Antidepressants Modulate Behavioral, Biochemical, and Histological Alterations Induced by Chronic Aluminum Chloride Administration in Wistar Rats

Shaik, Arshad Basha; Shenoy, Smita; Anupama, .; Rao, Muddanna S.; Amuthan, Arul

doi:10.4103/jpp.jpp_135_18

Cited by 7 publications

(5 citation statements)

References 40 publications

(55 reference statements)

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“…In addition, based on biochemical assay for markers of OS in hippocampal tissues, our data clearly demonstrate that Al-induced brain OS, this is due on the fact that Al exposure significantly elevated TBARS and NO levels whereas reducing SOD activity. Our results are in total agreement with recent published data (Auti and Kulkarni, 2019;Shaik et al, 2019). Similarly, the reports of Al-Amin et al ( 2019) are in line with our results in which Al treatment enhanced the level of LPO and NO in the hippocampus as well as a decrease in antioxidant status.…”

Section: Histopathological Resultssupporting

confidence: 94%

Neuroprotective Effects of Melatonin Against Neurotoxicity Induced by Intrahippocampal Injection of Aluminum in Male Wistar Rats: Possible Involvement of Oxidative Stress Pathway

Zghari¹,

Lamtai²,

Azirar³

et al. 2023

AAVS

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| Aluminum (Al) is a well-established neurotoxicant, affecting various regions of the brain and causing many neuropathological and neurobehavioral abnormalities as well as oxidative stress (OS). Conversely, melatonin (MEL) has been considered as an antidepressant, anxiolytic substance and protects neurons from OS. The present study was designed to evaluate the neuroprotection effect of MEL against Al neurotoxicity and OS in male Wistar rats. Rats received an intraperitoneal and/or a single intrahippocampal injection of NaCl, MEL or AlCl 3 . Before two weeks of intrahippocampal surgery period, MEL (4 mg/kg) was intraperitoneally injected (Group II and Group IV). Thereafter, control group (group I) received 2 µl NaCl (0.9%) and groups III and IV received 2 µl AlCl 3 (2 mg/kg) intracerebrally into the right ventral hippocampus. Five days after treatment period, all the rats were subjected to the neurobehavioral tests. The animals were then decapitated and the hippocampus was removed. Biochemical parameters of OS and the histology of Cornu Ammonis 3 (CA3) area of the hippocampus were evaluated. The results clearly showed that Al induced anxiety and depressive-like behaviour and cognitive impairment. In the hippocampus, Al also increased the levels of lipid peroxidation (LPO) and nitric oxide (NO) and reduced the activity of superoxide dismutase (SOD) as well mediates brain damage in CA3 hippocampal area. These alterations were reversed by MEL. It can be concluded that, by exerting its properties against the oxidative action of this metal in the hippocampus, MEL may play a potential role in protecting against the behavioral and histopathological alterations induced by Al.

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Section: Histopathological Resultssupporting

confidence: 94%

Neuroprotective Effects of Melatonin Against Neurotoxicity Induced by Intrahippocampal Injection of Aluminum in Male Wistar Rats: Possible Involvement of Oxidative Stress Pathway

Zghari¹,

Lamtai²,

Azirar³

et al. 2023

AAVS

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“…These results were in agreement with (Abdelghany et al, 2019) study. Also, our work was in the same line with (Shaik et al, 2019), who found that large numbers of the hippocampal CA3 neurons had flame-shaped soma and an unhealthy cellular architecture in rats that received AlCl 3 .…”

Section: Discussionsupporting

confidence: 86%

“…Aluminum reduces antioxidant enzymes and increases MDA levels as a result of lipid peroxidation (Shaik et al, 2019). All these findings give a shred of growing evidence that AD is related to apoptosis either through the accumulation of Ab, which can induce neuronal apoptosis or by oxidative stress, which causes a cytochrome c release and activates caspase-9 and caspase-3 and overproduction of free radicals (Xing et al, 2018).…”

Section: Discussionmentioning

confidence: 96%

“…It is widely used in manufacturing cooking kits, antiperspirants, and drugs such as antacids (Al-Okbi et al, 2017;Khalifa et al, 2020). Chronic administration of aluminum chloride (AlCl 3 ) causes deposition of aluminum in the brain tissues that produce cognitive impairment, dementia (Chiroma et al, 2019;Shaik et al, 2019), and development of many neurodegenerative diseases including AD (Maya et al, 2016).…”

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confidence: 99%

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Glucagon‐like peptide‐1 analog improves neuronal and behavioral impairment and promotes neuroprotection in a rat model of aluminum‐induced dementia

et al. 2020

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Background Alzheimer's disease (AD) is a worldwide severe medical and social burden. Liraglutide (LIR) has neuroprotective effects in preclinical animal models. Aim: To explore the probable neuroprotective impact of Glucagon‐like peptide‐1 (GLP‐1) on rats' behavior and to elucidate its underlying mechanisms. Methods: A total of 24 male albino rats were assigned to control, LIR (300 µg/kg subcutaneously (s.c.)), AD only (100 mg/kg aluminum chloride (AlCl3) orally) and LIR + AD treated groups. Eight radial arm maze was performed. Serum blood glucose, proinflammatory cytokines, oxidative stress markers were measured and hippocampal tissue homogenate neurotransmitters were evaluated. Histopathological and immunofluorescent examinations were performed. Results: LIR prevents the impairment of learning and improves both working memory and reference memory through significant reduction of serum tumor necrosis factor (TNF‐α), interleukin 6 (IL‐6) and interferon‐γ (INF‐γ) and malondialdehyde (MDA) and through the increase of superoxide dismutase (SOD), dopamine, adrenaline, and noradrenaline. LIR also improves hippocampal histological features of ALCL3 administrated rats and decreases the percentage of neuronal loss. Conclusion: LIR normalizes ALCL3‐induced dementia. It improves cognitive dysfunction and ameliorates cerebral damage.

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“…In our study, the decrease in AChE activity by DLX is in agreement with previous studies in which antidepressants, such as citalopram, fluoxetine, paroxetine, sertraline, and several structural derivatives of escitalopram, reduce cholinesterase expression (Müller et al, 2002; Munawar et al, 2015; Nisa et al, 2017; Rockwood et al, 2011). In particular, DLX‐treated rats show a decline in cholinesterase and improved cognition (Shaik et al, 2019). Furthermore, we assessed mTOR signaling, which is a key hub in the control of neuronal survival and spine protein synthesis, although either too much or too little mTOR can disturb neuronal networks and, by altering both glutamatergic and GABAergic synapses, contribute to autistic behavior (Fahnestock & Nicolini, 2015).…”

Section: Discussionmentioning

confidence: 99%

Duloxetine ameliorates valproicacid‐inducedhyperactivity, anxiety‐like behavior, and social interaction deficits in zebrafish

et al. 2021

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Syndromic autism spectrum disorders (ASDs) are characterized by impaired social communication and repetitive/stereotyped behaviors. Currently available therapeutic agents against ASD have limited efficacy. Thus, searching for novel and effective drugs ameliorating core symptoms, in particular social deficits, is of utmost importance. Duloxetine (DLX), an antidepressant that has been identified as an agonist mimetic for the cell adhesion molecule L1, exhibits beneficial functions in vitro and in vivo. Therefore, in this study, we focused on the rapid and persistent neuroprotective function of DLX following valproic acid (VPA)‐triggered hyperactivity, anxiety‐like behavior and social deficits in zebrafish. Embryonic exposure to VPA reduced survival in a dose‐ and time‐dependent manner, delayed hatching, and also resulted in a significant number of malformed larvae. After initial dose–response experiments in zebrafish larvae, 10 μM VPA exposure between 0.33 and 4.5 days post fertilization (dpf) was identified as an effective concentration that led to an early and persistent ASD‐like phenotype in zebrafish. ASD‐like elevated acetylcholine esterase (AChE) activity and reduced Akt–mTOR signaling was observed in zebrafish whole brain. Acute administration of DLX (4.5–6 dpf) reduced the VPA‐induced ASD‐like phenotype in zebrafish larvae. Additionally, such early‐life acute DLX treatment had long‐term effects in ameliorating social impairments, hyperactivity, and anxiety‐like behaviors through adulthood. This was accompanied by reduced AChE activity and by normalized Akt–mTOR signaling. Overall, DLX treatment showed a long‐term therapeutic effect on autistic‐like behaviors, and alteration of AChE activity and Akt–mTOR signaling were identified as crucial in the VPA‐induced ASD zebrafish model.

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Antidepressants Modulate Behavioral, Biochemical, and Histological Alterations Induced by Chronic Aluminum Chloride Administration in Wistar Rats

Cited by 7 publications

References 40 publications

Neuroprotective Effects of Melatonin Against Neurotoxicity Induced by Intrahippocampal Injection of Aluminum in Male Wistar Rats: Possible Involvement of Oxidative Stress Pathway

Neuroprotective Effects of Melatonin Against Neurotoxicity Induced by Intrahippocampal Injection of Aluminum in Male Wistar Rats: Possible Involvement of Oxidative Stress Pathway

Glucagon‐like peptide‐1 analog improves neuronal and behavioral impairment and promotes neuroprotection in a rat model of aluminum‐induced dementia

Duloxetine ameliorates valproicacid‐inducedhyperactivity, anxiety‐like behavior, and social interaction deficits in zebrafish

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