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用于糖尿病神经病变的口服霍诺基醇载体固体脂质纳米颗粒的制备,表征和药理应用

Tehmina Bibi¹, Shahar Bano¹, Fakhar Ud Din²

¹Pharmacological Sciences Research Lab, Department of Pharmacy, Faculty of Biological Sciences, Quaid-i-Azam University, Islamabad 45320, Pakistan; Department of Pharmacy, Faculty of Biological Sciences, Quaid-i-Azam University, Islamabad 45320, Pakistan.

International journal of pharmaceutics

|September 13, 2023

概括

含有Honokiol的固体脂质纳米颗粒 (SLN) 显著提高了糖尿病神经病变的口服生物可用性和神经保护. 这种配方有效地减少了氧化应激和亡,提供了一个有希望的治疗策略.

科学领域:

纳米技术纳米技术
药理学药理学是指药理学的学科.
神经科学是一个神经科学.

背景情况:

红是一种强大的植物化学物质,具有较差的溶解性和较低的口服生物可用性,限制了其治疗应用.
糖尿病神经病变 (DN) 是一种使人虚弱的疾病,通常与氧化应激和神经元损伤有关.

研究的目的:

为增强口服输送,制定和表征含有Honokiol的固体脂质纳米颗粒 (SLN).
在糖尿病神经病变的实验模型中评估Honokiol-SLNs的疗效.

主要方法:

诺基-SLN的配方和特征,包括颗粒大小,PDI,zeta潜力和捕获效率.
与纯Honokiol相比,体外药物释放研究和口服生物可用性的评估.
使用H2O2刺激的PC12细胞进行体外神经保护试验.
在糖尿病神经病变模型中的体内评估,评估氧化应激标志物 (NF-κB,Nrf2),离子通道表达 (TRPM8,TRPV1) 和亡 (caspase-3).

主要成果:

红-SLNs表现出最佳的特征:球形形态,粒子大小为~121nm,PDI为~0.25,ZP为~-20.8mV,和%EE为~88.7%.
与纯Honokiol相比,持续的体外释放和口服生物利用率增加了8倍.
通过NF-κB抑制和Nrf2上调调节显著减少氧化应激.
降低TRPM8,TRPV1和切割caspase-3表达的下调,表明神经炎症和亡的减少.
证明了体外和体外的神经保护作用.

结论:

霍诺基奥尔-SLN代表了一个成功的策略,以克服霍诺基奥尔的生物可用性限制.
增强的配方通过减轻氧化应激,神经炎症和亡,在糖尿病神经病变中提供显著的神经保护.
红-SLNs作为治疗糖尿病神经病变的有效治疗剂具有前途.

关键词:

细胞灭亡 (apoptosis) 是一种死亡的过程.糖尿病神经病变是一种神经病变.红-SLNs 在线链接在生物体内进行的研究.口服生物可用性口服生物可用性氧化应激是一种氧化应激.

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