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

• Published in: Dose-response Vol. 18; no. 4; p. 1559325820972205
• Main Authors: Yang, Xiaona, Du, Wanliang, Zhang, Yun, Wang, Hui, He, Maolin
• Format: Journal Article
• Language: English
• Published: Los Angeles, CA SAGE Publications 01.10.2020; SAGE PUBLICATIONS, INC
• Subjects: Aluminum; Apoptosis; Ketamine; Original; higenamine; cognitive impairment; Alzheimer’s disease; neuroprotective
• ISSN: 1559-3258; 1559-3258
• DOI: 10.1177/1559325820972205

The present investigation was envisaged to elucidate the neuroprotective effect of Higenamine (HGN) against aluminum chloride (AlCl3) 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, AlCl3 (100 mg/kg orally), HGN (50 mg/kg orally), HGN25, HGN50, HGN75 (HGN 25, 50 and 75 mg/kg respectively and AlCl3 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, Aβ1-42, β and γ secretases, Bax, Bad, caspases-9, cyto-c, pAkt and pGSK-3β, and oxidative markers. HGN significantly protected AlCl3 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 AlCl3 induced AD rat model.