Lim SM

References (6)

Title : Mahanimbine Improved Aging-Related Memory Deficits in Mice through Enhanced Cholinergic Transmission and Suppressed Oxidative Stress, Amyloid Levels, and Neuroinflammation - Mani_2021_Brain.Sci_12_12
Author(s) : Mani V , Mohd Azahan NS , Ramasamy K , Lim SM , Abdul Majeed AB
Ref : Brain Sci , 12 :12 , 2021
Abstract : Murraya koenigii leaves contain mahanimbine, a carbazole alkaloid, reported with improving cholinergic neuronal transmission and reducing neuroinflammation in the CNS. The current research investigated the effects of mahanimbine on age-related memory deficits, oxidative stress, cholinergic dysfunction, amyloid formation, and neuroinflammation in aged mice (16 months old). Mahanimbine was administered (1 and 2 mg/kg, p.o.) daily to groups of aged mice for 30 days. The Morris water maze (MWM) task was performed to study spatial learning (escape latency (EL) and swimming distance (SD)) and memory (probe test). The levels of malondialdehyde (MDA), glutathione (GSH), acetylcholine (ACh), acetylcholinesterase (AChE), beta-amyloid (Abeta(1-40) and Abeta(1-42)), beta-secretase (BACE-1), as well as neuroinflammation markers (total cyclooxygenase (COX) and COX-2 expression), were measured from the isolated brain. Mahanimbine reduced the EL time and SD in the MWM test. From the probe trial, the mahanimbine-treated group spent more time in the targeted quadrant related to the age-matched control, which indicated the enhancement of memory retention. From the biochemical tests, the treatment decreased MDA, AChE, Abeta(1-40), and Abeta(1-42), BACE-1, total COX activity, and COX-2 expression. It also raised the brain GSH and ACh levels in aged mice compared to age-matched control. These results have supported the reversal of memory dysfunctions by mahanimbine in aged mice and hypothesized that it could be a potential target to treat age-related neurodegenerative disease.
ESTHER : Mani_2021_Brain.Sci_12_12
PubMedSearch : Mani_2021_Brain.Sci_12_12
PubMedID: 35053756

Title : Virgin Coconut Oil-Induced Neuroprotection in Lipopolysaccharide-Challenged Rats is Mediated, in Part, Through Cholinergic, Anti-Oxidative and Anti-Inflammatory Pathways - Rahim_2020_J.Diet.Suppl__1
Author(s) : Rahim NS , Lim SM , Mani V , Hazalin N , Majeed ABA , Ramasamy K
Ref : J Diet Suppl , :1 , 2020
Abstract : Neuroinflammation is associated with neuronal cell death and could lead to chronic neurodegeneration. This study investigated the neuroprotective potential of virgin coconut oil (VCO) against lipopolysaccharide (LPS)-induced cytotoxicity of neuroblastoma SK-N-SH cells. The findings were validated using Wistar rats, which were fed with 1-10 g/kg VCO for 31 days, exposed to LPS (0.25 mg/kg) and subjected to the Morris Water Maze Test. Brain homogenate was subjected to biochemical analyses and gene expression studies. alpha-Tocopherol (alpha-T; 150 mg/kg) served as the positive control. VCO (100 microg/mL) significantly (p < 0.01) improved SK-N-SH viability (+57%) and inhibited reactive oxygen species (-31%) in the presence of LPS. VCO (especially 10 g/kg) also significantly (p < 0.05) enhanced spatial memory of LPS-challenged rats. Brain homogenate of VCO-fed rats was presented with increased acetylcholine (+33%) and reduced acetylcholinesterase (-43%). The upregulated antioxidants may have reduced neuroinflammation [malondialdehyde (-51%), nitric oxide (-49%), Cox-2 (-64%) and iNos (-63%)] through upregulation of IL-10 (+30%) and downregulation of IL-1beta (-65%) and Interferon-gamma (-25%). There was also reduced expression of Bace-1 (-77%). VCO-induced neuroprotection, which was comparable to alpha-T, could be mediated, in part, through inflammatory, cholinergic and amyloidogenic pathways.
ESTHER : Rahim_2020_J.Diet.Suppl__1
PubMedSearch : Rahim_2020_J.Diet.Suppl__1
PubMedID: 33962540

Title : Lactobacillus johnsonii CJLJ103 Attenuates Scopolamine-Induced Memory Impairment in Mice by Increasing BDNF Expression and Inhibiting NF-kappaB Activation - Lee_2018_J.Microbiol.Biotechnol_28_1443
Author(s) : Lee HJ , Lim SM , Kim DH
Ref : J Microbiol Biotechnol , 28 :1443 , 2018
Abstract : In the present study, we examined whether Lactobacillus johnsonii CJLJ103 (LJ) could alleviate cholinergic memory impairment in mice. Oral administration of LJ alleviated scopolamine-induced memory impairment in passive avoidance and Y-maze tasks. Furthermore, LJ treatment increased scopolamine-suppressed BDNF expression and CREB phosphorylation in the hippocampi of the brain, as well as suppressed TNF-alpha expression and NF-kappaB activation. LJ also increased BDNF expression in corticosterone-stimulated SH-SY5Y cells and inhibited NF-kappaB activation in LPS-stimulated microglial BV2 cells. However, LJ did not inhibit acetylcholinesterase activity. These findings suggest that LJ, a member of human gut microbiota, may mitigate cholinergic memory impairment by increasing BDNF expression and inhibiting NF-kappaB activation.
ESTHER : Lee_2018_J.Microbiol.Biotechnol_28_1443
PubMedSearch : Lee_2018_J.Microbiol.Biotechnol_28_1443
PubMedID: 30111074

Title : Enhanced memory in Wistar rats by virgin coconut oil is associated with increased antioxidative, cholinergic activities and reduced oxidative stress - Rahim_2017_Pharm.Biol_55_825
Author(s) : Rahim NS , Lim SM , Mani V , Abdul Majeed AB , Ramasamy K
Ref : Pharm Biol , 55 :825 , 2017
Abstract : CONTEXT: Virgin coconut oil (VCO) has been reported to possess antioxidative, anti-inflammatory and anti-stress properties. OBJECTIVE: Capitalizing on these therapeutic effects, this study investigated for the first time the potential of VCO on memory improvement in vivo. MATERIALS AND
METHODS: Thirty male Wistar rats (7-8 weeks old) were randomly assigned to five groups (n = six per group). Treatment groups were administered with 1, 5 and 10 g/kg VCO for 31 days by oral gavages. The cognitive function of treated-rats were assessed using the Morris Water Maze Test. Brains were removed, homogenized and subjected to biochemical analyses of acetylcholine (ACh) and acetylcholinesterase (AChE), antioxidants [superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), glutathione peroxidase (GPx) and glutathione reductase (GRx)], lipid peroxidase [malondialdehyde (MDA)] as well as nitric oxide (NO). alpha-Tocopherol (alphaT; 150 mg/kg) was also included for comparison purposes.
RESULTS: VCO-fed Wistar rats exhibited significant (p < 0.05) improvement of cognitive functions [reduced escape latency (>/= 1.8 s), reduced escape distance (>/= 0.3 m) and increased total time spent on platform (>/= 1 s)]. The findings were accompanied by elevation of ACh (15%), SOD (8%), CAT (>/= 54%), GSH (>/= 20%) and GPx (>/= 12%) and reduction of AChE (>/=17%), MDA (> 33%) and NO (>/= 34%). Overall, memory improvement by VCO was comparable to alphaT. DISCUSSION AND CONCLUSION: VCO has the potential to be used as a memory enhancer, the effect of which was mediated, at least in part, through enhanced cholinergic activity, increased antioxidants level and reduced oxidative stress.
ESTHER : Rahim_2017_Pharm.Biol_55_825
PubMedSearch : Rahim_2017_Pharm.Biol_55_825
PubMedID: 28118770

Title : Lactobacilli-fermented cow's milk attenuated lipopolysaccharide-induced neuroinflammation and memory impairment in vitro and in vivo - Musa_2017_J.Dairy.Res_84_488
Author(s) : Musa NH , Mani V , Lim SM , Vidyadaran S , Abdul Majeed AB , Ramasamy K
Ref : J Dairy Res , 84 :488 , 2017
Abstract : Nutritional interventions are now recommended as strategies to delay Alzheimer's disease (AD) progression. The present study evaluated the neuroprotective effect (anti-inflammation) of lactic acid bacteria (either Lactobacillus fermentum LAB9 or L. casei LABPC) fermented cow's milk (CM) against lipopolysaccharide (LPS)-activated microglial BV2 cells in vitro. The ability of CM-LAB in attenuating memory deficit in LPS-induced mice was also investigated. ICR mice were orally administered with CM-LAB for 28 d before induction of neuroinflammation by LPS. Learning and memory behaviour were assessed using the Morris Water Maze Test. Brain tissues were homogenised for measurement of acetylcholinesterase (AChE), antioxidative, lipid peroxidation (malondialdehyde (MDA)) and nitrosative stress (NO) parameters. Serum was collected for cytokine analysis. CM-LAB9 and CM-LABPC significantly (P < 0.05) decreased NO level but did not affect CD40 expression in vitro. CM-LAB attenuated LPS-induced memory deficit in mice. This was accompanied by significant (P < 0.05) increment of antioxidants (SOD, GSH, GPx) and reduction of MDA, AChE and also pro-inflammatory cytokines. Unfermented cow's milk (UCM) yielded greater cytokine lowering effect than CM-LAB. The present findings suggest that attenuation of LPS-induced neuroinflamation and memory deficit by CM-LAB could be mediated via anti-inflammation through inhibition of AChE and antioxidative activities.
ESTHER : Musa_2017_J.Dairy.Res_84_488
PubMedSearch : Musa_2017_J.Dairy.Res_84_488
PubMedID: 29154736

Title : Ciproxifan improves cholinergic transmission, attenuates neuroinflammation and oxidative stress but does not reduce amyloid level in transgenic mice - Mani_2017_Life.Sci_180_23
Author(s) : Mani V , Jaafar SM , Azahan NSM , Ramasamy K , Lim SM , Ming LC , Majeed ABA
Ref : Life Sciences , 180 :23 , 2017
Abstract : AIM: The present study is aimed to investigate the ability of ciproxifan, a histamine H3 receptor antagonist to inhibit beta-amyloid (Abeta)-induced neurotoxicity in SK-N-SH cells and APP transgenic mouse model. MATERIALS AND
METHODS: In vitro studies was designed to evaluate the neuroprotective effects of ciproxifan in Abeta25-35 - induced SK-N-SH cells. For the in vivo study, ciproxifan (1 and 3mg/kg, i.p.) was administrated to transgenic mice for 15days and behaviour was assessed using the radial arm maze (RAM). Brain tissues were collected to measure Abeta levels (Abeta1-40 and Abeta1-42), acetylcholine (ACh), acetylcholinesterase (AChE), nitric oxide (NO), lipid peroxidation (LPO), antioxidant activities, cyclooxygenases (COX) and cytokines (IL-1alpha, IL-1beta and IL-6), while plasma was collected to measure TGF-1beta.
RESULTS: The in vitro studies demonstrated neuroprotective effect of ciproxifan by increasing cell viability and inhibiting reactive oxygen species (ROS) in Abeta25-35-induced SK-N-SH cells. Ciproxifan significantly improved the behavioural parameters in RAM. Ciproxifan however, did not alter the Abeta levels in APP transgenic mice. Ciproxifan increased ACh and showed anti-oxidant properties by reducing NO and LPO levels as well as enhancing antioxidant levels. The neuroinflammatory analysis showed that ciproxifan reduced both COX-1 and COX-2 activities, decreased the level of pro-inflammatory cytokines IL-1alpha, IL-1beta and IL-6 and increased the level of anti-inflammatory cytokine TGF-1beta. CONCLUSION: This present study provides scientific evidence of the use of ciproxifan via antioxidant and cholinergic pathways in the management of AD.
ESTHER : Mani_2017_Life.Sci_180_23
PubMedSearch : Mani_2017_Life.Sci_180_23
PubMedID: 28501482