Combined Restraint Stress and Metal Exposure Paradigms in Rats: Unravelling Behavioural and Neurochemical Perturbations.

Accumulation of heavy metals (Mn and Ni) and prolonged exposure to stress are associated with adverse health outcomes. Various studies have shown the impacts of stress and metal exposures on brain function. However, no study has examined the effects of co-exposure to stress, Mn, and Ni on the brain.

Dopaminergic Perturbation in the Aetiology of Neurodevelopmental Disorders.

Brain development may be influenced by both genetic and environmental factors, with potential consequences that may last through the lifespan. Alterations during neurogenesis are linked to neurodevelopmental cognitive disorders. Many neurotransmitters and their systems play a vital role in brain development, as most are present prior to synaptogenesis, and they are involved in the aetiology of many neurodevelopmental disorders.

Caffeine Administration Mitigates Chronic Stress-Induced Behavioral Deficits, Neurochemical Alterations, and Glial Disruptions in Rats.

Prolonged exposure to stress has detrimental effects on health, and the consumption of caffeine, mostly contained in energy drinks, has become a widely adopted stress coping strategy. Currently, there is limited information regarding the effects of caffeine intake on chronic stress exposure. Thus, this study investigated the effects of caffeine administration on chronic stress-induced behavioral deficits, neurochemical alterations, and glial disruptions in experimental rats.

Necroptosis in the developing brain: role in neurodevelopmental disorders.

Cell death is vital to various organismal developmental processes including brain development. Apoptosis, the most recognized programmed cell death, has been linked to several developmental processes and implicated in pruning cells to provide the ultimate tissue integrity. However, more recently, other forms of non-apoptotic programmed cell death have been identified, of which necroptosis is of predominant interest.

Modulatory Role of Curcumin on Cobalt-Induced Memory Deficit, Hippocampal Oxidative Damage, Astrocytosis, and Nrf2 Expression.

Chemical overexposure is a growing environmental risk factor for many medical issues. Cobalt toxicity from environmental, industrial, and medical exposure has previously been linked to neurological impairment. Hence, the current study looked into the neuroprotective potential of curcumin, a natural polyphenol contained in the spice turmeric, against cobalt-induced neurotoxicity.

Neuroprotective effects of methyl jasmonate in male Wistar rats exposed to delayed acetic acid-induced ulcerative colitis: involvement of antioxidant status, GFAP, and IBA-1 immunoreactivities.

Neurobehavioral deficits have been severally reported as a comorbid outcome in inflammatory bowel diseases (IBDs). This study evaluated neurological changes in the experimental model of IBDs, as well potential protective effects of methyl jasmonate (MJ). The study used the acetic acid model of colitis and thereafter delayed the healing process by the administration of indomethacin (Indo) (2 mg/kg, SC).

Cobalt exposure triggers impairments in cognitive and anxiety-like behaviors, brain oxidative stress and inflammation, and hippocampo-amygdala histomorphological alterations: Protective role of aqueous seed extract.

Objectives: Cobalt toxicity has become a health concern in recent years, due to overexposure resulting in neurological impairments. With a growing interest in the therapeutic roles of herbs, in toxicity research, it's worth looking into the curative effects of aqueous seed extract, a plant rich in flavonoids on cobalt-induced neurotoxicity.

Materials And Methods: We treated rats with CoCl or CoCl in combination with aqueous PA seed extract (PAE) orally for 14 days.

Ferulic acid improves glucose homeostasis by modulation of key diabetogenic activities and restoration of pancreatic architecture in diabetic rats.

There are increasing concerns on the rising cases of diabetes mellitus with type 2 diabetes (T2D) being of major interest as well as the cost of its treatment. Plant phenolic compounds are natural and potent antioxidants that have been widely reported for their antidiabetic activities properties, one of which is ferulic acid. The effect of ferulic acid (FA) on major diabetogenic activities and pancreatic architecture linked to T2D was investigated in T2D rats.

Effect of chlorogenic acid plus donepezil on critical neurocortical enzyme activities, inflammatory markers, and synaptophysin immunoreactivity in scopolamine-assaulted rats, supported by multiple ligand simultaneous docking.

The effect of chlorogenic acid (a natural phenolic acid ubiquitous in plant foods) on selected therapeutic properties of donepezil (DON) in a scopolamine (SCOP)-induced rat model of amnesia was the focus of this study. Adult albino (Wister strain) rats were allocated into five groups (n = 11) consisting of control, SCOP, SCOP + chlorogenic acid (CGA), SCOP + DON, and SCOP + CGA + DON for 7 days. Post-treatment, the rat brain cerebral cortex homogenate was assayed for cholinesterase and monoamine oxidase activities.

Caffeic acid regulates glucose homeostasis and inhibits purinergic and cholinergic activities while abating oxidative stress and dyslipidaemia in fructose-streptozotocin-induced diabetic rats.

Objectives: The antidiabetic potential of caffeic acid in fructose/streptozotocin-induced type 2 diabetic rats was examined in this study.

Methods: Male Sprague-Dawley rats were supplied with 10% fructose solution for 14 days followed by an intraperitoneal injection of 40 mg/kg bw streptozotocin to induce type 2 diabetes (T2D). Rats were treated with both low (150 mg/kg bw) and high (300 mg/kg bw) doses of caffeic acid for 5 weeks, while the positive control group was treated with metformin (200 mg/kg bw).

Sex-dependent metal accumulation and immunoexpression of Hsp70 and Nrf2 in rats' brain following manganese exposure.

Manganese (Mn), although important for multiple cellular processes, has posed environmental health concerns due to its neurotoxic effects. In recent years, there have been extensive studies on the mechanism of Mn-induced neuropathology, as well as the sex-dependent vulnerability to its neurotoxic effects. Nonetheless, cellular mechanisms influenced by sex differences in susceptibility to Mn have yet to be adequately characterized.

D-Ribose-LCysteine attenuates manganese-induced cognitive and motor deficit, oxidative damage, and reactive microglia activation.

Due to overexposure, manganese (Mn) accumulation in the brain can trigger the inhibition of glutathione synthesis and lead to increased generation of reactive oxygen species (ROS) and oxidative stress. D-Ribose-L-Cysteine (RibCys) has been demonstrated to effectively support glutathione synthesis to scavenge ROS and protect cells from oxidative damage. In the present study, we examined the effects of RibCys on weight changes, cognitive and motor associated activities, oxidative stress markers, striatal and cortical histology, and microglia activation following Mn exposure.

Application of Fluorescence Microscopy and Behavioral Assays to Demonstrating Neuronal Connectomes and Neurotransmitter Systems in .

The nematode () is a prevailing model which is commonly utilized in a variety of biomedical research arenas, including neuroscience. Due to its transparency and simplicity, it is becoming a choice model organism for conducting imaging and behavioral assessment crucial to understanding the intricacies of the nervous system. Here, the methods required for neuronal characterization using fluorescent proteins and behavioral tasks are described.

Vanillin improves glucose homeostasis and modulates metabolic activities linked to type 2 diabetes in fructose-streptozotocin induced diabetic rats.

Objective: This study investigated the antidiabetic effect of vanillin using , , and experimental models.

Methodology: Type 2 diabetes (T2D) was induced in male Sprague-Dawley (SD) rats using fructose-streptozotocin (STZ), then orally administered low (150 mg/kg bodyweight) or high (300 mg/kg bodyweight) dose of vanillin for 5 weeks intervention period.

Results: Vanillin suppressed the levels of blood glucose, serum cholesterol, triglyceride, low-density lipoprotein cholesterol (LDL-c), alanine transaminase (ALT), aspartate transaminase (AST), creatinine, urea, uric acid, when elevated serum insulin, HDL-cholesterol, and concomitantly improved pancreatic β-cell function, glucose tolerance, and pancreatic morphology.

ERK/MAPK signalling in the developing brain: Perturbations and consequences.

The extracellular regulated kinase/microtubule-associated protein kinase (ERK/MAPK) signalling pathway transduces signals that cause an alteration in the ongoing metabolic pathways and modifies gene expression patterns; thus, influencing cellular behaviour. ERK/MAPK signalling is essential for the proper development of the nervous system from neural progenitor cells derived from the embryonic mesoderm. Several signalling molecules that regulate the well-coordinated process of neurodevelopment transduce developmental information through the ERK/MAPK signalling pathway.

Modulatory action of Lam. on L-arginine induced acute pancreatitis.

Objectives: Acute pancreatitis (AP) is an inflammatory disease of the pancreas with high morbidity and mortality. This study investigates the effect of (MO) on L-arginine-induced AP in Wistar rats.

Methods: Male Wistar rats were randomly divided into seven groups.

Vanillin modulates activities linked to dysmetabolism in psoas muscle of diabetic rats.

Skeletal muscles are important in glucose metabolism and are affected in type 2 diabetes (T2D) and its complications. This study investigated the effect of vanillin on redox imbalance, cholinergic and purinergic dysfunction, and glucose-lipid dysmetabolism in muscles of rats with T2D. Male albino rats (Sprague-Dawley strain) were fed 10% fructose ad libitum for 2 weeks before intraperitoneally injecting them with 40 mg/kg streptozotocin to induce T2D.

D-Ribose-L-Cysteine Improves Glutathione Levels, Neuronal and Mitochondrial Ultrastructural Damage, Caspase-3 and GFAP Expressions Following Manganese-Induced Neurotoxicity.

Repeated manganese (Mn) exposure may cause increased production of reactive oxygen species (ROS), with a consequent imbalance in the glutathione (GSH) antioxidant defence system, resulting in cellular dysfunctions, and eventually cell death, particularly in the brain. D-ribose-L-cysteine (RibCys) has been demonstrated to effectively promote the synthesis of glutathione, a potent neutralizer of ROS. In the present study, we examined the effects of RibCys on glutathione levels, apoptotic and astrocytic responses, neuronal ultrastructural integrity, following Mn exposure.

Impact of environmental toxicants on p38- and ERK-MAPK signaling pathways in the central nervous system.

There are several candidate signalling pathways that mediate the response of the central nervous system (CNS) cells to environmental toxins. However, much is still to be learned on how these pathways modulate neurotoxicity. The mitogen-activated protein kinases (MAPKs) signalling pathways, which include the extracellular signal-regulated protein kinase (ERK) and the p38-MAPK, are potentially key pathways to regulate CNS responses to environmental toxins.

Perturbed MAPK signaling in ASD: Impact of metal neurotoxicity.

The mitogen-activated protein kinase (MAPK) pathways are intracellular signaling pathways necessary for regulating various physiological processes, including neurodevelopment. The developing brain is vulnerable to toxic substances, and metals, such as lead, mercury, nickel, manganese, and others, have been proven to induce disturbances in the MAPK signaling pathway. Since a well-regulated MAPK is necessary for normal neurodevelopment, perturbation of the MAPK pathway results in neurodevelopmental disorders, including autism spectrum disorder (ASD).

Cola nitida infusion modulates cardiometabolic activities linked to cardiomyopathy in diabetic rats.

This study investigated the therapeutic mechanism of Cola nitida seeds on diabetic cardiomyopathy in hearts of diabetic rats. Type 2 diabetic (T2D) rats were treated with C. nitida infusion at 150 or 300 mg/kg body weight (bw).