Aluminum (Al) is an omnipresent mineral element in the environment. The brain is a central target of Al toxicity, being highly susceptible to oxidative damage. Therefore, recognition of drugs or natural products that guard against Al-mediated neuronal cell death is a powerful strategy for prevention and treatment of neurodegenerative disorders. This work aimed to explore the potential of a leaf extract from Harrisonia abyssinica to modulate the neurobehavioral, biochemical and histopathological activities induced experimentally by Al in vivo. Rats subjected to Al treatment displayed a reduction in learning and memory performance in a passive avoidance test accompanied by a decrease in the hippocampal monoamine and glutamate levels in addition to suppression of Bcl2 expression. Moreover, malondialdehyde (MDA), inflammatory markers (TNF-α, IL-1β), apoptotic markers (caspase-3 and expression of Bax) and extracellular regulated kinase (ERK1/2) levels were elevated along with acetylcholinesterase (AChE) activity, histological changes and marked deposition of amyloid β plaques in the hippocampus region of the brain tissues being observed in Al-treated animals. Concomitant administration of the high dose of H. abyssinica (200 mg/kg b.w.) restored nearly normal levels of all parameters measured, rather than the low dose (100 mg/kg b.w.), an effect that was comparable to the reference drug (rivastigmine). Molecular docking revealed the appropriate potential of the extract components to block the active site of AChE and ERK2. In conclusion, H. abyssinica leaf extract conferred neuroprotection against Al-induced neurotoxic effects, most likely due to its high phenolic and flavonoid content.

Background: Monosodium glutamate is a widely used flavor enhancer/food additive in meat, fish, milk and cheese or vegetable origins. Our present study aimed to assess the effect of utilization monosodium glutamate on the cardiac, splenic, hepatic and renal organs in mice. Thirty animals were divided into three groups: control group; glutamate 10 treated groups and glutamate 15 treated group. The experimental period was two successive weeks. Results: Oral administrations of monosodium glutamate for 10 days induced moderate histopathological changes in cardiac, splenic, hepatic and renal tissues and also resulted in significant increase of the nuclear factor-kB expression depend on time of administration as compared to the control group, while treatment with monosodium glutamate for 14 days resulted in severe histopathological changes as well as highly significant increase of the nuclear factor-kB expression as compared to the control group. Conclusions: It could be concluded that oral administration of monosodium glutamate induced histopathological alterations, and cytotoxicity in cardiac, splenic, hepatic and renal tissues dependent on time.

This current study aimed at detecting the potential protective role of Nano-fenugreek seed on acute lung injury induced by instillation gastric acid in male Swiss albino mice using histological, and histocemical studies. Forty animals grouped as follows: control group, HCl-treated group; low Nano-fenugreek + HCl treated group and high Nano-fenugreek + HCl treated group. Pretreatment with Nano-fenugreek in animal model of acute lung injury resulted in marked ameliorations of the lung histological lesions and injury induced by HCL instillation in a dose dependent manner. It also caused inhibition in the increase of the DNA content and prevented proliferation of goblet cells induced by HCl instillation alone. Pretreatment with Nano-fenugreek prior induction acute lung injury could suppress the aggregations of inflammatory cells, accumulation DNA content, and proliferation of goblet cells in a dose dependent manner. We suggest that Nano-fenugreek may be useful in combating lung injury induced.

Background: Gentamicin is one of aminoglycoside antibiotic used for treatment of many infections due to its availability and less cost. The aim of this study aimed to assess the modulation effect of fenugreek seed and its germinated seeds on pancreatic and testicular toxicity induced by gentamicin in male Swiss albino mice. Forty male albino mice were divided into four treatment groups as follows: (1) control group, (2) gentamicin treated group, (3) gentamicin-fenugreek treated group and (4) gentamicin-germinated fenugreek treated group. Pancreatic and testicular tissues were collected for histopathological examinations, histochemical, and biochemical analysis as well as genetic study. Results: Administration of gentamicin resulted in histopathological damage in pancreatic and testicular tissues as well as decreased glutathione peroxides, catalase and total antioxidant activity content in both pancreatic and testicular tissues compared to control group. Histopathological changes and antioxidant/oxidative alterations as well as DNA damage observed in gentamicin treated animals found were moderate improvement by fenugreek seeds administration and marked improvement by treatment with germinated fenugreek seeds. Conclusions: Treated with gentamicin induced histopathological lesions, antioxidant/oxidant imbalance and DNA damage in the pancreatic and testicular. Treatment with germinated fenugreek seeds was more effective than fenugreek seeds in amelioration of pancreatic and testicular lesions, preventing high appearance of carbohydrate and accumulation of collagen fibers as well as oxidative damage and genotoxicity induced by gentamicin administration.

Background: Monosodium glutamate is widely used as flavor enhancer/food additive. Many studies confirmed toxicity of monosodium glutamate even if in low concentrations especially in hepatic and renal organs. Therefore, our study aimed to examine ameliorative role of Nano-cerium oxide and L-arginine and their combination on the hepatic and renal toxicity induced by monosodium glutamate. Materials and Methods: Fifty mice were divided into five groups; 1st group served as control group; 2nd group treated oral with monosodium glutamate; animals of the 3rd group were administrated with monosodium glutamate and L-arginine. The 4th group was treated with monosodium glutamate and Nano-cerium oxide; and mice of the 5th group were treated with monosodium glutamate, L-arginine and Nano-cerium oxide. After 14 days, hepatic and renal tissues were removed for histological and histomorphometrical examinationsResults: Histological examination revealed hepatic and renal damages for animals treated with monosodium glutamate as well as highly significant declining of DNA content compared to control group. Administration of Nano-cerium oxide or L-argentine alone induced ameliorations of the hepatic and renal injuries induced by administration of monosodium glutamate but some pathological alterations still present. It also caused moderate improvement in the DNA content but still not reaches to normal value. Combined administration of Nano-cerium oxide and L-arginine caused marked ameliorations of the hepatic and renal changes induced by monosodium glutamate.Conclusions: The combined uses of L-arginine and Nano-cerium oxide more effective in preventing the hepatic and renal toxicity induced by monosodium glutamate in male albino rats than when they uses separately

Background: Lead, worldly is the most environmental pollutants that caused many health problems and affect all biological systems through exposure to air, water, and food sources. Aim: The aimed of our study is to evaluate protective effect of cerium oxide nanoparticle against toxicity of lead acetate in mice cardio-renal tissues using histopathological study.Materials and Methods: Forty male Swiss albino mice were divided into 4 groups as follows (1) control group, oral received distilled water (1ml/kg.bw); (2) lead treated group, animal injected interpertoneal by lead acetate at dose (150 mg /kg b.w, once); (3) cerium treated group: animals were given orally with cerium oxide nanoparticles at dose (0.5 mg/ kg, a and (4) cerium-lead treated group: animals given orally cerium oxide nanoparticles (0.5 mg/ kg bw) one hour prior injection of lead acetate(150 mg /kg bw). Renal and cardiac tissues were removed for histopathological and collagen deposition examinations. Results: Histopathological examinations revealed that treatment with lead acetate induced loss of architecture in both cardiac and renal tissues as evidenced by marked degenerative change in cardomyocyte, and glomeruli as well as congested dilated blood vessels, hemorrhage and lymphocytic cells aggregation compared to control group. While, pretreatment with cerium oxide nanoparticle prior lead acetate injection resulted in inhibition the histopathological lesions and injury in cardio-renal tissues induced by lead acetate treatment. In addition to, it also prevented collagen deposition observed in lead group compared to control group. Conclusion: In conclusions, the administration of cerium oxide nanoparticle could suppress the cytotoxicity of lead acetate and could combat tissue injury in cardio-renal tissues caused by lead acetate toxicity.