陈季强
呼吸及抗炎免疫药理
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- 姓名:陈季强
- 目前身份:
- 担任导师情况:
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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:呼吸及抗炎免疫药理
陈季强,1970年毕业于上海第二医学院儿科系6年制本科,1983年毕业于浙江医科大学药理专业研究生。现任浙江大学医学院基础医学部主任,教授,博士生导师,国家食品药品监督管理局浙江呼吸药物研究实验室副主任,主持实验室的工作和建设。中国药理学会临床药理学专业委员会理事,中国药学会海洋药物专业委员会理事,浙江省药理学会副理事长兼临床药理专业委员会主任委员,国家食品药品监督管理局新药审评专家。主要研究方向是呼吸及抗炎免疫药理。近几年作为课题负责人主持国家自然科学基金项目1项,作为第二负责人参加国家自然科学基金项目3项和国家重点科技(攻关)基金项目1项,浙江省自然科学基金重点项目l项。近五年发表研究论文40余篇,其中被SCI收录12篇,主编专著2部(《呼吸药理学与治疗学》,《药源性疾病一基础与临床》,由人民卫生出版社出版),参编大型专著5部。主编并由科学出版社出版教材三部(《基础医学教程》导论、各论[上、下])。获浙江省人民政府教学成果一等奖1项(2002年),二等奖1项(2004年),浙江省高校科技成果一等奖(2001年)和三等奖(2000年)各一项。
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【期刊论文】RR-福莫特罗和rac-福莫特罗对人支气管舒张作用的比较
陈季强, XUJ i-de, , XIE Qiang-min, CHEN Ji-qiang, et al
浙江大学学报( 医学版),2003,32(4):300~303,-0001,():
-1年11月30日
目的:比较RR-福莫特罗和rac-福莫特罗对人支气管舒张作用。方法:将内径2~4mm、长15mm的人支气管螺旋条置入持续供氧的浴槽内,静息张力为1g,以蓄积给药法测定RR-福莫特罗(10 pmol•L-1~3.2 Lmol•L-1)和rac-福莫特罗(10 pmol•L-1~3.2 Lmol•L-1)在静息情况下,及氨甲酰胆碱(10 Lmo l•L-1)或组胺(100 Lmol•L-1)引起收缩情况下的张力改变。结果:RR-福莫特罗在静息状况下支气管舒张作用强于rac-福莫特罗(P<0.05)。RR-福莫特罗和rac-福莫特罗对抗由氨甲酰胆碱和组胺引起的收缩,且RR-福莫特罗的对抗作用强于rac-福莫特罗(P<0.05)。结论:RR-福莫特罗对人支气管的舒张作用强于rac-福莫特罗。
支气管药物作用, 卡巴胆碱, 组胺类药, 立体异构现象, 福莫特罗, 支气管舒张
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陈季强, DENG Yang-Mei, XIE Qiang-Min, CHEN Ji-Qiang, BIAN Ru-Lian
Deng YM et al/Acta Pharmacol Sin 2003 Oct; 24 (10): 1039-1044,-0001,():
-1年11月30日
To explore the changes of leukotrienes (LT) in cerebral cortex and lung tissues in ovalbumin-induced rat asthma model and effects of different anti-asthma drugs on the changes. METHODS: Aerosol antigen-induced changes of inflammation in bronchoalveolar lavage fluids (BALF), pulmonary and brain histologic section in sensitized rats were investigated. Changes of LTB4 and LTC4 in lung and cerebral cortex homogenates were analyzed by reverse-phase high performance liquid chromatography (RP-HPLC). RESULTS: The number of inflammatory cells in BALF and the score of lung and brain histological examination from antigen- challenged rats were significantly higher than that from control group (P<0.05). Dexamethason (DXM, 0.5mg/kg, ip) and ketotifen fumarate (KF, 5mg/kg, ig) markedly reduced total leukocyte number in BALF, and inhibited eosinophil accumulation, reduced the infiltration of eosinophils, and improved mucous edema and epithelial lesion of bronchi and bronchioles. In addition, RP-HPLC results shown LTB4 in lung and cerebral cortex homogenates were increased in antigenchallenged rats [(4.1
leukotrienes, central nervous system, inflammation, asthma, rats
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陈季强, WANG Kai, CHEN Ji-Qiang, CHEN Zhong, CHEN Jun-Chun
Wang Ket al/Acta Pharmacol Sin 2002 Nov; 23 (11): 1013-1017,-0001,():
-1年11月30日
To study the inductive expression of human phosphodiesterase 4A (hPDE4A) in yeast cell GL62 and investigate the inhibitory effects of theophylline, rolipram, and acetamide-45 on PDE4A activity of the expressed product in yeast cell GL62. METHODS: Yeast cell GL62 were transfected with human PDE4A gene cloned in the expression plasmid p138NB. Expression was induced by adding CuSO4 to a final concentration of 150μmol/L, and the expressed product was extracted. The activity of PDE4A was detected by HPLC. RESULTS: Yeast cell GL62 expressed a certain protein at CuSO4 150μmol/L, the size of the expressed product was between 62 kDa and 83 kDa, the activity of PDE4A of the expressed product at 3 h was in maximum (188±23)μmol×g-1×min-1, and the Km was (17.7±2.6) mmol/L. Theophylline, rolipram, and acetamide-45 could inhibit the activity of PDE4A extracted from yeast cell GL62. The IC50 (95% confidence limits) of theophylline, rolipram, and acetamide-45 were 1642 (989-2727), 4.58 (3.45-6.08), and 275 (170-444) mmol/L respectively. CONCLUSION: PDE4A expressed in yeast cell GL62 is biologically active. Theophylline, rolipram, and acetamide-45 can inhibit the PDE4A activity. The expressed product in yeast cell GL62 may be used in the research work of PDE4 and its inhibitors.
3', ,, 5', -cyclic-nucleotide-phosphodiesterase, Saccharomyces cerevisiae, cyclic AMP, cyclic GMP, theophylline, rolipram, acetamide-45
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陈季强, XIE Qiang-MinI, CHEN li-Qiang, SHEN Wen-Hui, YANG Qiu-Huo, BIAN Ru-Lian
中国药理学,2002,23(3):243~247,-0001,():
-1年11月30日
目的:评价环孢素A气雾给药对豚鼠哮喘模型的药效。方法:用乙酰胆碱(ACh)或组胺诱导抗原攻击后的致敏豚鼠气道阻力pC200、支气管肺泡灌洗液(BALF)和肺组织切片中的嗜酸性粒细胞(EOS)变化观察环孢素A气雾给药后的抗气道高反应性和炎症作用。结果:环孢素AlOg•L-1、20g•L-1气雾给药和地塞米松(0.5mg-1kg ip)增加PC200值,能预防ACh或组胺引起的气道高反应性。环孢素A5g-L-1对组胺引起的气道高反应性也有作用,对Ach不显著.环孢素A10g•L-1、20g•L-1气雾给药能明显减少BAIF中的EOS浸润。与溶媒组比较,地塞米松0.5mg•kg-1增加了BALF中的中性粒细胞数日,与三组环孢素A比较有显著差异。在肺组织学研究中,环孢素A20g•L-1和地塞米松0.5mg•kg-1可抑制支气管和细支气管上皮和上皮表面结缔组织的EOS浸润。结论:环孢素A气雾吸入给药能明显对抗致敏豚鼠气道高反应性和炎症反应,为其治疗哮喘提供了一个可选择的给药途径。
环孢菌素类, 卵白蛋白, 己酰胆碱, 组胺, 嗜酸细胞, 哮喘, 豚鼠
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【期刊论文】致敏大鼠脑皮层和肺气道中干扰素-γ和白介素-4相关性的变化
陈季强, XIE Qiang-Min, CHEN Ji-Qiang, SHEN Wen-Hul, BIAN Ru-Lian
中国药理学,2002,23(3):248~252,-0001,():
-1年11月30日
目的:探讨致敏大鼠抗原攻击后脑皮层和肺气道中干扰素-γ(-IFN-γ)和白介素-4(IL-4)出现的相关性变化。方法:观察致敏大鼠吸入抗原诱导的支气管肺灌洗液(BAIF)和肺组织切片炎症变化,用ELISA法测定BALF和脑皮层-IFN-γ和JL-4水下变化。结果:抗原攻击组BAIF中的炎症细胞数目明显高于对照未攻击组(p<0.05)。地塞米松(DXM,0.5mg/kg,ip)明显减少BAIF中的白细胞总数,几乎完全抑制嗜酸性粒细胞(EOS)和淋巴细胞的聚集,但增加中性粒细胞数目。抗原攻击组的组织学检查积分(EOS浸润、粘膜水肿和上皮损伤)也明显高于对照未攻击组(P<O.05)。 DXM (0.5mg/kg,ip)减少支气管和细支气管的:EOS数目,改善粘膜水肿和上皮损伤。致敏人鼠抗原攻击后。BAIJF中的IFN,7水平降低伴随IL-4升高导致了IFN-γ/IL-4比例下降与此同时,脑皮层匀浆中也出现相似的改变。DXM(0.5mg/kg,Ip)能反转BALF和脑皮层匀浆中的IFN-γ/IL-4比例下降。结论:致敏大鼠抗原攻击后脑皮层和肺气道中的IFN-γ/IL-4出现相关性变化。
细胞因子类, 十扰素Ⅱ型, 白介素-4, 中枢神经系统, 炎症, 哮喘, 大鼠
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陈季强, XIE Qiang-Min, CHEN Ji-Qiang, SHEN Wen-Hui, YANG Qiu-Huo, BIAN Ru-Lian
Xie QM et a l/Acta Pharmacol Sin 2003 Mar; 24 (3): 277-282,-0001,():
-1年11月30日
To compare the bronchodilating and antiinflammatory effects of oral racemic formoterol (rac-FMT) and (R,R)-formoterol (R,R-FMT). METHODS: The changes of lung resistance (RL), dynamic lung compliance (Cdyn), and the accumulation of inflammatory cells in bronchoalveolar lavage fluids (BALF) induced by ovalbumin aerosol in sensitized guinea pigs and mice were investigated in vivo. RESULTS: Mean value increase of RL and mean value reduction of Cdyn from 1 to 30 min after antigen challenge were up to 101%
formoterol, bronchodilator agents, inflammation, eosinophils, asthma, guinea pigs, mice
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【期刊论文】TGF-h1 induces alveolar epithelial to mesenchymal transition in vitro
陈季强, Hong-Wei Yao*, Qiang-Min Xie, Ji-Qiang Chen, Yang-Mei Deng, Hui-Fang Tang
H.-W. Yao et al./Life Sciences 76 (2004) 29-37,-0001,():
-1年11月30日
The aim of this study was to investigate whether transforming growth factor-h1 (TGF-h1) could induce alveolar epithelial to mesenchymal transition (EMT) in vitro. Alveolar epithelial cells (AECs) from SD rats were isolated by elastase cell dispersion and IgG panning. Expression of a-smooth muscle actin (a-SMA) was assayed using Western blotting and immunostaining analysis. Morphological changes, the markers of epithelial cell (E-cadherin), and stress fiber by actin reorganization were detected by an indirect immunostaining. The contents of collagen I were determined by spectrophotometry. The levels of endogenous TGF-h1 were measured with ELISA. Incubation of AECs with TGF-h1 (0.1~10ng/mL) induced abundant expression of a-SMA protein, and a-SMA expression in AECs reached a plateau when TGF-h1 was N 3ng/mL. Furthermore, we found that TGF-h1 (3ng/mL) exposure of AECs induced an authentic EMT characterized by abundant expression of a-smooth muscle actin, transformation of myofibroblastic morphology, increased formation of stress fiber by actin reorganization, and loss of epithelial marker E-cadherin. Meanwhile, significant increase in the levels of collagen I from 32.0 F 6.6mg/g in control to 98 F 10.8mg/g in TGF-h1-treated group was found over a 72h incubation period. Moreover, following stimulated by TGF-h1 (3ng/mL), a marked and time-dependent increase in endogenous TGF-h1 released from AECs was observed. At time points 72h, TGFh1 release mounted to 3451pg/ml, which was much enough to induce EMT in vitro. These results demonstrated that AECs, under stimulation of TGF-h1, underwent a conversion process into myofibroblasts in vitro.
Transforming growth factor-h1, Alveolar epithelial cells, Epithelial to mesenchymal transition
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【期刊论文】硝普钠与异丙肾上腺素松弛犬气管平滑肌的协同作用*
陈季强, CHEN Ji-Qiang, ZHOU Han-Liang
中国药理学通报,1997,13(1):35~38,-0001,():
-1年11月30日
目的:研究硝普钠(SNP)与异丙肾上腺素(ISO)对犬气管平滑肌松弛作用是否存在协同关系,并分析协同的机制。方法:采用放射免疫分析法测定犬气管平滑肌环核苷酸量,并用磷酸二酯酶(PDE)同工酶抑制剂为工具分析SNP与ISO相互作用的机制。结果:SNP(1~100Lmol•L-1)增强ISO(30Lmol•L-1)对3Lmol•L-1乙酰甲胆碱预收缩的犬气管平滑肌的松弛作用。SNP(100Lmol•L-1) 与ISO(30Lmol•L-1)对犬气管平滑肌松弛的协同作用伴有气管平滑肌中CAMP积聚比SNP与ISO单独时分别增加112倍与014倍。PDEÍ 抑制剂扎普司特(3 Lmol•L-1)使SNP的气管平滑肌CGM P积聚由214倍增加到416倍,可进一步增加气管松弛作用112倍。合并PDEË抑制剂氰胍哒嗪(30Lmol•L-1)和PDEÌ抑制剂咯利普兰(30Lmol•L-1)或合并SNP(100Lmol•L-1) 和咯利普兰(30Lmol•L-1)均能进一步增强ISO的气管cAMP积聚与松弛作用。结论:SNP是通过气管平滑肌cGMP含量增加而抑制PDEË,导致SNP与ISO对气管松弛的协同作用。
硝普钠, 异丙肾上腺素, 环腺苷酸, 环鸟苷酸, 3', 5', 2环核苷酸磷酸二酯酶, 磷酸二酯酶抑制剂
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陈季强, Jun-chun CHEN, Ji-qiang CHEN, Qiang-min Xie, Yi-liang ZHU
Chen JC et al/Acta Pharmacol Sin 2004 Sep; 25 (9): 1171-1175,-0001,():
-1年11月30日
human PDE4A was improved by ammonium sulfate fractionation, DEAE Sephadex A-50 chromatography, and Sephadex G-100 chromatography. The activity of PDE4A was measured by high performance liquid chromatography (HPLC). RESULTS: Induced PDE4A activity expressed in crude yeast cell GL62 supernatant and pellet was (340±21) nmol•g-1•min-1 and (250±25) nmol•g-1•min-1 respectively. The specific activity of recombinant PDE4A in supernatant was improved 6.4 fold. Ciclamilast, piclamilast, and rolipram could inhibit PDE4A activity. The IC50 values (95% confidence limits) of ciclamilast, piclamilast, and rolipram were 1.27 (0.84-1.91), 66.4 (33.3-132.2), and 3.73 (2.51-5.53) μmol/L respectively. Zaprinast, aspirin, and indomethacin had no obvious inhibitory effect on PDE4A activity. CONCLUSION: The specific activity of PDE4A expressed in yeast cell GL62 can be improved by ammonium sulfate fractionation, DEAE Sephadex A-50 chromatography, and Sephadex G-100 chromatography. Ciclamilast, piclamilast, and rolipram can inhibit PDE4A activity while zaprinast, aspirin, and indomethacin have no obvious inhibitory effect on PDE4A activity. Human PDE4A expressed in GL62 might be useful in the research and screening of new selective PDE4 inhibitors.
phosphodiesterase inhibitors, ciclamilast, 3-(, cyclopentyloxy), -N-(, 3,, 5-dichloro-4-pyridyl), -4-methoxybenzamide, rolipram, zaprinast, 3', ,, 5', -cyclic-nucleotide phosphodiesterase, Saccharomyces cerevisiae
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【期刊论文】扎普司特和谷胱甘肽翻转豚鼠离体气管对硝普钠的耐受性1
陈季强, LU Yun-B i, CHEN Ji-Q iang, ZHOU Han-Liang
中国药理学与毒理学杂志,1997,11(4):271~274,-0001,():
-1年11月30日
上皮完整或去上皮的豚鼠离体气管以300Lmol•L-1硝普钠(SNP)预处理1h,使SNP对抗乙醋甲胆碱气管收缩作用的剂量反应曲线右移1.3-1.5倍,最大舒张率下降41%-58%,形成SNP气管松弛作用的耐受性82溴环鸟苷酸可模拟SNP在豚鼠离体气管形成的SNP耐受性,谷胱甘肽(1mmol•L-1)及环核苷酸磷酸二酯酶(PDE)V抑制剂扎普司特(30Lmol•L-1)均可部分翻转SNP的气管松弛作用耐受性,而蛋白合成抑制剂环己酰亚胺(10Lmol•L-1)对SNP的耐受性无预防作用。结果表明SNP可产生豚鼠离体气管松弛耐受性,这可能是由于气管平滑肌中环鸟苷酸(CGMP)积聚而下调鸟苷酸环化酶(GC)活性和上调PDEÍ活性。
血管舒张药, 药物耐受性, 磷酸二酯酶 抑制剂, 硝普钠, 谷胱甘肽, 气管
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