Premium
P3‐491: NEUROPROTECTIVE EFFECT OF NARINGIN IN QUINOLINIC ACID‐INDUCED HUNTINGTON'S DISEASE: ROLE OF BAX/BCL‐2 AND CASPASE‐3
Author(s) -
Mukherjee Anwesha A.,
Kandhare Amit D.,
Bodhankar Subhash L.
Publication year - 2018
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2018.06.1855
Subject(s) - naringin , neuroprotection , pharmacology , chemistry , malondialdehyde , oxidative stress , superoxide dismutase , nitric oxide synthase , biochemistry , medicine , endocrinology , chromatography , enzyme
Background:Huntington’s disease (HD) is a dominant autosomal inherited disorder characterized by chorea, cognitive impairment, and psychiatric disturbances. Naringin, flavanone glycoside exhibits the anti-inflammatory and antioxidant effect. The aim of present investigation was to evaluate the neuroprotective effect of naringin in quinolinic acid (QA) induced HD in laboratory rats. Methods:HD was induced in male Wistar rats by single intrastriatal injection of QA (300 nmol/4 ul saline) in striatum except normal. Sham rats received an equal volume of saline. Rats were divided into various groups viz., normal, sham, QA control, Naringin (20, 40 and 80 mg/kg, p.o.). Rats were treated for 21 days. Various behavioral, biochemical and histological parameters were evaluated. Results: Naringin (40 and 80 mg/kg) treatment significantly (p < 0.05) attenuated QA-induced behavioral (motor and memory function) activity. QA-induced elevated neural oxido-nitrosative stress (Superoxide dismutase, glutathione, malondialdehyde and nitric oxide) was significantly inhibited (p < 0.05) by naringin (40 and 80 mg/kg) treatment. Decreased level of biogenic amines (dopamine, 5-hydroxytryptamine, and g-Aminobutyric acid) and mitochondrial complex (I-IV) was significantly increased (p < 0.05) by it. Triphenyl tetrazolium chloride (TTC) scanning also showed a significant reduction (p< 0.05) in QA-induced striatal degeneration by naringin treatment. QA-induced alterations in Bcl-2-associated X protein (BAX), Bcl-2 and caspase-3 mRNA expression was significantly (p < 0.05) attenuated by naringin (40 and 80 mg/kg) treatment. Conclusions:Neuroprotective effect of naringin could be via modulation of oxido-nitrosative stress, brain monoamines, and BAX/Bcl-2-caspase-3 pathway.