朱依纯
从事高血压心血管系统重构的机制及干预的研究
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- 姓名:朱依纯
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学术头衔:
博士生导师, 教育部“新世纪优秀人才支持计划”入选者
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学科领域:
生物药物学
- 研究兴趣:从事高血压心血管系统重构的机制及干预的研究
朱依纯,1987年毕业于上海第二医科大学医疗系。1994年毕业于德国海德堡大学,获药理学博士学位。现任复旦大学上海医学院生理与病理生理学系副主任、教育部分子医学重点实验室副主任。
从事高血压心血管系统重构的机制及干预的研究。1998年列入上海市曙光计划,被评为第四届上海市高校优秀青年教师,2000年入选教育部跨世纪优秀人才培养计划,2004年获教育部自然科学奖二等奖一项(第一完成人),获中国专利授权一项(第一发明人)。发表研究论文35篇,论文被国际刊物引用190次(他引)。第一作者论文所发表的刊物中,最高影响因子是Diabetes.(其2002年影响因子为9.019)。此外,2002年在Science网站上发表了一篇论文。
近年来在科学研究上的创新性工作包括提出诱导分化逆转心肌重构的新思路,已获发明专利并在国外重要刊物发表论文。其中,全反式维甲酸在整体高血压动物上的作用填补了国际同领域的空白。此外,还找到降压作用显著并具有心脏保护作用的天然植物单体成分,具有很大的应用价值,可进一步申报国家一类新药。近年的研究工作还包括:1.研究了血管紧张素转换酶(ACE)抑制剂改善心功能的机制,观察到缓激肽增强介导了ACE抑制剂的部分心脏作用。2.观察到ACE在心脏中的细胞分布主要是在血管内皮细胞。其基因表达取决于内皮细胞所处的解剖部位,即在心肌小动脉中,几乎所有的内皮细胞均表达ACE;在毛细血管内皮细胞中为部分表达;在冠状静脉的内皮细胞中则完全不表达。还观察到ACE和血管紧张素受体基因表达在心肌重构过程中表达的变化,以及AT1和AT2两种受体亚型在心肌细胞中的共存3.最近观察到Urotensin II受体GPR14在心肌重构过程中的变化及其与血管紧张素受体在心肌细胞中的共存,有关结果的论文正在撰写中。4.天然植物中分离到一种有效成分KHR96,观察到其不但在SHR中有明显、持久的降压作用,而且对心脏有直接作用,包括降低心率、室壁张力、心肌耗氧量并抑制成纤维细胞的增殖。已明确该有效成分的分子结构,有关结果正在申报发明专利,目前还在深入研究其作用机制。
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朱依纯, BY Y. Z. ZHUY. C. ZHU
,-0001,():
-1年11月30日
The Yellow Emperor's Internal Classics, an 18-volume medical reference work, was published some 2000 years ago in China. Written by several generations of traditional Chinese medicine (TCM) practitioners, it describes-with remarkable accuracy-the human body in terms of its anatomy, physiology, and psychology. The book also focuses a great deal of attention on the medicinal uses of plants-particularly herbs. Together with The Yellow Emperor’s Internal Classics, contemporary books such as The Poetry Classics and The Mountain and Sea Classics identified close to 200 therapeutic plants, including herbs with tonic, contraceptive, antidotal, and antiparasitic effects. There are now over 9000 reports of TCM medicines; however, only about 500 of these are commonly used by TCM practitioners, and only 80 or so (see the box for some examples) have amply demonstrated pharmacological effects--from the perspective of "modern" medicine.
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朱依纯, Hui Gong, Yan-Xia Wang, Yi-Zhun Zhu, Wen-Wei Wang, Ming-Jie Wang, Tai Yao, and Yi-Chun Zhu
J Appl Physiol VOL 97 DECEMBER 2004,-0001,():
-1年11月30日
Cellular distribution of GPR14 and the positive inotropic role of urotensin II in the myocardium in adult rat. J Appl Physiol 97: 000-000, 2004. First published July 23; oi: 10.1152/japplphysiol.00540.2004.-Urotensin II is a cyclic neuropeptide recently shown to play a role viaits receptor GPR14 in regulating vascular tone in the mammalian cardiovascular system. The existence of GPR14 in rat heart has been validated by ligand binding assay and RT-PCR. In the present study, we investigated the cellular distribution of GPR14 protein in rat heart by using immunohistochemistry and confocal microscopic immunofluorescence double staining with antipeptide polyclonal antibodies against GPR14 and cell type markers for myocytes and endothelial cells. The direct effect of urotensin II on left ventricular contractility was further evaluated in isolated left ventricular papillary muscles of the rat. In paraffin-embedded heart sections, positive immunohistochemical staining was observed in the left ventricle but not in the right ventricle and atria. Immunofluorescence double staining revealed the cardiac myocyte as the only cell type expressing GPR14 protein in frozen heart sections as well as in isolated cardiac myocytes. There was no visible signal for GPR14 in intramyocardial coronary arteries and capillaries. The existence of GPR14 protein in rat heart was further validated by immunoprecipitation and Western blot analysis. In isolated rat left ventricular papillary muscle preparations, urotensin II induced an increase in active contractile force. GPR14 mRNA was also detected in rat heart by RT-PCR. These data provide the first direct evidence for the cellular localization of GPR14 receptor protein and a positive inotropic effect of urotensin II in normal rat heart.
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朱依纯, Lei L
Am J Physiol Heart Circ Physiol 285: H1370-H1377, 2003.,-0001,():
-1年11月30日
Chronic all-trans retinoic acid treatment prevents medial thickening of intramyocardial and intrarenal arteries in spontaneously hypertensive rats. Am J Physiol Heart Circ Physiol 285: H1370-H1377, 2003. First published May 29, 2003; 10.1152/ajpheart.00260.2003.-There are in vitro data linking all-trans retinoic acid (atRA) with inhibition of hypertrophy and hyperplasia in cardiomyocytes, vascular smooth muscle cells, and fibroblasts. In the present study, we tested the hypothesis that chronic treatment with atRA may blunt the process of myocardial remodeling in spontanously hypertensive rats (SHR). Four-week-old male SHR were treated with atRA (5 or 10 mg kg 1 day 1) given daily for 3 mo by gavage; age-and sex-matched Wistar-Kyoto rats (WKY) and placebo-treated SHR served as controls. At the end of the treatment period, cardiac geometry and function were assessed by Doppler echocardiography. Histological examination and RIA were performed to evaluate medial thickening of intramyocardial and renal arteries, perivascular and interstitial collagen content, and atrial natriuretic peptide (ANP) and IGF-I in the heart, respectively. The novel finding of the present study is that atRA prevented hypertrophy of intramyocardial and intrarenal arteries and ventricular fibrosis. However, at RAtreatment did not lower blood pressure or left ventricular weight and left ventricular weight-to-body weight ratio in SHR. atRA did not change cardiac geometry and function as assessed by Doppler echocardiography. atRA showed no influence on either ANP or IGF-I levels. In conclusion, the present study suggests that chronic atRA treatment prevents medial thickening of intramyocardial and intrarenal arteries and ventricular fibrosis during the development of hypertension. Left ventricular hypertrophy and cardiac geometry and function are not changed by atRA treatment.
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【期刊论文】Effects of all-trans retinoic acid on angiotensin II-induced myocyte hypertrophy
朱依纯, HAO-JIE WANG, YI-CHUN ZHU, AND TAI YAO
J Appl Physiol 92: 2162-2168, 2002.,-0001,():
-1年11月30日
We used cultured neonatal rat cardiac myocytes to test the hypothesis that all-trans retinoic acid (atRA) may act to modulate ANG II actions in inducing myocyte hypertrophy. Our observations were as follows. 1) atRA (10-7 to~10-5 M) inhibited ANG II-induced hyperplasia of fibroblasts in a dose-dependent manner. 2) Treatment of atRA attenuated the ANG II-induced increase in total cell protein content. 3) Treated with ANG II (10-7 M) for 5 days, the cultured neonatal rat cardiac myocytes demonstrated an apparent accumulation of sarcomeric fiber proteins and Golgi's complex, as well as reorganization of the sarcomeric unit within individual myocytes. atRA (10-6 M) treatment reduced the accumulation of contractile proteins and Golgi's complex without affecting the ANG II-induced reorganization of the sarcomeric unit. 4) atRA attenuated the ANG II-induced increase in intracellular Ca2. Our results show that atRA inhibits some effects of ANG II on neonatal rat cardiac myocytes and suggest that atRA may be a therapeutic candidate for the prevention and therapy of cardiac hypertrophy and remodeling.
cardiac hypertrophy, dedifferentiation, intracellular calcium, hyperplasia,, induction of myocyte differentiation
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【期刊论文】Antioxidants in Chinese herbal medicines: a biochemical perspective
朱依纯, Y. Z. Zhu, a S. H. Huang, b B. K. H. Tan, a J. Sun, a M. Whitemanb and Y.-C. Zhu c
Nat. Prod. Rep., 2004, 21, 478-489,-0001,():
-1年11月30日
Recently, intense interest has focused on the antioxidant properties of natural products. In particular, Chinese herbal medicines (CHM) have become hot topics for life science researchers since many are reported to possess cardioprotective compounds, many of which remain to be identified. Indeed, the exact mechanisms by which CHM work remain unknown. Although many of these herbal remedies are undoubtedly efficacious, few have been scientifically investigated for their active chemical constituents and biological activities. We have previously reported higher activities of antioxidant defence enzymes such as superoxide dismutase, catalase, glutathione peroxidase and glutathione S-transferases in the liver of rats treated with the herb Salvia miltiorrhiza in a model of acute myocardial infarction. Using well established in vitro antioxidant assays employing 2, 2-azino-bis (3-ethylbenzthiazoline-6-sulfonic acid) (ABTS) and diphenyl-1-picrylhydrazyl (DPPH) we have shown that in addition to elevating endogenous antioxidant enzyme activity, Salvia miltiorrhiza and other CHM traditionally used for cardiovascular disorders (such as Rhizoma ligustici, Herba leonuri, Radix achyranthis bidentatae, and Camellia sinensis) contain potent antioxidant moieties in addition to their phenolic constituents. Furthermore, these novel non-phenolic components are effective inhibitors of oxidative reactions mediated by the inflammatory oxidants, peroxynitrite, hypochlorous acid and hydroxyl radical as well as iron-dependent lipid peroxidation. In this review, we discuss the various antioxidant properties of CHM in the context of their biochemical mechanisms.
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