Enhanced Neuroprotection of Acetyl-11-Keto-β-Boswellic Acid (AKBA)-Loaded O-Carboxymethyl Chitosan Nanoparticles Through Antioxidant and Anti-Inflammatory Pathways

Mol Neurobiol. 2016 Aug;53(6):3842-3853. doi: 10.1007/s12035-015-9333-9. Epub 2015 Jul 11.

Abstract

Acetyl-11-keto-β-boswellic acid (AKBA), a main active constituent from Boswellia serrata resin, is a novel candidate for therapy of cerebral ischemia-reperfusion (I/R) injury. Nevertheless, its poor solubility in aqueous solvent, bioavailability, and rapid clearance limit its curative efficacy. To enhance its potency, in our study, AKBA-loaded o-carboxymethyl chitosan nanoparticle (AKBA-NP) delivery system was synthesized. The transmission electron microscopy and transmission electron microscope images of AKBA-NPs suggested that particle size was 132 ± 18 nm, and particles were spherical in shape with smooth morphology. In pharmacokinetics study, AKBA-NPs apparently increases the area under the curve of plasma concentration-time and prolonged half-life compared with AKBA. The tissue distribution study confirmed that AKBA-NPs had a better brain delivery efficacy in comparison with AKBA. The results from our pharmacodynamic studies showed that AKBA-NPs possess better neuroprotection compared with AKBA in primary neurons with oxygen-glucose deprivation (OGD) model and in animals with middle cerebral artery occlusion (MCAO) model. Additionally, AKBA-NPs modulate antioxidant and anti-inflammatory pathways more effectively than AKBA by increasing nuclear erythroid 2-related factor 2 and heme oxygenase-1 expression, and by decreasing nuclear factor-kappa B and 5-lipoxygenase expression. Collectively, our results suggest that AKBA-NPs serve as a potent delivery vehicle for AKBA in cerebral ischemic therapy.

Keywords: Boswellic acid; Cerebral ischemia; Nanoparticle; Neuroprotective effects; Pharmacokinetics.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Administration, Intravenous
  • Animals
  • Anti-Inflammatory Agents / metabolism*
  • Antioxidants / metabolism*
  • Apoptosis / drug effects
  • Cells, Cultured
  • Chitosan / analogs & derivatives*
  • Chitosan / chemistry
  • Disease Models, Animal
  • Glucose / deficiency
  • Glutathione Peroxidase / metabolism
  • Infarction, Middle Cerebral Artery / drug therapy
  • Infarction, Middle Cerebral Artery / pathology
  • Interleukin-1beta / metabolism
  • L-Lactate Dehydrogenase / metabolism
  • Nanoparticles / chemistry*
  • Nanoparticles / ultrastructure
  • Neurons / drug effects
  • Neurons / metabolism
  • Neuroprotection / drug effects*
  • Neuroprotective Agents / pharmacology
  • Neuroprotective Agents / therapeutic use
  • Oxygen
  • Rats, Sprague-Dawley
  • Superoxide Dismutase / metabolism
  • Tissue Distribution / drug effects
  • Triterpenes / pharmacokinetics
  • Triterpenes / pharmacology*
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Anti-Inflammatory Agents
  • Antioxidants
  • Interleukin-1beta
  • Neuroprotective Agents
  • O-carboxymethylchitosan
  • Triterpenes
  • Tumor Necrosis Factor-alpha
  • acetyl-11-ketoboswellic acid
  • Chitosan
  • L-Lactate Dehydrogenase
  • Glutathione Peroxidase
  • Superoxide Dismutase
  • Glucose
  • Oxygen