TY - JOUR
T1 - A novel nanoformulation of ellagic acid is promising in restoring oxidative homeostasis in rat brains with alzheimer’s disease
AU - Harakeh, Steve
AU - Qari, Mohamad H.
AU - Ramadan, Wafaa S.
AU - Al Jaouni, Soad K.
AU - Almuhayawi, Mohammed S.
AU - Al Amri, Turki
AU - Ashraf, Ghulam Md
AU - Bharali, Dhruba J.
AU - Mousa, Shaker A.
N1 - Publisher Copyright:
© 2021 Bentham Science Publishers.
PY - 2021
Y1 - 2021
N2 - Background: Aluminum toxicity induces neurodegenerative changes in the brain and results in Alzheimer’s disease (AD). Objective: Here, the aim was to evaluate the antioxidant therapeutic effects of ellagic acid (EA) and EA-loaded nanoparticles (EA-NP) in an aluminum chloride-induced AD rat model. Methods: The nanoparticles’ loading of EA was 0.84/1 w/w. The in vitro release kinetics of EA from EA-NP in fetal bovine serum showed 60% release in the first 1-5 hours, followed by sustained release at 60-70% over 6-24 hours. Six groups were implemented; group 1 served as the control, group 2 received EA, group 3 received EA-NP, group 4 was the AD rat model administered AlCl3 (50 mg/kg) for 4 weeks, groups 5 (AD+EA) and 6 (AD+EA-NP) were treated with EA and EA-NP, respectively, for 2 weeks after AlCl3 was stopped. The neurotoxicity in the rat brain was examined by measuring the brain antioxidant biomarkers catalase, glu-tathione, and total antioxidant activity and lipid peroxidation (thiobarbituric acid, TBA). Histopathological studies using hematoxylin and eosin, cresyl violet, silver stains, and the novel object recognition test were ex-amined. Results: Data revealed significant increase of antioxidant biomarkers and decreased TBA in the EA-NP group. The pathological hallmarks of AD-vacuolation of the neurons, chromatolysis, neurofibrillary tangles, and the se-nile plaques in brains of the AD rat model were decreased and restoration of Nissl granules was noted. The cal-culated discrimination index in the behavioral test increased more in cases treated with EA-NP. Conclusion: The treatment of AD with EA-NP was more effective than EA in alleviating the oxidative neuro-toxic effects on AD rat brains.
AB - Background: Aluminum toxicity induces neurodegenerative changes in the brain and results in Alzheimer’s disease (AD). Objective: Here, the aim was to evaluate the antioxidant therapeutic effects of ellagic acid (EA) and EA-loaded nanoparticles (EA-NP) in an aluminum chloride-induced AD rat model. Methods: The nanoparticles’ loading of EA was 0.84/1 w/w. The in vitro release kinetics of EA from EA-NP in fetal bovine serum showed 60% release in the first 1-5 hours, followed by sustained release at 60-70% over 6-24 hours. Six groups were implemented; group 1 served as the control, group 2 received EA, group 3 received EA-NP, group 4 was the AD rat model administered AlCl3 (50 mg/kg) for 4 weeks, groups 5 (AD+EA) and 6 (AD+EA-NP) were treated with EA and EA-NP, respectively, for 2 weeks after AlCl3 was stopped. The neurotoxicity in the rat brain was examined by measuring the brain antioxidant biomarkers catalase, glu-tathione, and total antioxidant activity and lipid peroxidation (thiobarbituric acid, TBA). Histopathological studies using hematoxylin and eosin, cresyl violet, silver stains, and the novel object recognition test were ex-amined. Results: Data revealed significant increase of antioxidant biomarkers and decreased TBA in the EA-NP group. The pathological hallmarks of AD-vacuolation of the neurons, chromatolysis, neurofibrillary tangles, and the se-nile plaques in brains of the AD rat model were decreased and restoration of Nissl granules was noted. The cal-culated discrimination index in the behavioral test increased more in cases treated with EA-NP. Conclusion: The treatment of AD with EA-NP was more effective than EA in alleviating the oxidative neuro-toxic effects on AD rat brains.
KW - Aluminum
KW - Alzheimer’s disease
KW - Antioxidant biomarkers
KW - Ellagic acid
KW - Nano-ellagic acid
KW - Nanoformulation
KW - Neuro-protection
KW - Oxidative stress
UR - http://www.scopus.com/inward/record.url?scp=85110396445&partnerID=8YFLogxK
U2 - 10.2174/1389200221666201216170851
DO - 10.2174/1389200221666201216170851
M3 - Article
C2 - 33327909
AN - SCOPUS:85110396445
SN - 1389-2002
VL - 22
SP - 299
EP - 307
JO - Current Drug Metabolism
JF - Current Drug Metabolism
IS - 4
ER -
