Exercise protects the hypothalamus morphology from the deleterious effects of high sucrose diet consumption.

A growing body of evidence suggests that elevated sucrose intake may contribute to the development of neurological disorders. Recognizing that regular exercise has the potential to reduce the occurrence of neuromuscular disorders, the present research investigated the impact of exercise on the redox status of the hypothalamus in mitigating the adverse effects associated with high sucrose intake. Forty Wistar albino rats were subjected to a high sucrose diet, with some groups engaging in exercise for a duration of 3 months. The exercise regimen was found to sustain the redox balance in the hypothalamus. In summary, the consumption of a high sucrose diet resulted in the disturbance of the histological morphology of the hypothalamus, accompanied by an increased percentage of caspase-3 positive cells. Additionally, the high sucrose diet disrupted the oxidant/antioxidant ratio in favor of oxidants, leading to elevated levels of AOPPs and AGEP. Conversely, exercise was effective in restoring most of these values to levels approximating the control group, indicating a potential protective effect of regular exercise against the detrimental impacts of high sucrose dietary consumption on the hypothalamus. Graphical abstract.

Role of canagliflozin in ameliorating isoprenaline induced cardiomyocyte oxidative stress via the heme oxygenase-1 mediated pathway.

Canagliflozin (CZ) is commonly prescribed for management of type-2 diabetes mellitus (T2DM); it also can reduce the risk of myocardial infarction. We used 80 albino Wistar rats to investigate the cardioprotective potential of CZ against oxidative stress caused by administration of isoprenaline (ISO). We found that ISO stimulates production of reactive oxygen species and that CZ administration caused up-regulation of antioxidants and down-regulation of oxidants due to nuclear factor erythroid-2 related factor-2, as well as by enhancement of the heme oxygenase-1 mediated cascade. CZ monotherapy may play a cardioprotective role in diabetic patients. CZ possesses strong antioxidant potential that ameliorates cardiac damage induced by ISO administration.

Potential of Ascorbic Acid Supplements to Ameliorate the Deleterious Effects of Hyperuricemia on Albino Wistar Rats' Hippocampus (Structural and Functional Study).

INTRODUCTION: Diet rich in purines may increase the serum level of uric acid causing hyperuricemia, contributing to learning and memory to impairments. Ascorbic acid has a potent antioxidant potential. The hippocampus is a pivotal component of human brains and other vertebrates that plays crucial roles in the consolidation of information and spatial memory. Our study was mainly designated to examine the potential palliative role of ascorbic acid supplements on harmful effects induced hyperuricemia on the hippocampus of albino Wistar rats. METHODS: Forty rats were subgrouped into the control group, ascorbate-only group, hyperuricemic group, and combined hyperuricemia and ascorbate group. RESULTS: Ascorbic acid has strongly preserved the histological architecture and maintained the normal hippocampal functions in the hyperuricemic group. CONCLUSION: The anti-inflammatory and antioxidant properties of ascorbic acid could protect the hippocampus of albino Wistar rats against the hazardous impact of hyperuricemia.

Plasma D-dimer level in early and late-onset neonatal sepsis.

BACKGROUND: Neonatal sepsis is a life-threatening disease. Early diagnosis is essential, but no single marker of infection has been identified. Sepsis activates a coagulation cascade with simultaneous production of the D-dimers due to lysis of fibrin. D-dimer test reflects the activation of the coagulation system. AIM: To assess the D-dimer plasma level, elaborating its clinicopathological value in neonates with early-onset and late-onset neonatal sepsis. METHODS: The study was a prospective cross-sectional study that included ninety neonates; divided into three groups: Group I: Early-onset sepsis (EOS); Group II: Late-onset sepsis (LOS); and Group III: Control group. We diagnosed neonatal sepsis according to our protocol. C-reactive protein (CRP) and D-dimer assays were compared between EOS and LOS and correlated to the causative microbiological agents. RESULTS: D-dimer was significantly higher in septic groups with a considerably higher number of cases with positive D-dimer. Neonates with LOS had substantially higher levels of D-dimer than EOS, with no significant differences in CRP. Neonates with LOS had a significantly longer hospitalization duration and higher gram-negative bacteriemia and mortality rates than EOS (P < 0.01). Gram-negative bacteria have the highest D-dimer levels (Acinetobacter, Klebsiella, and Pseudomonas) and CRP (Serratia, Klebsiella, and Pseudomonas); while gram-positive sepsis was associated with relatively lower levels. D-dimer had a significant negative correlation with hemoglobin level and platelet count; and a significant positive correlation with CRP, hospitalization duration, and mortality rates. The best-suggested cut-off point for D-dimer in neonatal sepsis was 0.75 mg/L, giving a sensitivity of 72.7% and specificity of 86.7%. The D-dimer assay has specificity and sensitivity comparable to CRP in the current study. CONCLUSION: The current study revealed a significant diagnostic value for D-dimer in neonatal sepsis. D-dimer can be used as an adjunct to other sepsis markers to increase the sensitivity and specificity of diagnosing neonatal sepsis.

Hesperidin Preserves Cognitive Functions and Hippocampus Histological Architecture in Albino Wistar Rats Subjected to Stress Through Enhancement of Brain-Derived Neurotrophic Factor.

Hesperidin (HSD) is a natural compound with antioxidant potential. On the other hand, chronic stress had been linked to impaired cognitive functions as it affects many neurotransmitters and brain regions such as the hippocampus. The current study was conducted to examine the effect of HSD on learning and memory after chronic mild stress. Albino Wistar rats were subjected to chronic mild stress with HSD administered as supplements. HSD was found to decrease hippocampal amyloid beta and malondialdehyde levels, in addition, to preserve cognitive functions together with preserving hippocampus histological architecture. In conclusion, the present study sheds the light on the potential of HSD to ameliorate the deleterious effects of chronic mild stress on cognitive functions through brain-derived neurotrophic factor enhancement and reduction in Aß formation in addition to activation of the antioxidant pathway.

Potential effect of fish oil to preserve expression of cell cycle and tight junction regulating genes in colon after di-isononyl phthalate ingestion in albino Wistar rats.

Di-isononyl phthalate (DIP) is considered a high molecular-weight subtype of phthalates that are commonly used and could easily affect the gastrointestinal tract (GIT). Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are the main active components of fish oil (FO), and their anti-inflammatory potential was previously documented. The current study was designed to investigate the protective potential of fish oil against the impacts of DIP exposure on the colon of albino Wistar rats. Sixty albino Wistar rats were divided into Control group received corn oil for ten days. Di-isononyl phthalate treated group received DIP. Di-isononyl phthalate + fish oil treated group received both DIP and FO. FO was found to preserve the histological architecture, tight junction and cell cycle of the colon. In conclusion, the current study provided an evidence that FO has a protective potential against DIP further examinations to be done to fully understand the molecular basis of this potential as a step for further clinical applications.

Potential of Amantadine to Ameliorate Glutamate-Induced Pyramidal Cells Toxicity in Juvenile Rat' Brain Cortex.

Glutamate (Gt) neurotoxicity contributes to a wide spectrum of neurological conditions. Loss of glutamate transporters leads to intracellular Gt accumulation. Amantadin (AMn) is a non-competitive N-methyl-D-aspartate (NMDA) antagonist that can partially inhibit Gt transporters and influence protein phosphatase 2A subunit B (PP-2A-B) activity. Herein, we investigate the potential of AMn administered in the early life stages to reverse the Gt-induced changes in the cerebral cortex in the rat model. We report that AMn can reverse Gt-induced structural changes in the brain cortex and increase PP-2A activity. Additionally, PP-2A-B activity in the AMn + Gt-treated group was comparable to controls. Moreover, administration of AMn leads to a decrease of apoptotic index in the Gt-treated individuals. We suggest that severe histopathological changes observed in Gt group could be attributed to the decreased PP-2A expression causing an imbalance between phosphatase and protein kinase activities and leading to a strong positive TUNEL reaction. We provide a short summary of the current state of knowledge regarding the role of PP-2A-B in the Gt-induced neurotoxicity and AMn treatment and discuss the potential of amantadine as a potential therapeutic agent.

Mitigation of cadmium-induced lung injury by Nigella sativa oil.

Induction of oxidative stress and inflammation are considered the primary mechanism of cadmium (Cd) toxicity. Nigella sativa (NS) seeds and their oil (NSO) have been reported to possess antioxidant and anti-inflammatory potential. This study was conducted to assess the protective effect of NSO on Cd-induced lung damage in rat. Forty adult male Wistar rats were divided equally into 4 groups. Animals in groups I, II, and III received 1 ml of isotonic saline intraperitoneally (IP), 2 mg/kg of cadmium chloride (CdCl2) dissolved in isotonic saline IP, and 1 ml/kg of NSO by gastric gavage, respectively. Group IV rats received NSO an hour prior to CdCl2 administration via the same routes and doses as previously described. All animals were treated for 28 days. At the end of the study, animals were sacrificed; lungs were harvested for histopathological studies using light and electron microscopy. Saline-treated and NSO-treated rats showed normal lung parenchyma. However, CdCl2-treated rats showed massive degenerative changes in alveolar epithelial lining, disrupted interalveolar septa, and hemolytic debris in alveoli. Rats treated with both NSO and CdCl2 (group IV) showed amelioration of most Cd-induced lung damage with minimal histopathological changes in lung architecture. This study elucidates the protective effects of NSO on Cd-induced lung injury in rats and highlights the possibility of using NSO as a protective agent in individuals at high risk of Cd-induced lung toxicity.