目的观察金钗石斛生物总碱对外源性内毒素脂多糖(lipopolysaccharide,LPS)激活大鼠大脑皮层星形胶质细胞(astrocyte)及诱导其产生和释放炎症介质的影响,探讨石斛生物总碱对星形胶质细胞的抗炎作用。方法通过MTS检测细胞存活率,ELISA法检...目的观察金钗石斛生物总碱对外源性内毒素脂多糖(lipopolysaccharide,LPS)激活大鼠大脑皮层星形胶质细胞(astrocyte)及诱导其产生和释放炎症介质的影响,探讨石斛生物总碱对星形胶质细胞的抗炎作用。方法通过MTS检测细胞存活率,ELISA法检测TNF-α炎性因子蛋白的表达,实时定量多聚酶链反应(real time RT-PCR)检测炎症相关基因TNF-α、IL-6 mRNA的表达。结果①LPS刺激星形胶质细胞后,MTS检测吸光度明显升高,与正常组比较差异有显著性;②金钗石斛生物总碱能够降低LPS所致的TNF-α蛋白的高表达(P<0.05);③金钗石斛生物总碱能够降低LPS诱导的星形胶质细胞吸光度的升高,同时明显抑制LPS所致的TNF-α、IL-6 mRNA的高表达。结论金钗石斛生物总碱能够拮抗LPS所引起的炎症反应,其作用与抑制星形胶质细胞的激活及其炎症因子的释放密切相关。展开更多
目的研究安宫牛黄丸对脑缺血再灌注损伤和脑外伤大鼠的保护作用。方法成年雄性SD大鼠连续7 d灌胃给予安宫牛黄丸,灌胃第4天线栓法致脑缺血1 h再灌注72 h后检测大鼠行为学、脑梗死百分比及脑组织炎症因子肿瘤坏死因子α(TNF-α)、白介素-...目的研究安宫牛黄丸对脑缺血再灌注损伤和脑外伤大鼠的保护作用。方法成年雄性SD大鼠连续7 d灌胃给予安宫牛黄丸,灌胃第4天线栓法致脑缺血1 h再灌注72 h后检测大鼠行为学、脑梗死百分比及脑组织炎症因子肿瘤坏死因子α(TNF-α)、白介素-1β(IL-1β)和诱导型一氧化氮合酶(i NOS)mRNA的表达。此外,大鼠连续7 d灌胃给予安宫牛黄丸后,采用重物打击法诱导大鼠脑外伤模型,24 h后检测大鼠行为学改变并通过real time RT-PCR检测脑内炎症因子TNF-α、IL-1β和i NOS mRNA的表达。结果与脑缺血再灌注损伤模型组比较,安宫牛黄丸(1.5 g/kg)能够改善模型大鼠行为学改变,减少大鼠脑梗死面积,下调脑组织内TNF-α、IL-1β和i NOS mRNA的表达;与脑外伤模型组比较,安宫牛黄丸(1.5 g/kg)可以改善大鼠行为学改变,下调脑组织内TNF-α、IL-1β和i NOS mRNA的表达。结论安宫牛黄丸对大鼠脑缺血再灌注损伤和脑外伤有保护作用。展开更多
Objective: To evaluate the effects and possible mechanisms of rutaecarpine on angiotensin Ⅱ (Ang Ⅱ )-induced proliferation in cultured rat vascular smooth muscle cells (VSMCs). Methods: VSMCs were isolated fro...Objective: To evaluate the effects and possible mechanisms of rutaecarpine on angiotensin Ⅱ (Ang Ⅱ )-induced proliferation in cultured rat vascular smooth muscle cells (VSMCs). Methods: VSMCs were isolated from Male Sprague-Dawley rat aorta, and cultured by enzymic dispersion method. Experiments were performed with cells from passages 3-8. The cultured VSMCs were randomly divided into control, model (Ang Ⅱ 0.1 μ moVL), and rutaecarpine (0.3-3.0μmol/L) groups. VMSC proliferation was induced by Ang Ⅱ, and was evaluated by the 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide assay and cell counting. To examine the mechanisms involved in anti-proliferative effects of rutaecarpine, nitric oxide (NO) levels and NO synthetase (NOS) activity were determined. Expressions of VSMC proliferation-related genes including endothelial nitric oxide synthase (eNOS), and c-myc hypertension related gene-1 (HRG-1) were determined by real-time reverse chain reaction (RT-PCR). Results: Rutaecarpine (0.3-3.0μmol/l_) inhibited Ang R-induced VSMC proliferation and the best effects were achieved at 3.0 μmol/L. The Ang Ⅱ-induced decreases in cellular NO contents and NOS activities were antagonized by rutaecarpine (P〈0.05). Ang Ⅱ administration suppressed the expressions of eNOS and HRG-1, while increased c-myc expression (P〈0.05). All these effects were attenuated by 3.0μmol/L rutaecarpine (P〈0.05). Conclusion: Rutaecarpine is effective against Ang Ⅱ-induced rat VSMC proliferation, and this effect is due, at least in part, to NO production and the modulation of VMSC proliferation-related gene expressions.展开更多
文摘目的观察金钗石斛生物总碱对外源性内毒素脂多糖(lipopolysaccharide,LPS)激活大鼠大脑皮层星形胶质细胞(astrocyte)及诱导其产生和释放炎症介质的影响,探讨石斛生物总碱对星形胶质细胞的抗炎作用。方法通过MTS检测细胞存活率,ELISA法检测TNF-α炎性因子蛋白的表达,实时定量多聚酶链反应(real time RT-PCR)检测炎症相关基因TNF-α、IL-6 mRNA的表达。结果①LPS刺激星形胶质细胞后,MTS检测吸光度明显升高,与正常组比较差异有显著性;②金钗石斛生物总碱能够降低LPS所致的TNF-α蛋白的高表达(P<0.05);③金钗石斛生物总碱能够降低LPS诱导的星形胶质细胞吸光度的升高,同时明显抑制LPS所致的TNF-α、IL-6 mRNA的高表达。结论金钗石斛生物总碱能够拮抗LPS所引起的炎症反应,其作用与抑制星形胶质细胞的激活及其炎症因子的释放密切相关。
文摘目的研究安宫牛黄丸对脑缺血再灌注损伤和脑外伤大鼠的保护作用。方法成年雄性SD大鼠连续7 d灌胃给予安宫牛黄丸,灌胃第4天线栓法致脑缺血1 h再灌注72 h后检测大鼠行为学、脑梗死百分比及脑组织炎症因子肿瘤坏死因子α(TNF-α)、白介素-1β(IL-1β)和诱导型一氧化氮合酶(i NOS)mRNA的表达。此外,大鼠连续7 d灌胃给予安宫牛黄丸后,采用重物打击法诱导大鼠脑外伤模型,24 h后检测大鼠行为学改变并通过real time RT-PCR检测脑内炎症因子TNF-α、IL-1β和i NOS mRNA的表达。结果与脑缺血再灌注损伤模型组比较,安宫牛黄丸(1.5 g/kg)能够改善模型大鼠行为学改变,减少大鼠脑梗死面积,下调脑组织内TNF-α、IL-1β和i NOS mRNA的表达;与脑外伤模型组比较,安宫牛黄丸(1.5 g/kg)可以改善大鼠行为学改变,下调脑组织内TNF-α、IL-1β和i NOS mRNA的表达。结论安宫牛黄丸对大鼠脑缺血再灌注损伤和脑外伤有保护作用。
基金Supported by the National Natural Science Foundation of China(No.81160528)the Governor Foundation of Guizhou Province(No.2006-07)Administration of Traditional Chinese Medicine of Guizhou Province Foundation(No.2009-79)
文摘Objective: To evaluate the effects and possible mechanisms of rutaecarpine on angiotensin Ⅱ (Ang Ⅱ )-induced proliferation in cultured rat vascular smooth muscle cells (VSMCs). Methods: VSMCs were isolated from Male Sprague-Dawley rat aorta, and cultured by enzymic dispersion method. Experiments were performed with cells from passages 3-8. The cultured VSMCs were randomly divided into control, model (Ang Ⅱ 0.1 μ moVL), and rutaecarpine (0.3-3.0μmol/L) groups. VMSC proliferation was induced by Ang Ⅱ, and was evaluated by the 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide assay and cell counting. To examine the mechanisms involved in anti-proliferative effects of rutaecarpine, nitric oxide (NO) levels and NO synthetase (NOS) activity were determined. Expressions of VSMC proliferation-related genes including endothelial nitric oxide synthase (eNOS), and c-myc hypertension related gene-1 (HRG-1) were determined by real-time reverse chain reaction (RT-PCR). Results: Rutaecarpine (0.3-3.0μmol/l_) inhibited Ang R-induced VSMC proliferation and the best effects were achieved at 3.0 μmol/L. The Ang Ⅱ-induced decreases in cellular NO contents and NOS activities were antagonized by rutaecarpine (P〈0.05). Ang Ⅱ administration suppressed the expressions of eNOS and HRG-1, while increased c-myc expression (P〈0.05). All these effects were attenuated by 3.0μmol/L rutaecarpine (P〈0.05). Conclusion: Rutaecarpine is effective against Ang Ⅱ-induced rat VSMC proliferation, and this effect is due, at least in part, to NO production and the modulation of VMSC proliferation-related gene expressions.