钱之玉
长期从事药理学实验研究工作
个性化签名
- 姓名:钱之玉
- 目前身份:
- 担任导师情况:
- 学位:
-
学术头衔:
博士生导师
- 职称:-
-
学科领域:
药物化学
- 研究兴趣:长期从事药理学实验研究工作
钱之玉,1965年毕业于南京药学院药学专业,毕业后留校一直从事药学教育和科研工作。任中国药科大学药理学教研室主任,教授,博士生导师,中国药理学会理事,江苏省药理学会副理事长,国家和江苏省药品评审专家,江苏省学科评议组成员,《中草药》、《中国药科大学学报》、《中国处方药》、《中国执业药师》等杂志编委。
1987年率先在中国药科大学,为研究生开设细胞生物学课程,为促进药学教育向化学和生物学相结合模式转变做出了自己的切实努力。1997年,主持申请了国家教育部"药理学课程体系和教学内容改革"的课程,已通过教育部结题验收,报告已被收集出版。1998年主编"药学和医学基础"教材,供理科基地班使用,为搭建药学和医学之间桥梁的一门重要专业课。1999年主持"药学的医学基础"课程教学改革研究,申请了教育部"国家理科基地创建名牌课程项目",现已完成。1987年开始招收研究生,1997年获准招收博士生。先后为国家培养硕士生30余名,博士生10余名,在读硕士9人,博士11人。
长期从事药理学实验研究工作,先后在国内外发表论文百余篇。70年代末,主持"水飞蓟宾注射剂研制"的药效和毒理研究,顺利完成临床前研究工作。1982年10月,受世界卫生组织资助,赴英、美留学,从事男性生殖生物学研究,分别在Cell Biology和Biology of Reproduction等杂志发表论文。1985年回国后,向WHO申请了"棉酚抗生精作用的生化机制"课题,并圆满完成了研究任务。1990年后,采用价格低廉、来源广泛的栀子果实替代价格昂贵、药源奇缺的西红花,成功地提取分离西红花总苷、西红花苷-1及西红花酸,2000年获得此项研究国家发明专利授权,获国家新药证书二本《血脉清片,证书号:国家证字Z20040052及栀子提取物(主要成分西红花苷)证书号:国药证字Z20040053》。近年来还承担了省级及企业联合的研究课题。
-
主页访问
1699
-
关注数
0
-
成果阅读
218
-
成果数
6
钱之玉, Shuguo Zheng, Zhiyu Qian*, Futian Tang, Liang Sheng
Biochemical Pharmacology 70(2005)1192-1199,-0001,():
-1年11月30日
To elucidate the molecular mechanism by which antioxidants alleviate atherosclerosis, we nvestigated the effect of crocetin, a naturally occurred carotinoid with potent antioxidant power, on vascular cell adhesion molecule-1 (VCAM-1) expression in atherosclerotic rabbits. Twenty-four male New Zealand White rabbits were allocated to three groups fed on standard diet (control group), high lipid diet (HLD group) or high lipid diet supplemented with crocetin (crocetin group), respectively. After 8 weeks of treatment, rabbits in HLD group developed severe hypercholesterolemia and atherosclerosis in aortas, together with a significantly up-regulated expression of both protein and mRNA for VCAM-1. In contrast, supplementation with crocetin resulted in markedly ameliorated atherosclerosis, coupled with a significantly decreased VCAM-1 expression, though plasma lipids level remained comparable to that of HLD group. Regression analysis revealed a positive correlation between VCAM-1 expression and the extent of atherosclerosis (P<0.01). In addition, immunohistochemical analysis showed an increased activation of nuclear factor kappa B (NF-kB), a redox sensitive transcription factor essential for VCAM-1 expression, in aortas from rabbits fed on high lipid diet, which was evidently suppressed by crocetin supplementation. These findings suggest that the antiatherosclerotic effect of crocetin might be attributed, at least in part, to the suppressed expression of VCAM-1, which might result from reduced NF-kB activation. This study provides a further insight into the molecular mechanism by which antioxidants attenuate atherosclerosis and suggests a potential target for the treatment of atherosclerosis with antioxidants.
Atherosclerosis, Cell adhesion molecule, Trans, c, r, i, p, t, ion factor, Reactive oxygen species, Antioxidants, Crocetin
-
27浏览
-
0点赞
-
0收藏
-
0分享
-
122下载
-
0评论
-
引用
【期刊论文】Effect of crocin on experimental atherosclerosis in quails and its mechanisms☆
钱之玉, Shu-Ying He, Zhi-Yu Qian*, Fu-Tian Tang, Na Wen, Guang-Lin Xu, Liang Sheng
Life Sciences 77(2005)907-921,-0001,():
-1年11月30日
In the present study, we examined the prophylaxis effect of crocin on experimental atherosclerosis and it spossible mechanisms. The atherosclerosis formation was induced by hyperlipidamic diet in quails. At the 9th week, serum lipid, MDA and NO were measured, and HE staining was used to investigate the histopathological changes of aorta. Bovine aortic endothelial cells (EC) were obtained from the thoracic aorta of newborn calves. After incubation of the cells with Ox-LDL (50mg·L-1) for 24h, the activities of LDH, NO in culture media and activity of NOS in endothelial cells were measured, flow cytometer was used to determine the rate of endothelial cells apoptosis. Peritoneal macrophages were obtained from thioglycolate-injected mice. Cholesterol and free cholesterol in cells were assayed after incubation of the cells with Ox-LDL. Bovine aortic smooth muscle cells (SMC) were obtained from the thoracic aorta of newborn calf. Proliferation was induced by 100 Agd L 10X-LDL and antiproliferative effect of crocin on SMCs were observed. SMCs cycle phases were measured by flow cytometry. SMCs were loaded with Fluo-3/AM and [Ca2+]i was measured by Laser Scanning Confocal Microscope (LSCM). Crocin could reduce the level of serum TC, TG, LDL-C and inhibit the formation of aortic plaque. Crocin could reduce MDA and inhibit the descending of NO in serum. Compared with control, Ox-LDL group could increase the activity of LDH and decrease activity of NO in culture media and activity of NOS in endothelial cells, preincubated with crocin, the effects of Ox-LDL were inhibited. Crocin could decrease the EC apoptosis induced by Ox-LDL. Crocin concentration-dependently inhibited the TC and CE elevation induced by Ox-LDL in macrophages. Crocin could inhibit the proliferation of SMCs induced by Ox-LDL. In the presence or absence of extracellular Ca2+, crocin concentration-dependently inhibited the [Ca2+]i elevation induced by 120mgd L 1Ox-LDL, In the absence of extracellular Ca2+, crocin could inhibit the [Ca2+]i elevation induced by CHCl3 in a concentration-dependent manner. The results indicated that crocin could inhibit the formation of atherosclerosis in quails. Crocin had protective effects on endothelial cells. Crocin could decrease CE in macrophages and uptake of Ox-LDL, inhibiting the formation of foam cell, which would promote the initiation and progression of atherosclerosis. Crocin could inhibit the [Ca2+]i elevation in smooth muscle cell, Ca2+ is an important second messenger that regulates a variety of cellular processes, including smooth muscle cell proliferation and gene expression. Crocin exerted antiatherosclerotic effects through decreasing the level of Ox-LDL that plays an important role in the initiation and progression of atherosclerosis.
Atherosclerosis, Crocin, Quail, Endothelial cells, Macrophages, SMCs, Ox-LDL, NO, NOS, CE, Apoptosis, Flow cytometer, Laser Scanning Confocal Microscope (, LSCM), , Calcium, Fluo-3/, AM
-
48浏览
-
0点赞
-
0收藏
-
0分享
-
169下载
-
0评论
-
引用
钱之玉, 何书英, 唐富天
Acta Pharmaceutica Sinica 2004, 39(10)778-781,-0001,():
-1年11月30日
目的 研究西红花苷对血管平滑肌细胞内钙离子浓度的影响。方法 以Fluo-3/AM作为Ca2+荧光探针,采用激光扫描共聚焦显微镜观察牛主动脉平滑肌细胞内钙离子浓度的变化。结果 无论细胞外有无钙离子,西红花苷(1×10-8,1×10-7,1×10-6mol·L-1)均能明显抑制1×10-2mol·L-1 H202引起的细胞内钙离子浓度的升高,其抑制率含钙条件下分别为34.1%,57.1%和74.3%(P<0.01),无钙条件下分别为26.2%,32.1%和50.0%(P<0.01);在胞外无钙的条件下,西红花苷(1×10-8,1×10-7,1×10-6mol·L-1)能抑制70 mmol·L-1 CHC13导致雷洛丁敏感钙池的释放,其抑制率分别为27.8%,27.8%和50.0%(P<0.01)。结论 西红花苷能抑制胞外钙离子的内流及内质网上钙离子的释放。
西红花苷, 激光共聚焦显微镜, 平滑肌细胞, Fluo-3/, AM, 钙离子
-
35浏览
-
0点赞
-
0收藏
-
0分享
-
83下载
-
0评论
-
引用
钱之玉, 沈祥春, 钱之玉*
Acta Pharmaceutica Sinica 2004, 39(3)172-175,-0001,():
-1年11月30日
目的 研究西红花酸对压力超负荷所致大鼠心肌肥厚的影响。方法 腹主动脉部分狭窄术致心肌肥厚,采用试剂盒测定Na+-K+ ATPase和Ca2+-Mg2+ ATPase的活力及羟脯氨酸的含量,SDS-PAGE检测MMPs的活力。结果 模型组ATPase活性降低更加明显,羟脯氨酸的含量明显增加,MMPs活力明显增强。西红花酸能显著提高心肌组织的ATPase活力,降低胶原的含量,抑制MMPs的活力。结论 西红仡酸对斥力超负荷所致大鼠心肌肥厚具有一定的改善作用,抑制MMPs的活性可能是其作用机制之一。
西红花酸, 压力超负荷, 心肌肥厚, 基质金属蛋白酶
-
24浏览
-
0点赞
-
0收藏
-
0分享
-
91下载
-
0评论
-
引用
【期刊论文】西红花酸对去甲肾上腺素所致原代培养心肌细胞能量代谢和凋亡的影响
钱之玉, 沈祥春**, 钱之玉*, 陈琦, 王雅娟
Acta Pharmaceutica Sinica 2004, 39(10)787-791,-0001,():
-1年11月30日
目的 研究西红花酸对去甲肾上腺素(NE)诱导原代培养心肌细胞能量代谢障碍和细胞凋亡的保护作用。方法 1μmol·L-1 NE损伤原代培养的心肌细胞,检测细胞培养上清液的LDH、心肌细胞ATPase、线粒体琥珀酸脱氢酶(MSDH)的活力,线粒体膜电位的变化,流式细胞仪检测细胞凋亡,观察西红花酸保护作用。结果模型组细胞培养上清液LDH增加,心肌细胞MSDH和ATPase的活力降低,线粒体膜电位降低,心肌细胞凋亡率增加。西红花酸明显降低培养上清液LDH增加,提高MSDH和ATPase的活力、线粒体膜电位的水平,对心肌细胞的凋亡具有明显的保护作用。结论西红花酸对NE所致的心肌细胞能量代谢障碍和凋亡具有明显的保护作用。
西红花酸, 去甲肾上腺素, 心肌细胞, 线粒体膜电位, 细胞凋亡
-
36浏览
-
0点赞
-
0收藏
-
0分享
-
73下载
-
0评论
-
引用
钱之玉, 龚国清*, 刘同征, 李立文
中国药科大学学报,2001,32(4):306~309,-0001,():
-1年11月30日
目的 探讨西红花提取物中西红花酸的椿外抗氧化作用。方法 采用H2O2和Vc-Fe2+两种径自由基发生丰统,观察了西红花酸对H2O2。系统的径自由基的清除能力,对肝匀浆及肝线粒椿的Vc-Fe2+系统引起的脂质过氧化的抑制作用。结果 西缸花酸对H2O2系列的羟自由基有较强的清除能力,并能押制肝匀莱自氧化和Vc-Fe2+束统羟自由基引起的脂质过氧化,对肝线拉体也有保护作用。结论 西红花酸具有较强的抗氧化作用。
西红花酸, 抗氧化, 羟自由基, 丙二醛, H2O2, 维生素C
-
48浏览
-
0点赞
-
0收藏
-
0分享
-
41下载
-
0评论
-
引用