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<PublisherName>isfcppharmaspire</PublisherName>
<JournalTitle>Pharmaspire</JournalTitle>
<PISSN>C</PISSN>
<EISSN>o</EISSN>
<Volume-Issue>Volume 12, Issue 1</Volume-Issue>
<PartNumber/>
<IssueTopic>Multidisciplinary</IssueTopic>
<IssueLanguage>English</IssueLanguage>
<Season>January-March, 2020</Season>
<SpecialIssue>N</SpecialIssue>
<SupplementaryIssue>N</SupplementaryIssue>
<IssueOA>Y</IssueOA>
<PubDate>
<Year>-0001</Year>
<Month>11</Month>
<Day>30</Day>
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<ArticleType>Pharmaceutics</ArticleType>
<ArticleTitle>Orally administered chebulinic acid negated neurobehavioral deficits in intracerebroventricular streptozotocin and Amyloid-__ampersandsignbeta;-induced experimental model of dementia</ArticleTitle>
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<ArticleLanguage>English</ArticleLanguage>
<ArticleOA>Y</ArticleOA>
<FirstPage>20</FirstPage>
<LastPage>27</LastPage>
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<Author>
<FirstName>Rimpi</FirstName>
<LastName>Arora</LastName>
<AuthorLanguage>English</AuthorLanguage>
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<CorrespondingAuthor>N</CorrespondingAuthor>
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<Abstract>Background: With the constant failure of the clinical trials and continuous exploration of a therapeutic target against Alzheimer’s disease (AD) is the utmost need. Chebulinic acid (ChA) has been reported to possess neuroprotective potential in various neurodegenerative models such as anxiety and depression. In the current study, the ChA was challenged on the progression of AD induced by intracerebroventricular (ICV)-streptozotocin (STZ)-and A__ampersandsignbeta; induced neurotoxicity to determine its therapeutic potential in experimental dementia. Material and Methods: STZ and A__ampersandsignbeta; were infused bilaterally (3 mg/kg/icv) on day 1st and 3rd after surgery. ChA (25, 50 and 100 mg/kg/p.o) was administered from 7th day onwards up to 21st day following 1st ICV-STZ and A__ampersandsignbeta; infusion. Cognitive impairment was evaluated by actophotometer, Morris water maze (MWM) and object recognition task (ORT) in rats whereas biochemical and neurochemical, using hipoocampal brain regions on day 22nd. Results: Ventricular administration of STZ and A__ampersandsignbeta; in rats found to significantly shorten the latency time on the MWM and ORT which was associated with significant alterations in hippocampal biochemistry, including elevation in oxidative stress and compromised antioxidant defense (reduced glutathione). Conclusion: ChA treatment significantly prevented the ICV-STZ and A__ampersandsignbeta; induced memory compromised antioxidant defense and cholinergic deficits in rats. These results clearly pointed to the pivotal role of ChA in ICV-STZ and A__ampersandsignbeta; induced neurotoxicity and its association may be a promising alternative to be investigated in the treatment of AD-like dementia.</Abstract>
<AbstractLanguage>English</AbstractLanguage>
<Keywords>Alzheimer’s dementia, chebulinic acid, hippocampus, neuroprotection, streptozotocin</Keywords>
<URLs>
<Abstract>https://isfcppharmaspire.com/ubijournal-v1copy/journals/abstract.php?article_id=13836&title=Orally administered chebulinic acid negated neurobehavioral deficits in intracerebroventricular streptozotocin and Amyloid-__ampersandsignbeta;-induced experimental model of dementia</Abstract>
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<References>
<ReferencesarticleTitle>References</ReferencesarticleTitle>
<ReferencesfirstPage>16</ReferencesfirstPage>
<ReferenceslastPage>19</ReferenceslastPage>
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