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环氧合酶-2抑制剂NS398对食管癌细胞迁移的抑制作用及其机制 被引量:1
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作者 文卉 刘涛 +1 位作者 余宗涛 李胜保 《华中科技大学学报(医学版)》 CAS CSCD 北大核心 2016年第3期302-305,共4页
目的探讨COX-2选择性抑制剂NS398对食管癌细胞株EC109迁移能力的影响及其可能机制。方法选用食管癌细胞株EC109为靶细胞,分别加入不同浓度(0、50、100μmol/L)的NS398,利用细胞划痕实验,观测细胞48h内迁移能力变化;采用逆转录PCR方法检... 目的探讨COX-2选择性抑制剂NS398对食管癌细胞株EC109迁移能力的影响及其可能机制。方法选用食管癌细胞株EC109为靶细胞,分别加入不同浓度(0、50、100μmol/L)的NS398,利用细胞划痕实验,观测细胞48h内迁移能力变化;采用逆转录PCR方法检测目标基因COX-2、RhoA、CDC42及Rac-1的表达变化。结果细胞划痕实验显示,50μmol/L NS398组迁移距离[24h:(50.81±8.51)μm,48h:(109.67±18.38)μm]及100μmol/L NS398组迁移距离[24h:(53.15±9.58)μm,48h:(97.42±13.20)μm]与对照0μmol/L NS398组迁移距离[24h:(68.72±5.68)μm,48h:(129.68±10.79)μm]相比均明显减少(均P<0.05),说明加入NS398后细胞迁移能力下降。50μmol/L NS398组及100μmol/L NS398组与对照0μmol/L NS398组相比,COX-2、RhoA、CDC42、Rac-1表达均降低(均P<0.05)。结论 NS398可抑制食管癌细胞EC109迁移运动能力,其机制可能与抑制COX-2表达,调节迁移基因RhoA、CDC42及Rac-1的表达有关。 展开更多
关键词 环氧合酶抑制剂 食管癌 rhoa/cdc42/rac-1信号通路 细胞迁移
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Houshiheisan and its components promote axon regeneration after ischemic brain injury 被引量:14
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作者 Yue Lu Flora Hsiang +5 位作者 Jia-Hui Chang Xiao-Quan Yao Hui Zhao Hai-Yan Zou Lei Wang Qiu-Xia Zhang 《Neural Regeneration Research》 SCIE CAS CSCD 2018年第7期1195-1203,共9页
Houshiheisan,a classic prescription in traditional Chinese medicine,contains Flos Chrysanthemi,Radix Saposhnikoviae,Ramulus Cinnamomi,Rhizoma Chuanxiong,Radix et Rhizoma Asari,Radix Platycodonis,Rhizoma Atractylodis m... Houshiheisan,a classic prescription in traditional Chinese medicine,contains Flos Chrysanthemi,Radix Saposhnikoviae,Ramulus Cinnamomi,Rhizoma Chuanxiong,Radix et Rhizoma Asari,Radix Platycodonis,Rhizoma Atractylodis macrocephalae,Poria,Rhizoma Zingiberis,Radix Angelicae sinensis,Radix et Rhizoma Ginseng,Radix Scutellariae and Concha Ostreae.According to traditional Chinese medicine theory,Flos Chrysanthemi,Radix Saposhnikoviae,Ramulus Cinnamomi,Rhizoma Chuanxiong,Radix et Rhizoma Asari and Radix Platycodonis are wind-dispelling drugs;Rhizoma Atractylodis macrocephalae,Poria,Rhizoma Zingiberis,Radix Angelicae sinensis and Radix et Rhizoma Ginseng are deficiency-nourishing drugs.A large number of randomized controlled trials have shown that Houshiheisan is effective in treating stroke,but its mechanism of action is unknown.Axonal remodeling is an important mechanism in neural protection and regeneration.Therefore,this study explored the effect and mechanism of action of Houshiheisan on the repair of axons after cerebral ischemia.Rat models of focal cerebral ischemia were established by ligating the right middle cerebral artery.At 6 hours after model establishment,rats were intragastrically administered 10.5 g/kg Houshiheisan or 7.7 g/kg wind-dispelling drug or 2.59 g/kg deficiency-nourishing drug.These medicines were intragastrically administered as above every 24 hours for 7 consecutive days.Houshiheisan,and its wind-dispelling and deficiency-nourishing components reduced the neurological deficit score and ameliorated axon and neuron lesions after cerebral ischemia.Furthermore,Houshiheisan,and its wind-dispelling and deficiency-nourishing components decreased the expression of proteins that inhibit axonal remodeling:amyloid precursor protein,neurite outgrowth inhibitor protein A(Nogo-A),Rho family small GTPase A(Rho A) and Rho-associated kinase 2(Rock2),and increased the expression of growth associated protein-43,microtubule-associated protein-2,netrin-1,Ras-related C3 botulinum toxin substrate 1(Rac1) and cell division cycle 42(Cdc42).The effect of Houshiheisan was stronger than wind-dispelling drugs or deficiency-nourishing drugs alone.In conclusion,Houshiheisan,and wind-dispelling and deficiency-nourishing drugs promote the repair of axons and nerve regeneration after cerebral ischemia through Nogo-A/Rho A/Rock2 and Netrin-1/Rac1/Cdc42 signaling pathways.These effects are strongest with Houshiheisan. 展开更多
关键词 nerve regeneration Houshiheisan wind-dispelling drug deficiency-nourishing drug cerebral ischemia Nogo-A/Rho A/Rock2 signaling pathway axonal recovery Netrin-1/Rac1/cdc42 signaling pathway neuroprotection neural regeneration
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