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Ferulic Acid-Loaded Nanostructured Lipid Carriers: A Promising Nanoformulation Against the Ischemic Neural Injuries Publisher Pubmed



Hassanzadeh P1 ; Arbabi E2 ; Atyabi F1 ; Dinarvand R1
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Authors Affiliations
  1. 1. Nanotechnology Research Center, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran
  2. 2. Research Center for Gastroenterology and Liver Disease, Shahid Beheshti University of Medical Sciences, Tehran, Iran

Source: Life Sciences Published:2018


Abstract

Aims Treatment of the ischemic stroke has remained a major healthcare challenge. The phenolic compound, ferulic acid (FA), has shown promising antioxidant and neuroprotective effects, however, low bioavailability may negatively affect its efficiency. This, prompted us to incorporate FA into the nanostructured lipid carriers (FA-NLCs) and evaluate its therapeutic potential in in vitro and in vivo models of ischemic stroke. Main methods FA-NLCs were prepared by high-pressure homogenization followed by physicochemical characterization, evaluation of the bioactivity of FA-NLCs in oxygen-glucose deprivation (OGD) and global cerebral ischemia/reperfusion (I/R) injury and implication of phosphatidylinositol 3-kinase (PI3K) pathway in this regard. Key findings Formation of FA-NLCs which exhibited a controlled release profile, was confirmed by scanning electron microscope and differential scanning calorimetry. 1- and 8-h OGD followed by 24 h re-oxygenation significantly reduced PC12 cell viability, increased lactate dehydrogenase activity and number of condensed nuclei, and induced oxidative stress as revealed by increased malondialdehyde and decreased glutathione content and superoxide dismutase and catalase activities. FA (80 and 100 μM) reduced the cytotoxicity, oxidative stress, and cellular damage only after 1-h OGD, while, FA-NLCs (containing 80 and 100 μM of FA) were effective at both time points. Intravenous injections of FA-NLCs (20 and 25 mg/kg) into rats significantly attenuated I/R-induced neurobehavioural deficits, cellular damage, and oxidative stress, while, FA failed. Pre-treatment with PI3K inhibitor, LY294002, abolished the protective effects against OGD or I/R. Significance FA-NLCs by improving the pharmacological profile of FA and activating PI3K pathway might be of therapeutic value in cerebral stroke. © 2017
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