TY - JOUR
T1 - Neuroprotective role of asiatic acid in aluminium chloride induced rat model of Alzheimer’s disease
AU - Rather, Mashoque Ahmad
AU - Thenmozhi, Arokiasamy Justin
AU - Manivasagam, Thamilarasan
AU - Bharathi, Mathiyazahan Dhivya
AU - Essa, Musthafa Mohamed
AU - Guillemin, Gilles J.
N1 - Publisher Copyright:
© 2018 Frontiers in Bioscience. All Rights Reserved.
PY - 2018/1/1
Y1 - 2018/1/1
N2 - Alzheimer’s disease (AD) is the most common form of dementia, characterized by memory loss, cognitive impairment and personality disorders accompanied by diffuse structural abnormalities in the brain of elderly people. The current investigation explored the neuroprotective potential of asiatic acid (AA), a natural triterpene of Centella asiatica on aluminium chloride (AlCl3) induced rat model of AD. Oral administration of AlCl3 (100 mg/kg b.w.) for 42 days significantly elevated the levels of Al, activity of acetyl cholinesterase and expressions of amyloid precursor protein, amyloid beta1–42, beta and gamma secretases, glial fibrillary acidic protein, ionized calcium binding adaptor molecule 1, interleukins -1β, 6, 4, 2, tumor necrosis factor alpha, inducible nitric oxide synthase, nuclear factor- k beta and cyclooxygenase-2 in the hippocampus and cortex compared to the control group. Our observations suggested that AA treatment mitigated AlCl3 induced AD associated pathologies, which might be due to its multiple pharmacological actions. Further studies are necessary in order to explore the link between AlCl3-mediated oxidative stress and associated apoptosis to establish its neuroprotective role in AD.
AB - Alzheimer’s disease (AD) is the most common form of dementia, characterized by memory loss, cognitive impairment and personality disorders accompanied by diffuse structural abnormalities in the brain of elderly people. The current investigation explored the neuroprotective potential of asiatic acid (AA), a natural triterpene of Centella asiatica on aluminium chloride (AlCl3) induced rat model of AD. Oral administration of AlCl3 (100 mg/kg b.w.) for 42 days significantly elevated the levels of Al, activity of acetyl cholinesterase and expressions of amyloid precursor protein, amyloid beta1–42, beta and gamma secretases, glial fibrillary acidic protein, ionized calcium binding adaptor molecule 1, interleukins -1β, 6, 4, 2, tumor necrosis factor alpha, inducible nitric oxide synthase, nuclear factor- k beta and cyclooxygenase-2 in the hippocampus and cortex compared to the control group. Our observations suggested that AA treatment mitigated AlCl3 induced AD associated pathologies, which might be due to its multiple pharmacological actions. Further studies are necessary in order to explore the link between AlCl3-mediated oxidative stress and associated apoptosis to establish its neuroprotective role in AD.
KW - Alzheimer’s disease
KW - Amyloid Pathology
KW - Asiatic Acid
KW - Inflammation
KW - Memory Deficits
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U2 - 10.2741/s514
DO - 10.2741/s514
M3 - Article
C2 - 28930532
AN - SCOPUS:85037979871
SN - 1945-0516
VL - 10
SP - 262
EP - 275
JO - Frontiers in Bioscience - Scholar
JF - Frontiers in Bioscience - Scholar
IS - 2
ER -