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Icariin/HAP纳米凝胶剂的处方优化及体外释放研究
[目的]对Icariin/HAP纳米凝胶剂处方进行优化并考察其体外释放特性.[方法]物理吸附法制备Icariin/HAP纳米混悬液,研和法制备Icariin/HAP纳米凝胶,采用正交设计对处方进行优化,透析法测定Icariin/HAP纳米凝胶中药物的释放.[结果]Icariin/HAP纳米凝胶优选处方为卡波姆浓度为1％,三乙醇胺用量为1.5％,丙二醇用量为5％.Icariin/HAP纳米凝胶剂、Icariin凝胶剂和Icariin溶液体外释放均符合一级模型和Weibull模型.[结论]以卡波姆为基质制备Icariin/HAP纳米凝胶,处方简单,质量稳定,可提高Icariin/HAP纳米混悬液的稳定性.
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The Neuropharmacological Effects of Herba Epimedii and its Main Bioactive Components:Icariin,IcarisideⅡand Icartin
Herba Epimedii,a traditional & Chinese medicine(T&CM),is used as a tonic, remedy for calming the nerves and anti-rheumatic agent in some Chinese proprietary medicine. Icariin,icarisideⅡ and icartin,are main bioactive products present in this herb. Previous studies have demonstrated that these compounds possess broad therapeutic capabilities,especially anti-osteoporosis, anti-oxidative stress and anti-cancer effects. In recent years,growing numbers of researches have focused on pharmacological actions of Herba Epimedii in central nervous system. Numerous preclinical studies have demonstrated that Herba Epimedii as agent for neurological disease,and our reports showed powerful neruoprotective effects of icariin and icarisideⅡ in Alzheimer's disease(AD)and ischemic brain injury. Mechanistically,icariin increased cerebral blood flow and amyloidβ-protein (Aβ)clearance,enhanced neurogenesis and memory,promoted synaptic plasticity may through the PDE5/NO/cGMP signaling pathway. Moreover,icariin is also efficient at anti-depression,and possible molecular mechanisms involve in decrease of the hyper-responsiveness of corticotropin-releasing factor (CRF),regulation of 5-hydroxytryptamine system and anti-inflammation effect. Although some Chinese proprietary medicine which are contain icariin have been used for osteoporosis in clinic,but no agents for neurological diseases. To further promote the researches on prevention and treatment of Herba Epimedii on central nervous system diseases,this review aim to summarize the anti-AD,anti-aging, and anti-ischemic brain injury effects of compounds of Herba Epimedii with reference to published data. Base on the literature compiled,the compounds of Herba Epimedii have tremendous potential to be developed therapeutic drugs for AD,ischemic stroke and depression. It is our hope that traditional Chinese medicine health industry could promote the development of health and contribute to the health welfare for all.
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Protective Effects and Mechanism of Icariin on LPS-induced Dopaminergic Neuronal Damage
Objective:To observe the protective effects of Icariin(ICA)on lipopolysaccharide (LPS)-induced dopaminergic(DA)neuronal damage and explore the possible mechanisms. Methods:Thirty SD rats were randomly divided into control,ICA(20 mg·kg-1)alone,model(LPS,5μg), LPS+ICA(10 mg·kg-1)and LPS+ICA(20 mg·kg-1).The DA neuronal damage was induced by injecting LPS into one side of rat midbrain substantia nigra(SN). After seven daily intragastric administration of ICA,rat behavior changes were analyzed by the rotarod test and then brains were collected to detect the expression of tyrosine hydroxylase(TH,a marker of DA neuron)and OX-42(a marker of microglia activation)by double-labelimmunofluorescent analysis. Primary rat midbrain neuron-glia co-cultures were applied to further elucidate the ICA-exerted neuroprotection in vitro. The cultures were randomly divided into control,ICA(0.1μmol·L-1)alone,LPS(10 ng·mL-1), LPS+ICA(0.01 μmol·L-1)and LPS+ICA(0.1 μmol·L-1). LPS-induced DA neuronal damage and microglia activation were evaluated by immunofluorescent analysis and western blot analysis. The levels of NO,TNF-α and IL-1β in the culture supernatantwere measured with Griess reagent and ELISA,respectively. In addition,BV2 cell lines were prepared to investigate the effects of ICA on LPS-induced protein expressions of TLR4,MyD88,p65 and phosphorylated-p65(p-p65). Results:ICA attenuated the loss of DA neurons and microglia activation induced by LPS-injected SN in vivo.Inneuron-glia co-cultures,ICA ameliorated LPS-induced DA neuronal damage and microglia activation. Moreover,ICA reduced LPS-elevated NO,TNF-α and IL-1β production in the culture supernatant. In addition,ICA suppressed LPS-induced activation of TLR4,MyD88 and NF-κBpathways. Conclusion:ICA could afford neuroprotection against LPS-induced DA neurotoxicity both in vivo and in vitro through the inhibition of microglia activation and the subsequent production of neuroinflammatory factors.
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淫羊藿苷后处理对心肌缺血再灌注损伤的保护作用研究
目的：观察淫羊藿苷（ icariin，ICA）后处理对心肌缺血／再灌注损伤的保护作用及其可能机制。方法：将24只家兔分为3组：假手术组、I／R组以及ICA后处理组。采用家兔在体模型，家兔麻醉后，开胸短暂结扎冠状动脉左前降支模拟缺血，缺血30min后松开结扎线进行再灌注，再灌注前10min耳缘静脉注射给药。灌注过程中检测左心室内压等心功能指标，再灌注180min后采血检测血清中SOD、MDA；随后处死动物，心脏染色测定心肌梗死面积，检测心肌组织中Bcl－2、Bax蛋白水平。结果：与假手术组比较，I／R组中LVSP、±dp／dtmax下降，LVEDP升高，HR降低；血清中SOD活性降低，MDA含量增高；Bcl－2、Bax蛋白表达量增高（P＜0．01，P＜0．05）。与I／R组比较，ICA后处理组中LVSP、±dp／dtmax升高，LVEDP下降；心梗面积减少；血清中SOD活性增高，MDA含量降低；Bcl－2蛋白表达量增高，Bax蛋白表达量降低，（P＜0．05）。结论：ICA后处理对MIRI造成的心脏损伤具有保护作用，能明显改善心功能各项指标，缩小心梗面积，其保护机制与减轻心肌氧化应激反应、抑制心肌细胞凋亡有关。
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活性甾体分子Icariin对人脐静脉内皮细胞功能的影响及其机制
目的 观察活性甾体分子Icariin (ICA)对人脐静脉内皮细胞(HUVEC)功能的影响,探讨其分子机制.方法 培养HUVEC并采用10-9 ～ 10-3 mol/L的ICA分别干预细胞12、24、36 h以确定佳干预条件.实时定量聚合酶链反应(Real-time PCR)和Western blot检测ICA干预后成血管相关基因血管内皮生长因子(VEGF)、磷酸肌醇3激酶(PI3K)、蛋白激酶B(Akt)、丝裂原细胞外激酶(MEK)、细胞外信号调节激酶(ERK) mRNA和蛋白表达水平.体外成血管实验验证ICA对HUVEC成血管能力的影响.利用PI3K抑制剂LY294002和MEK抑制剂PD98059与ICA同时干预细胞,观察可否逆转ICA对HUVEC功能的影响,探讨ICA调控HUVEC功能的分子机制.结果 ICA对HUVEC具有促增殖作用,10-4 mol/L的ICA干预36 h后细胞增殖活性达到峰值[(179.90±0.04)％],与对照组比较差异有统计学意义(P＜0.05).ICA干预后VEGF、MEK、ERK、PI3K、Akt基因的mRNA相对扩增倍数(分别为4.01 ±0.03、3.35 ±0.05、4.07±0.03、3.99±0.05、2.64±0.02)及VEGF、磷酸化Akt (p-Akt)、磷酸化ERK(p-ERK)的蛋白表达量均显著高于对照组(P＜0.05).ICA干预后的管腔形成数为(15.60±0.06)个,较对照组的(7.20±0.03)个比较差异有统计学意义(P＜0.05).LY294002、PD98059可逆转ICA对HUVEC功能的影响.结论 ICA通过VEGF介导激活PI3K/Akt、MEK/ERK通路促进HUVEC的增殖与血管形成能力.
