Evaluation of neuroprotective effects of Canna indica L against aluminium chloride induced memory impairment in rats

Ojha, Prachi S.; Biradar, Prakash R.; Tubachi, S.; Patil, Vishal S.

doi:10.1007/s13596-021-00627-x

Cited by 6 publications

(6 citation statements)

References 54 publications

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“…The EPM test was used in this work to evaluate memory function, and it was found that AlCl 3 rats showed considerable memory loss. The results are similar with previously published studies on memory loss caused by aluminium [ 24 , 25 ]. In contrast, TRF therapy prevented memory loss in AlCl 3 rats.…”

Section: Discussionsupporting

confidence: 93%

Tocotrienol-Rich Fraction Ameliorates the Aluminium Chloride-Induced Neurovascular Dysfunction-Associated Vascular Dementia in Rats

Shaikh

Muthuraman

2023

Pharmaceuticals

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Neurovascular dysfunction leads to the second most common type of dementia, i.e., vascular dementia (VaD). Toxic metals, such as aluminium, increase the risk of neurovascular dysfunction-associated VaD. Hence, we hypothesized that a natural antioxidant derived from palm oil, i.e., tocotrienol-rich fraction (TRF), can attenuate the aluminium chloride (AlCl3)-induced VaD in rats. Rats were induced with AlCl3 (150 mg/kg) intraperitoneally for seven days followed by TRF treatment for twenty-one days. The elevated plus maze test was performed for memory assessment. Serum nitrite and plasma myeloperoxidase (MPO) levels were measured as biomarkers for endothelial dysfunction and small vessel disease determination. Thiobarbituric acid reactive substance (TBARS) was determined as brain oxidative stress marker. Platelet-derived growth factor-C (PDGF-C) expression in the hippocampus was identified using immunohistochemistry for detecting the neovascularisation process. AlCl3 showed a significant decrease in memory and serum nitrite levels, while MPO and TBARS levels were increased; moreover, PDGF-C was not expressed in the hippocampus. However, TRF treatment significantly improved memory, increased serum nitrite, decreased MPO and TBARS, and expressed PDGF-C in hippocampus. Thus, the results imply that TRF reduces brain oxidative stress, improves endothelial function, facilitates hippocampus PDGF-C expression for neovascularisation process, protects neurons, and improves memory in neurovascular dysfunction-associated VaD rats.

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Section: Discussionsupporting

confidence: 93%

Tocotrienol-Rich Fraction Ameliorates the Aluminium Chloride-Induced Neurovascular Dysfunction-Associated Vascular Dementia in Rats

Shaikh

Muthuraman

2023

Pharmaceuticals

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“…Nehru and Anand ( 2005 ) observed that decreased activities of SOD and CAT in rat’s brains exposed to AlCl 3 may be attributed to a decrease in the synthesis of enzyme proteins. Similarly, numerous studies stated that declines in activities of SOD and CAT are connected with AD (Jadhav and Kulkarni 2022 ; Ekundayo et al 2022 ; Ojha 2023 ; Chen et al 2021 ).…”

Section: Discussionmentioning

confidence: 95%

“…Our findings indicated an increase in brain TNF-α and IL-1β, which may be related to an increase in oxidative stress induced by aluminum in the AlCl 3 group. According to Popa-Wagner et al ( 2013 ), ROS produced in brain cells can alter synaptic and non-synaptic transmission among neurons, leading to neuro-inflammation, cell death, neuro-degeneration, and memory loss. Previous studies have shown that neuro-inflammatory cytokines reduce the efflux transfer of amyloid (A β) , which results in increased A β concentrations in the brain (Blasko et al 1999 ).…”

Section: Discussionmentioning

confidence: 99%

Myco-fabricated ZnO nanoparticles ameliorate neurotoxicity in mice model of Alzheimer’s disease via acetylcholinesterase inhibition and oxidative stress reduction

et al. 2023

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Alzheimer’s disease (AD) is one of the primary health problems linked to the decrease of acetylcholine in cholinergic neurons and elevation in oxidative stress. Myco-fabrication of ZnO-NPs revealed excellent biological activities, including anti-inflammatory and acetylcholinesterase inhibitory potentials. This study aims to determine if two distinct doses of myco-fabricated ZnO-NPs have a positive impact on behavioral impairment and several biochemical markers associated with inflammation and oxidative stress in mice that have been treated by aluminum chloride (AlCl3) to induce AD. Sixty male mice were haphazardly separated into equally six groups. Group 1 was injected i.p. with 0.5 ml of deionized water daily during the experiment. Mice in group 2 received AlCl3 (50 mg/kg/day i.p.). Groups 3 and 4 were treated i.p. with 5 and 10 mg/kg/day of ZnO-NPs only, respectively. Groups 5 and 6 were given i.p. 5 and 10 mg/kg/day ZnO-NPs, respectively, add to 50 mg/kg/day AlCl3. Results showed that the AlCl3 caused an increase in the escape latency time and a reduction in the time spent in the target quadrant, indicating a decreased improvement in learning and memory. Moreover, acetylcholinesterase enzyme (AChE) activity and malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-α), and interleukin 1β (IL-1β) levels were significantly increased, and the content of glutathione (GSH), activities of superoxide dismutase (SOD), catalase (CAT), alanine aminotransferase (ALT), and aspartate aminotransferase (AST), as well as levels of serotonin and dopamine, were decreased in brain tissues only in AlCl3 treated mice. However, treatment of mice with myco-fabrication of ZnO-NPs at doses of 5 or 10 mg/kg improves learning and memory function through ameliorate all the previous parameters in the AD mice group. The low dose of 5 mg/kg is more effective than a high dose of 10 mg/kg. In accordance with these findings, myco-fabricated ZnO-NPs could enhance memory and exhibit a protective influence against memory loss caused by AlCl3.

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“…The concentration of ACh and BuCh, which are neurotransmitters involved in normal functioning of the brain, is found to decrease in AD pathological state due to quick hydrolysis by AChE and BuChE, respectively [35]. The in vitro AChE decreases in concentration of photobiomodulation on the cerebral cortex and hippocampus.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective effects of photobiomodulation by hormesis on scopolamine induced neurodegenerative diseases of memory disorders in rats a paradigm shift

Danappanvar

Biradar

Jalalpure

et al. 2023

Journal of Biophotonics

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The loss and progressive dysfunction of neurons are hallmarks of neurodegenerative diseases. The aim of the current study is to explore the effects of photobiomodulation at 460–660 nm (100–1000 lux units) on the progression of scopolamine‐induced cognitive dysfunctions in Wistar male rats. Photobiomodulation (PBM) is defined as “the use of monochromatic or quasi‐monochromatic light from a low‐power laser or light‐emitting diode (LED) source to modify or modulate biological functions.” Neuroprotective activity was assessed by in vivo models such as the Morris water maze, the elevated plus maze (EPM), and the T‐maze. After using scopolamine (1 mg/kg/day) as a dementia induction model for 21 days, the induction was primarily due to impairments in cholinergic transmission, oxidative stress, and inflammation. The in vitro determinations, including acetylcholinesterase (AChE), butyrylcholinesterase (BChE), reduced glutathione (GSH), malondialdehyde (MDA), superoxide dismutase (SOD), tumor necrosis factor‐alpha (TNF‐α), Interleukin 1 beta (IL‐1β), and alkaline phosphatase (ALP), were assessed biochemicals and biomarkers. The structural and morphological integrity of the cortex and hippocampus was investigated through histopathology. In vivo studies of exteroceptive behavior models such as the Morris water maze, the EPM, and the T‐maze revealed that administration of scopolamine resulted in enhanced escape latency time (ELT), transfer latency (TL), and decreased percentage alternation, respectively. The levels of AChE, BChE, reduced, GSH, SOD, TNF‐α, IL‐1β and ALP were increased, while MDA level was decreased. In contrast to normal and control groups with treatment groups, histopathology of the cortex and hippocampus examination revealed the maintenance of structural integrity and densities of CA1 and CA3 neuronal cells. However, network pharmacology predicted Ca+2 modulation of various pathways, among the treatments with red LED light showed highly significant amelioration compared with normal and control groups. Photobiomodulation by hormesis, chromophores in cells, and tissues excitation can influence neuroprotective effect mainly by scavenging of ROS, variation in the level of GSH MDA and SOD mitochondrial electron transfer, the improved abscopal effects on improved in gut microbiome by resembles the of fecal ALP level correlation of intestinal microbiome, cholinergic neurotransmissions, anti‐inflammatory, and antioxidant activities.

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Evaluation of neuroprotective effects of Canna indica L against aluminium chloride induced memory impairment in rats

Cited by 6 publications

References 54 publications

Tocotrienol-Rich Fraction Ameliorates the Aluminium Chloride-Induced Neurovascular Dysfunction-Associated Vascular Dementia in Rats

Tocotrienol-Rich Fraction Ameliorates the Aluminium Chloride-Induced Neurovascular Dysfunction-Associated Vascular Dementia in Rats

Myco-fabricated ZnO nanoparticles ameliorate neurotoxicity in mice model of Alzheimer’s disease via acetylcholinesterase inhibition and oxidative stress reduction

Neuroprotective effects of photobiomodulation by hormesis on scopolamine induced neurodegenerative diseases of memory disorders in rats a paradigm shift

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