Neuroprotective Effects of Higenamine Against the Alzheimer’s Disease Via Amelioration of Cognitive Impairment, A Burden, Apoptosis and Regulation of Akt/GSK3β Signaling Pathway

The present investigation was envisaged to elucidate the neuroprotective effect of Higenamine (HGN) against aluminum chloride (AlCl 3 ) triggered experimental Alzheimer’s disease (AD) rat model. Thirty-six male albino Wister rats were randomized and divided in 6 groups and subjected to experimentati...

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Main Authors: Xiaona Yang PhD, Wanliang Du PhD, Yun Zhang PhD, Hui Wang PhD, Maolin He MD
Format: Article
Language:English
Published: SAGE Publishing 2020-12-01
Series:Dose-Response
Online Access:https://doi.org/10.1177/1559325820972205
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author Xiaona Yang PhD
Wanliang Du PhD
Yun Zhang PhD
Hui Wang PhD
Maolin He MD
author_facet Xiaona Yang PhD
Wanliang Du PhD
Yun Zhang PhD
Hui Wang PhD
Maolin He MD
author_sort Xiaona Yang PhD
collection DOAJ
description The present investigation was envisaged to elucidate the neuroprotective effect of Higenamine (HGN) against aluminum chloride (AlCl 3 ) triggered experimental Alzheimer’s disease (AD) rat model. Thirty-six male albino Wister rats were randomized and divided in 6 groups and subjected to experimentation for 6 weeks. Control group, AlCl 3 (100 mg/kg orally), HGN (50 mg/kg orally), HGN25, HGN50, HGN75 (HGN 25, 50 and 75 mg/kg respectively and AlCl 3 100 mg/kg orally). After completion of 42 days protocol, the animals were subjected to passive avoidance test. The animals were then anesthetized by intramuscularly injecting ketamine hydrochloride (24 mg/kg body weight) and euthanized by cervical amputation. Cortical and hippocampal tissues were carefully removed and were employed for quantification of aluminum and acetylcholinesterase. The tissues were quantified using Western blotting and detection kits for APP, Aβ 1-42 , β and γ secretases, Bax, Bad, caspases-9, cyto-c, pAkt and pGSK-3β, and oxidative markers. HGN significantly protected AlCl 3 induced memory and learning impairments, Al overload, AChE hyperactivity, amyloid β (Aβ) burden and apoptosis in brain tissues via activating Akt/GSK3β pathway. HGN attenuated oxidative damage induced by Al by modulation of oxidative markers. Our findings advocate the neuroprotective effect of HGN in AlCl 3 induced AD rat model.
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spelling doaj.art-c0236b040112408bb0f72fc5781fa3212022-12-21T18:35:11ZengSAGE PublishingDose-Response1559-32582020-12-011810.1177/1559325820972205Neuroprotective Effects of Higenamine Against the Alzheimer’s Disease Via Amelioration of Cognitive Impairment, A Burden, Apoptosis and Regulation of Akt/GSK3β Signaling PathwayXiaona Yang PhD0Wanliang Du PhD1Yun Zhang PhD2Hui Wang PhD3Maolin He MD4 Department of Neurology, Beijing Shijitan Hospital, , Beijing, China Department of Neurology, Beijing Tiantan Hospital, , Beijing, China Department of Neurology, Beijing Shijitan Hospital, , Beijing, China Department of Neurology, Beijing Shijitan Hospital, , Beijing, China Department of Neurology, Beijing Shijitan Hospital, , Beijing, ChinaThe present investigation was envisaged to elucidate the neuroprotective effect of Higenamine (HGN) against aluminum chloride (AlCl 3 ) triggered experimental Alzheimer’s disease (AD) rat model. Thirty-six male albino Wister rats were randomized and divided in 6 groups and subjected to experimentation for 6 weeks. Control group, AlCl 3 (100 mg/kg orally), HGN (50 mg/kg orally), HGN25, HGN50, HGN75 (HGN 25, 50 and 75 mg/kg respectively and AlCl 3 100 mg/kg orally). After completion of 42 days protocol, the animals were subjected to passive avoidance test. The animals were then anesthetized by intramuscularly injecting ketamine hydrochloride (24 mg/kg body weight) and euthanized by cervical amputation. Cortical and hippocampal tissues were carefully removed and were employed for quantification of aluminum and acetylcholinesterase. The tissues were quantified using Western blotting and detection kits for APP, Aβ 1-42 , β and γ secretases, Bax, Bad, caspases-9, cyto-c, pAkt and pGSK-3β, and oxidative markers. HGN significantly protected AlCl 3 induced memory and learning impairments, Al overload, AChE hyperactivity, amyloid β (Aβ) burden and apoptosis in brain tissues via activating Akt/GSK3β pathway. HGN attenuated oxidative damage induced by Al by modulation of oxidative markers. Our findings advocate the neuroprotective effect of HGN in AlCl 3 induced AD rat model.https://doi.org/10.1177/1559325820972205
spellingShingle Xiaona Yang PhD
Wanliang Du PhD
Yun Zhang PhD
Hui Wang PhD
Maolin He MD
Neuroprotective Effects of Higenamine Against the Alzheimer’s Disease Via Amelioration of Cognitive Impairment, A Burden, Apoptosis and Regulation of Akt/GSK3β Signaling Pathway
Dose-Response
title Neuroprotective Effects of Higenamine Against the Alzheimer’s Disease Via Amelioration of Cognitive Impairment, A Burden, Apoptosis and Regulation of Akt/GSK3β Signaling Pathway
title_full Neuroprotective Effects of Higenamine Against the Alzheimer’s Disease Via Amelioration of Cognitive Impairment, A Burden, Apoptosis and Regulation of Akt/GSK3β Signaling Pathway
title_fullStr Neuroprotective Effects of Higenamine Against the Alzheimer’s Disease Via Amelioration of Cognitive Impairment, A Burden, Apoptosis and Regulation of Akt/GSK3β Signaling Pathway
title_full_unstemmed Neuroprotective Effects of Higenamine Against the Alzheimer’s Disease Via Amelioration of Cognitive Impairment, A Burden, Apoptosis and Regulation of Akt/GSK3β Signaling Pathway
title_short Neuroprotective Effects of Higenamine Against the Alzheimer’s Disease Via Amelioration of Cognitive Impairment, A Burden, Apoptosis and Regulation of Akt/GSK3β Signaling Pathway
title_sort neuroprotective effects of higenamine against the alzheimer s disease via amelioration of cognitive impairment a burden apoptosis and regulation of akt gsk3β signaling pathway
url https://doi.org/10.1177/1559325820972205
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