小鼠外周血中白细胞总数无明显影响;THS iv(6,3,1.5ms/kS)对正常大鼠外周血中白细胞总数、骨髓有核细胞数、体重、胸腺及脾脏无明显影响;THS iv(8,4,2ms/ks)对小鼠的血清溶血素及巨噬细胞吞噬能力无明显影响。结论:在有效剂量范围内,THS对实验性动物造血功能及免疫功能无明显影响。
藤黄酸, 荷瘤, 小鼠大鼠, 造血功能, 免疫功能
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【期刊论文】藤黄酸促进bax和p53表达诱导人肝癌细胞SMMC-7721凋亡
郭青龙, GU Hong-Yan, GUO Qing-Long*, YOU Qi-Dong, LIU Wei, QI Qi, ZHAO Li, YUAN Sheng-Tao, ZHANG Kun
中国天然药物,2005,3(3):168~672,-0001,():
-1年11月30日
目的:观察藤黄酸(gambogic acids, GA)对肝癌细胞凋亡的诱导作用并探讨其分子作用机制。方法与结果:采用MTT比色法检测藤黄酸对人肝癌和人正常肝细胞增殖作用的影响,结果表明,藤黄酸对人肝细胞性肝癌SMMC27721细胞株和QGY27701细胞株有明显增殖抑制作用,并呈剂量依赖性,而对正常人肝组织L202细胞株作用相对较弱;光镜及电镜形态学观察结果显示,给予GA后,肝癌细胞发生明显的细胞凋亡形态学变化,如细胞体积变小,细胞核固缩,出现凋亡小体等;采用RT2PCR和Western blotting方法检测bax mRNA以及bax和p53蛋白表达变化,结果表明GA可诱导bax mR2NA及bax和p53蛋白表达上调;琼脂糖凝胶电泳显示,给予GA后,SMMC-7721裸小鼠移植瘤组织呈现典型的DNA ladder电泳梯状条带。结论:藤黄酸可显著抑制人肝癌细胞的增殖,其分子作用机制可能通过促进bax和p53表达上调,从而诱导人肝细胞性肝癌细胞凋亡。
肝癌, 藤黄酸, 凋亡, bax, p53
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【期刊论文】藤黄总酸对实验性肿瘤及肿瘤细胞体外生长的抑制作用
郭青龙, WU Zhao-Qiu, GU Qing-Long*, YOU Qi-Dong, ZHAO Li
中国天然药物,2003,1(2):99~102,-0001,():
-1年11月30日
目的:研究藤黄总酸的体内外抗肿瘤活性。方法:以抑瘤率和生命延长率观察药物的体内抗肿瘤活性,以药物对肿瘤细胞株的抑制率为指标,探讨其体外抗瘤作用。结果:藤黄总酸(8,4,2 mg/kg)iv对Heps、Ec及s180的肿瘤生长具有明显的抑制作用(P<0.01);ip(1.5,0.75,0.375 mg/kg)能显著延长Heps、EAc、S180腹水型小鼠移植瘤的存活天数;藤黄总酸对人肝癌细胞BEL-7402及人肺腺癌细胞SPC-A1有较强的抑制作用。结论:藤黄总酸对肿瘤细胞的体内外生长有明显抑制作川。
藤黄总酸, 抑瘤率, 生命延长率, 肿瘤细胞
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郭青龙, GUO Qing-Long, WU Min-Shu, CHEN Zhen
Guo QL et al I Acta Pharmacol Sin 2002 Oct; 23(10):946~951,-0001,():
-1年11月30日
AIM: To investigate the antitumor effect of recombinant L-asparaginase on the growth of several tumors such as P388, L1210, hepatocellular carcinoma (Heps), K562, P815, and sarcoma 180 (S180). METHODS: Tumor cells (K562, L1210, and P815) were cultured in vitro and the morphology of those cells was observed with inverse microscope and transmission electron microscope. MTT assay was performed to measure the cell proliferation and inhibition rate. DNA content was assayed by flow cytometry. According to protocols of transplant tumor research, mice were transplanted with tumor cells LI210, P388, Heps, and S180. The survival rate and weight of tumor were observed after the treatment of test drugs. RESULTS: The antimmor effects of L-asparaginase were observed in vitro with tumor cells K562, L1210, and P815 (P<0.01). In vivo experiments showed that ip adminis-tration of L-asparaginase significantly increased the survival rate and life span of mice with P388 or LI210 tumor cells (P<0.01). Tumor growth induced with Heps was also significantly suppressed. Furthermore, significant suppression of tumor growth was observed in mice induced with Heps and S180 by iv administration of L-asparaginase. CONCLUSION: Recombinant L-asparaginase markedly inhibited tumors tested in this study and the results strongly suggest that recombinant L-asparagiuase has great potential for clinical treatment of these tumors.
recombinant proteins, L-asparaginase, antineoplastic agents, leukemia LI210, leukemia P388, hepa-tocellular carcinoma, sarcoma 180, K562 cells, P815 cells, DBA/, 2 mice
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郭青龙, Wei Liu, Qing-Long Guo, Qi-Dong You, Li Zhao, Hong-Yan Gu, Sheng-Tao Yuan
World Journal of Gastroenterology ISSN 1007~9327,-0001,():
-1年11月30日
is on nude mice xenografts was observed by Annexin-V/PI doubling staining flow cytometry assay and DNA fragmentation assay. To further determine the molecular mechanism of apoptosis induced by GA, the changes on the expression of bcl-2 and bax genes were detected by RT-PCR. RESULTS: After incubation with GA, low differential human gastric cancer line BGC-823 was dramatically inhibited in a dose-dependent manner. After these cells were exposed to GA for 24, 48 and 72 h, the IC50 value was 1.02±0.05, 1.41±0.20 and 1.14±0.19 μmol/L, respectively. Apoptosis in BGC-823 cells induced by GA was observed by Annexin-V/PI doubling staining flow cytometry assay. The apoptotic population of BGC-823 cells was about 12.96% and 24.58%, respectively, when cells were incubated with 1.2 μmol/L GA for 48 and 72 h. T/C (%) of human gastric carcinoma adenocarcinoma BGC-823 nude mice xenografts was 44.3, when the nude mice were treated with GA (8 mg/kg). Meanwhile, apoptosis induced by GA was observed in human gastric carcinoma adenocarcinoma BGC-823 nude mice xenografts. The increase of bax gene and the decrease of bc1-2 gene expressions were found by RT-PCR. CONCLUSION: The inhibition of GA on human gastric cancer line BGC-823 was confirmed. This effect connects with the inducing apoptosis in BGC-823 cells and the molecular mechanism might be related to the reduction of expression of apoptosis-regulated gene bcl-2, and the improvement of the expression of apoptosis-regulated gene bax. The result was also confirmed in vivo.
Gambogic acid, Apoptosis, bcl-2, bax
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郭青龙, Zhao-Qiu WU, a, ) Qing-Long GUO, *, a Qi-Dong YOU, b Li ZHAO, a and Hong-Yan GUa
,-0001,():
-1年11月30日
We determined the in vivo and in vitro antitumor activities of gambogic acid (GA) and one of the possible mechanisms for its inhibitory activities. In vivo antitumor activity of GA was evaluated by the relative tumor growth ratio (T/C) in nude mice, and in vitro inhibition of SPC-A1 cells was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay and trypan blue exclusion assay. Telomere repeats amplification protocol (TRAP)-polymerase chain reaction (PCR)-enzyme-linked immunosorbent assay (ELISA) and RT-PCR were used to quantitatively detect telomerase activity and the expression of human telomerase reverse transcriptase (hTERT) mRNA, respectively. Results from our in vivo study showed that transplantable tumor growth remained suppressed for up to 21 d with minimal animal weight loss in nude mice treated with gambogic acid (i.v.). Proliferation of SPC-A1 cells cultured in vitro was significantly inhibited (p0.01), showing time-dependent and dose-dependent inhibition. Telomerase activity and hTERT mRNA expression were both decreased significantly, when cells were exposed to gambogic acid for 24, 48 and 72 h (for 24 h p0.05, and for 48, 72 h, p0.01). These results suggeste that gambogic acid could inhibit the growth of SPC-A1 cells and its tumor xenografts, and when treated with gambogic acid for a period of time, telomerase activity and expression of hTERT mRNA in the tumor cells were both inhibited significantly. It is safe, at least in part, to conclude that the down-regulating telomerase activity of GA by modifying partly the expression of hTERT mRNA in SPC-A1 cells may be one possible mechanism for the inhibitory activity of GA in the cells.
gambogic acid, SPC-A1 cell, antitumor effect, telomerase, human telomerase reverse trans, c, r, i, p, t, ase (, hTERT), mRNA
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郭青龙, Li ZHAO, Qing-Long GUO, *, a Qi-Dong YOU, b Zhao-Qiu WU, and Hong-Yan GU
,-0001,():
-1年11月30日
The selective induction of apoptosis of gambogic acid (GA) on MGC-803 cells and its probable molecular mechanism were studied. GA greatly inhibited (24, 48, 72 h) the growth of MGC-803 cells (by MTT); the IC50 value was 0.96m g/ml at 48 h. Meanwhile, no influence was observed on body weight, number of WBC (white blood cells) in blood or karyote in marrow of rats after GA was injected intravenously. We conclude that GA does not affect normal cells, but that it can induce apoptosis in tumor cells selectively and there were marked morphological changes. A great quantity of apoptotic cells and increasing G2/M phase cells were observed by flow cytometry, and a significant percentage of early apoptotic cells were observed by Annexin-V/PI double staining assay. The increase of bax gene and the decrease of bc1-2 gene expressions were detected by immunohistochemistry. Activation of bax and suppression of bc1-2 may contribute to the apoptosis mechanism.
gambogic acid, MGC-803, apoptosis, inhibition rate, bax, bc1-2
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郭青龙, Qing-Long Guo a, *, Sen-Sen Lin a, Qi-Dong You b, Hong-Yan Gu a, Jun Yu a, Li Zhao a, Qi Qi a, Fei Liang a, Zi Tan c, Xiaotang Wang c
Q.-L. Guo et al./Life Sciences xx(2005)1~8,-0001,():
-1年11月30日
The activation of human telomerase, a process regulated by the human telomerase reverse transcriptase (hTERT), is a crucial step during cellular immortalization and malignant transformation. We have reported that gambogic acid (GA), a natural product isolated from the gamboges resin of Garcinia hanburyi tree, is an effective telomerase inhibitor and thus displays potent anticancer activity both in vitro and in vivo. Here we present the direct interaction of GA with oncogene c-MYC, a ubiquitous transcription factor involved in the control of cell proliferation and differentiation, as the molecular mechanism of GA's inhibitory effect on telomerase activity. Consistent with the recently reported association between c-MYC overexpression and induction of telomerase activity, we find here that GA treatment of a human hepatoma cell line SMMC-7721 significantly reduced the expression of c-MYC in a time-and concentration-dependent manner accompanied with the down-regulation of the hTERT transcription and the ultimate reduction in telomerase activity. Our results indicate that the hTERT is a target of c-MYC activity and identify a feasible mechanism of GA's potent anticancer activity.
Gambogic acid, Human hepatoma, hTERT, c-MYC, Telomerase
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郭青龙, Qing-long GUO, Qi-dong YOU, Zhao-qiu WU, Sheng-tao YUAN, Li ZHAO
Guo QL et al/Acta Pharmacol Sin 2004 Jun; 25(6):769~774,-0001,():
-1年11月30日
To study the inhibitory effect of general gambogic acids (GGA) on transplantation tumor SMMC-7721 in experimental animal model and SMMC-7721 cells in vitro. METHODS: Anti-tumor activity of GGA in the experimental transplantation tumor SMMC-7721 was evaluated by relative tumor growth ratio. Cell morphology was observed with inverted microscope and electron microscope. Cell proliferation was measured by MTT assay and the telomerase activity was determined by PCR. RESULTS: In vivo study indicated that GGA (2, 4, and 8 mg/kg, iv, 3 times per week for 3 weeks) displayed an inhibitory effect on the growth of transplantation tumor SMMC-7721 in nude mice compared with the normal saline group (P<0.01). At the concentrations of 0.625-5.0 mg/L, GGA remarkably inhibited the proliferation of SMMC-7721 cells in vitro. GGA 2 mg/L dramatically changed morphology of SMMC-7721 cells and inhibited the telomerase activity in SMMC-7721 cells. CONCLUSION: GGA had inhibitory effect on the growth of SMMC-7721, which might be related to its inhibition of telomerase activity.
gamboge, gambogic acid, hepatoma, SMMC-7721 cells, telomerase, nude mice
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