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北京市自然科学基金(7122097)

作品数:4 被引量:68H指数:3
相关作者:叶加高小力蒋益民万丹徐风更多>>
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发文基金:北京市自然科学基金国家自然科学基金更多>>
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The protective effects of thalidomide derivative ZSN-12 on acute lung injury被引量:1
2013年
The aim of this study was to evaluate the protective effect of thalidomide derivative ZSN-12 on acute lung injury induced by oleic acid in mice, and to investigate the possible mechanisms. The results showed that ZSN-12 (200 mg/kg) markedly improved the pathological changes of acute lung injury. The proportion of polymorphonuclear neutrophils (PMN) was reduced by 48% (P〈0.01) and the content of nitric oxide (NO) in bronchoalveolar lavage fluid (BALF) was decreased by 33% (P〈0.05). ZSN-12 produced significant anti-inflammatory effects in the models of xylene induced ear edema and carrageenan induced paw edema, in which ZSN-12 inhibited ear edema and paw swelling in a dose-dependent manner. The inhibition rates by ZSN-12 dosed at 200, 100, 50 mg/kg were 62%, 43%, and 30% in ear edema, respectively and 60%, 47%, and 33% in paw edema, respectively, at 3 h. Meanwhile, ZSN-12 (10, 5, 1 μmol/L) significantly restrained the ConA-induced T lymphocyte proliferation, with the inhibition rates of 33%, 30% and 22%, respectively (P〈0.01). In conclusion, the present study showed that administration of thalidomide derivative ZSN-12 exerted significant protective effect in acute lung injury induced by oleic acid in mice, which may be related to its anti-inflammation effect. ZSN-12 inhibited the effusion of PMN, reduced the release of NO, and suppressed the proliferation of T lymphocyte.
高小力孟祥豹蒋益民李中军叶加
关键词:ANTI-INFLAMMATION
Buyang Huanwu Decoction ameliorates ischemic stroke by modulating multiple targets with multiple components: In vitro evidences被引量:19
2018年
Buyang Huanwu Decoction (BYHWD) is a well-known traditional Chinese medicine prescription which is used to treat ischaemic stroke and stroke-induced disabilities. However, the exact mechanism underlying BYHWD's amelioration of ischaemic stroke and its effective constituents remain unclear. The present study aimed to identify the effective constituents of BYHWD and to further explore its action mechanisms in the amelioration of ischaemic stroke by testing the activities of 15 absorbable chemical constituents of BYHWD with the same methods under the same conditions. The following actions of these 15 compounds were revealed: 1) Ferulic acid, calycosin, formononetin, astrapterocarpan-3-O-β-D-glucoside, paeonol, calycosin-7-O-β-D-glucoside, astraisofla- van-7-O-β-D-glucoside, ligustrazine, and propyl gallate significantly suppressed concanavalin A (Con A)-induced T lymphocyte proliferation; 2) Propyl gallate, calycosin-7-O-β-D-glucoside, paeonol, and ferulic acid markedly inhibited LPS-induced apoptosis in RAW264.7 cells; 3) Propyl gallate and formononetin significantly inhibited LPS-induced NO release; 4) Hydroxysaffior yellow A and inosine protected PC12 cells against the injuries caused by glutamate; and 5) Formononetin, astragaloside IV, astraisofiavan-7-O-β-D- glucoside, inosine, paeoniflorin, ononin, paeonol, propyl gallate, ligustrazine, and ferulic acid significantly suppressed the constriction of the thoracic aorta induced by KCI in rats. In conclusion, the results from the present study suggest that BYHWD exerts its ischaemic stroke ameliorating activities by modulating multiple targets with multiple components.
ZHANG Wei-WeiXU FengWANG DingYE JiaCAI Shao-Qing
关键词:NEUROPROTECTIONVASODILATION
化合物DXL-A-22抗神经病理性疼痛作用及机制研究被引量:3
2019年
目的研究螺环哌嗪季铵盐化合物DXL-A-22抗神经病理性疼痛作用及机制。方法以坐骨神经慢性压迫性损伤(CCI)模型评价DXL-A-22的抗神经病理性疼痛作用;Westernblot和qPCR技术研究DXL-A-22的作用机制;极限实验评价DXL-A-22的急性毒性。结果与溶媒组比较,DXL-A-22(2、1、0.5mg·kg^-1,i.g.)剂量依赖性提高CCI大鼠机械刺激缩足反应阈值和热刺激缩足潜伏期(P<0.05,P<0.01),术后d7痛阈提高率分别为108%、86%和71%,最大镇痛百分率分别为77%、56%和43%;DXL-A-22(2mg·kg^-1)明显降低背根神经节(DRG)p-CaMKⅡα、p-CREB,p-JAK2、p-STAT3蛋白表达,以及TNF-α、c-FosmRNA表达(P<0.05,P<0.01),抑制率分别为37%、48%、35%、58%、39%和32%;明显降低脊髓TNF-α、c-FosmRNA表达(P<0.01),抑制率分别为47%和72%;无明显毒性反应。结论螺环哌嗪季铵盐化合物DXL-A-22能明显抑制大鼠坐骨神经慢性压迫性损伤引起的神经病理性疼痛,无明显毒性,其机制可能与抑制DRGCaMKⅡα/CREB和JAK2/STAT3信号通路,降低DRG及脊髓TNF-α、c-FosmRNA表达相关。
梁莹莹王欣刘芹王丁杜小雷李润涛蒋益民叶加
关键词:CCIJAK2/STAT3信号通路
甲基丁香酚镇痛抗炎作用及机制研究被引量:45
2017年
目的甲基丁香酚是细辛挥发油的主要成分之一,对甲基丁香酚镇痛抗炎效果进行评价,探索其镇痛作用机制。方法本研究以醋酸刺激痛、福尔马林刺激痛、热刺激痛实验和二甲苯致小鼠耳肿胀实验评价甲基丁香酚的镇痛、抗炎作用,并以受体阻断实验、一氧化氮(NO)检测实验探讨其镇痛作用机制。结果 (1)甲基丁香酚(6,3,1.5 mg·kg^(-1)),在醋酸刺激痛实验中,显著抑制小鼠扭体次数,抑制率分别为56.58%,51.25%,40.93%;在福尔马林刺激痛实验中,缩短Ⅱ相舔足、咬足时间,抑制率分别为56.62%,47.03%,33.98%;在热刺激痛实验中明显延长小鼠热痛潜伏期,在2 h镇痛作用达高峰,痛阈提高率分别为57.32%,42.14%,26.29%。(2)甲基丁香酚(6,3,1.5 mg·kg^(-1))明显抑制二甲苯所致小鼠耳肿胀,抑制率分别为76.43%,57.23%,35.00%。(3)受体阻断实验显示甲基丁香酚(6 mg·kg^(-1))镇痛作用可被GABA_A受体阻断剂荷包牡丹碱(3 mg·kg^(-1))阻断,不能被阿片受体阻断剂纳洛酮(3 mg·kg^(-1))阻断。NO检测实验显示甲基丁香酚(6 mg·kg^(-1))可抑制醋酸致痛小鼠血清NO水平。结论本研究表明细辛挥发油成分甲基丁香酚有明显镇痛抗炎作用,其镇痛作用机制与激动GABAA受体,抑制NO水平相关。
杨华徐风万丹高小力蒋益民叶加
关键词:细辛甲基丁香酚镇痛抗炎
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