Tualang Honey and its Methanolic Fraction Improve LPS-induced Learning and Memory Impairment in Male Rats: Comparison with Memantine

Wan, Muhammad Hilmi; Long, Idris; Zakaria, Rahimah; Othman, Zahiruddin

doi:10.2174/1573401315666181130103456

Cited by 18 publications

(19 citation statements)

References 48 publications

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“…Tualang honey has also been reported to mitigate memory impairment induced by hypoxia [ 47 ] and lipopolysaccharide [ 48 ]. Hypoxia exposure may cause oxidative stress, alteration in cholinergic and glutamate neurotransmissions, as well as neuronal apoptosis in the cortex, striatum, and hippocampal cells, ultimately causing memory impairment [ 49 , 50 ].…”

Section: Resultsmentioning

confidence: 99%

“…Tualang honey administration at 200 mg/kg body weight for 14 days to hypoxia-induced rats resulted in significant improvement in spatial and recognition memory as well as reduced neuronal damage in the hippocampus compared to hypoxia-induced rats treated with sucrose [ 47 ]. In lipopolysaccharide-induced rats, a rat model of Alzheimer’s disease, a similar dose and duration of Tualang honey treatment significantly improved spatial and recognition memory comparable to the group treated with memantine, a medication used to treat Alzheimer’s disease [ 48 ]. It was also discovered that 150 mg/kg of methanolic fraction of Tualang honey produced similar effects [ 48 ].…”

Section: Resultsmentioning

confidence: 99%

“…In lipopolysaccharide-induced rats, a rat model of Alzheimer’s disease, a similar dose and duration of Tualang honey treatment significantly improved spatial and recognition memory comparable to the group treated with memantine, a medication used to treat Alzheimer’s disease [ 48 ]. It was also discovered that 150 mg/kg of methanolic fraction of Tualang honey produced similar effects [ 48 ]. Further investigation revealed that Tualang honey and its methanolic fraction exhibited significant neuroprotective effects against oxidative stress, hippocampal neurodegeneration, and amyloid deposition in the lipopolysaccharide-induced rats, although pure Tualang honey exhibited slightly higher protective activity than its methanolic fraction [ 51 ].…”

Section: Resultsmentioning

confidence: 99%

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Tualang Honey: A Decade of Neurological Research

et al. 2021

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Tualang honey has been shown to protect against neurodegeneration, leading to improved memory/learning as well as mood. In addition, studies have also demonstrated its anti-inflammatory and antioxidant properties. However, a substantial part of this research lacks systematization, and there seems to be a tendency to start anew with every study. This review presents a decade of research on Tualang honey with a particular interest in the underlying mechanisms related to its effects on the central nervous system. A total of 28 original articles published between 2011 and 2020 addressing the central nervous system (CNS) effects of Tualang honey were analysed. We identified five main categories, namely nootropic, antinociceptive, stress-relieving, antidepressant, and anxiolytic effects of Tualang honey, and proposed the underlying mechanisms. The findings from this review may potentially be beneficial towards developing new therapeutic roles for Tualang honey and help in determining how best to benefit from this brain supplement.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

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Tualang Honey: A Decade of Neurological Research

et al. 2021

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“…Minocycline (USP, 12601Twinbrook Pkwy, Rockville, MD) and memantine (USP, 12601Twinbrook Pkwy, Rockville, MD) were administered intraperitoneally once daily for 2 weeks consequently, starting from day 1 to day14. LPS was obtained from E.coli 0111:B4 (Sigma-Aldrich, St. Louis, MO) and injected intraperitoneally once on day 5 at the dose of 5 mg/kg (Yaacob et al, 2018). After 2 weeks of treatment, all rats were subjected to OFT from day 15 to day 18.…”

Section: Experimental Designmentioning

confidence: 99%

Minocycline attenuates lipopolysaccharide-induced locomotor deficit and anxiety-like behavior via upregulation of the BDNF/CREB protein expression in the rat medial prefrontal cortex (mPFC)

Qaid

Abdullah

Zakaria

et al. 2022

Preprint

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Introduction: Neuroinflammation following lipopolysaccharide (LPS) administration induces locomotor deficit and anxiety-like behavior. In this study, minocycline was compared to memantine, the NMDA receptor antagonist, for its effects on LPS-induced locomotor deficit and anxiety-like behavior in rats. Methodology: Adult male Sprague Dawley rats were administered either two different doses of minocycline (25 or 50 mg/kg/day, i.p.) or 10 mg/kg/day of memantine (i.p.) for 14 days four days prior to LPS (5 mg/kg, i.p.) injection. The locomotor activity and anxiety-like behavior were assessed using the open field test (OFT). The phosphorylated tau protein level was measured using ELISA while the expression and density of brain-derived neurotrophic factor (BDNF) and cAMP response element-binding protein (CREB) protein in the medial prefrontal cortex (mPFC) were measured using immunohistochemistry and western blot, respectively. Results: In the mPFC, minocycline treatment reduced the locomotor deficit and anxiety-like behavior, reduced phosphorylated tau protein level, and upregulated BDNF/CREB protein expression comparable to memantine, with the higher dose of minocycline having better benefits. Conclusion: Minocycline treatment attenuated LPS-induced locomotor deficit and anxiety-like behavior in rats, possibly via a decrease in phosphorylated tau protein levels and an increase in the expression of the BDNF/CREB proteins.

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“…Acetylcholinesterase (AChE) inhibitors (prevent the degradation of Ach and enhance ACh levels) including donepezil, rivastigmine, and galantamine cause nausea, anorexia, vomiting, and diarrhea. [5][6][7]. The glutamate antagonist memantine is another FDA-approved anti-Alzheimer medication that acts as an antagonist of nicotinic receptors (nAChRs) non-competitively that produces fast desensitization of nAChR activity [8] and lowers neuronal excitotoxicity [9].…”

Section: Introductionmentioning

confidence: 99%