Introduction: Epilepsy is a chronic neurological condition characterized by behavioral, molecular, and neurochemical alterations. Current antiepileptic drugs are associated with various adverse impacts. The main goal of the current study is to investigate the possible anticonvulsant effect of selenium nanoparticles (SeNPs) against pentylenetetrazole (PTZ)mediated epileptic seizures in mice hippocampus. Sodium valproate (VPA) was used as a standard anti-epileptic drug. Methods: Mice were assigned into five groups (n=15): control, SeNPs (5 mg/kg, orally), PTZ (60 mg/kg, intraperitoneally), SeNPs+PTZ and VPA (200 mg/kg)+PTZ. All groups were treated for 10 days. Results: PTZ injection triggered a state of oxidative stress in the hippocampal tissue as represented by the elevated lipoperoxidation, heat shock protein 70 level, and nitric oxide formation while decreased glutathione level and antioxidant enzymes activity. Additionally, the blotting analysis showed downregulation of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) in the epileptic mice. A state of neuroinflammation was recorded following the developed seizures represented by the increased pro-inflammatory cytokines. Moreover, neuronal apoptosis was recorded following the development of epileptic convulsions. At the neurochemical level, acetylcholinesterase activity and monoamines content were decreased in the epileptic mice, accompanied by high glutamate and low GABA levels in the hippocampal tissue. However, SeNP supplementation was found to delay the onset and decreased the duration of tonic, myoclonic, and generalized seizures following PTZ injection. Moreover, SeNPs were found to provide neuroprotection through preventing the development of oxidative challenge via the upregulation of Nrf2 and HO-1, inhibiting the inflammatory response and apoptotic cascade. Additionally, SeNPs reversed the changes in the activity and levels of neuromodulators following the development of epileptic seizures. Conclusion: The obtained results suggest that SeNPs could be used as a promising anticonvulsant drug due to its potent antioxidant, anti-inflammatory, and neuromodulatory activities.

Eimeria coecicola causes intestinal coccidiosis in rabbits and, thereby, enormous economic losses in rabbit farms. This study aimed to investigate the effect of intestinal coccidial infection, E. coecicola on metabolic status and growth of rabbits. Animals were allocated into two groups with eight rabbits each; one group was orally inoculated with saline and served as control while the other group was orally inoculated with 5 × 10(4) sporulated oocysts. On day 7 postinfection, fecal expulsion of E. coecicola oocysts is maximal (1.2 × 10(6) oocyst/g feces) and rabbits have lost approximately 23% of their weight. Infection induced a severe depletion in plasma growth hormone level. In addition, the energy metabolic status was significantly (P ≤ 0.05) altered by the infection as, both blood glucose and total lipid levels were significantly elevated with mutual depletion in carbohydrate stores in liver sections. Also, the thyroid-stimulating hormone and cortisol concentrations were raised as a consequence of the infection. Moreover, protein status was affected by the infection as both liver and plasma total proteins were significantly decreased with concurrent disturbance in the blood protein electrophoretic pattern and duplication of blood urea nitrogen concentration. Finally, the infection induced plasma electrolyte imbalance as indicated by a significant decrease in sodium, potassium, calcium, phosphorus, ferrous, and selenium ions. Our data suggested that the intestinal coccidial infection of rabbits with E. coecicola has serious effects on rabbit growth and metabolism and could disrupt endocrine and electrolyte homeostasis.

Monosodium glutamate (MSG), a commonly used avor enhancer, has been reported to induce hepatic and renal dysfunctions. In this study, the palliative role of protocatechuic acid (PCA) in MSG-administered rats was elucidated. Adult male rats were assigned to four groups, namely control, MSG (4 mg/kg), PCA (100 mg/kg), and the last group was co-administered MSG and PCA at aforementioned doses for seven days. Results showed that MSG augmented the hepatic (AST and ALT) and renal (urea and creatinine) functions markers as well as glucose, triglycerides, total cholesterol and LDL levels. Moreover, marked increases in MDA levels accompanied by declines in GSH levels and notable decreases in the activities of SOD, CAT, GPx, and GR were observed in MSG-treated group. The MSG-mediated oxidative stress was further con rmed by down-regulation of Nfe2l2 gene expression levels in both tissues. In addition, MSG enhanced the hepatorenal in ammatory response as witnessed by increased in ammatory cytokines (IL-1b and TNF-α) and elevated NF-κB levels in both tissues. Further, signi cant increases in Bax (proapoptotic biomarker) levels together with decreases in Bcl-2 (anti-apoptotic marker) levels were observed in MSG administration. Hepatic and renal histopathological screening supported the biochemical and molecular ndings. On the contrary, co-treatment of rats with PCA resulted in remarkable enhancement of the antioxidant cellular capacity, suppression of in ammatory mediators and apoptosis. These effects are possibly endorsed for activation of Nrf-2 and suppression of NF-kB signaling pathways. Collectively, addition of PCA counteracted MSG-induced hepatic and renal injurious effects through modulation of oxidative, in ammatory and apoptotic alterations.

Malaria is a major health problem that still affects numerous countries. The current study aimed to identify the role of leaf extract in regulating mouse spleen macrophages during the progression of infection. Three doses of the leaf extract (100, 200, and 300 mg/kg) were administered to mice inoculated with infected erythrocytes. The weight of the infected mice improved after the treatment with. The infection causes disorganization of macrophage distribution in the spleen. After the mice had been treated with the leaf extract, the macrophages appeared to be reorganized in the white and red pulp areas. In addition, the leaf extract (IOLE) significantly increased the total antioxidant capacity of the mice spleens infected with. The phagocytic activity of spleen macrophages was increased in the infected group as indicated by the significant decrease in the number of fluorescent particles in the spleen sections. This number increased in the mice spleens after treatment with IOLE. Based on these results, it is suggested that IOLE regulate macrophage response of the spleen during the blood stage of malaria in mice.

Monosodium glutamate (MSG), a commonly used flavor enhancer, has been reported to induce hepatic and renal dysfunctions. In this study, the palliative role of protocatechuic acid (PCA) in MSG-administered rats was elucidated. Adult male rats were assigned to four groups, namely control, MSG (4 mg/kg), PCA (100 mg/kg), and the last group was co-administered MSG and PCA at aforementioned doses for seven days. Results showed that MSG augmented the hepatic (AST and ALT) and renal (urea and creatinine) functions markers as well as glucose, triglycerides, total cholesterol and LDL levels. Moreover, marked increases in MDA levels accompanied by declines in GSH levels and notable decreases in the activities of SOD, CAT, GPx, and GR were observed in MSG-treated group. The MSG-mediated oxidative stress was further confirmed by down-regulation of Nfe2l2 gene expression levels in both tissues. In addition, MSG enhanced the hepatorenal inflammatory response as witnessed by increased inflammatory cytokines (IL-1b and TNF-α) and elevated NF-κB levels in both tissues. Further, significant increases in Bax (pro-apoptotic biomarker) levels together with decreases in Bcl-2 (anti-apoptotic marker) levels were observed in MSG administration. Hepatic and renal histopathological screening supported the biochemical and molecular findings. On the contrary, co-treatment of rats with PCA resulted in remarkable enhancement of the antioxidant cellular capacity, suppression of inflammatory mediators and apoptosis. These effects are possibly endorsed for activation of Nrf-2 and suppression of NF-kB signaling pathways. Collectively, addition of PCA counteracted MSG-induced hepatic and renal injurious effects through modulation of oxidative, inflammatory and apoptotic alterations.