Schistosomiasis is a condition characterized by high rates of morbidity and cognitive impairment. It afflicts many people in tropical and sub-tropical countries. Our study aimed to investigate the protective role of gold nanoparticles (GNPs) on the brain of mice infected with Schistosoma mansoni. Characterizations of GNPs were determined by using high-resolution transmission electron microscopy. Three doses of GNPs (0.25, 0.5, and 1.0 mg/kg body weight) were used to treat animals after S. mansoni infection. The infection induced impairments in histological picture as a result of schistosome infection resulting in a disturbance in the content of the brain neurotransmitters, norepinephrine (NE), and dopamine (DA). Also, the infection induced significant reduction in glutathione level; oppositely, the levels of nitric oxide and malondialdehyde were increased significantly. In addition, S. mansoni was able to disregulate the infected mice brain Cacnb4, Cabp4, Vdac3, Glrb, and Adam23 messenger RNA (mRNA). On the other hand, treatment of mice with GNPs could alleviate the histological impairments, the changes in the content of NE and DA, and the brain oxidative damage. Also, GNPs could regulate the gene expression due to S. mansoni infection. Generally, GNPs could decrease the neurooxidative stress and regulated the gene expression in the brain of infected mice. Consequently, our results revealed an anti-neuroschistosomal effect of GNPs in mice infected with S. mansoni.

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Nanomedicine is one of the most important methods used to treat human diseases including parasitic diseases. Schistosomiasis is a major parasitic disease that affects human health in tropical regions. Whilst Praziquantel is the main classic antischistosomal drug, new drugs are required due to the poor effect of the drug on the parasite juveniles and immature worms, and the emergence of drug resistant strains of Schistosoma. The present study aimed to examine the curative roles of both gold and selenium nanoparticles on jejunal tissues of mice infected with Schistosoma mansoni. Transmission electron microscopy was used for characterization of nanoparticles. Gold nanoparticles of 1 mg/kg mice body weight and selenium nanoparticles 0.5 mg/kg body weight were inoculated separately into mice infected with S. mansoni. The parasite induced a significant decrease in glutathione levels; however, the levels of nitric oxide and malondialdehyde were significantly increased. Additionally, the parasite introduced deteriorations in histological architecture of the jejunal tissue. Treatment of mice with metal nanoparticles reduced the levels of body weight changes, oxidative stress and histological impairment in the jejunal tissue significantly. Therefore, our results revealed the protective role of both selenium and gold nanoparticles against jejunal injury in mice infected with S. mansoni.

In recent years, gold nanoparticles (AuNPs) have become the focus of much attention in biomedical research, especially in the context of nanomedicine, due to their distinctive physicochemical properties. The current study was planned to assess the effect of three dose levels of AuNPs on the gene expression, histology, and oxidative stress status of Schistosoma mansoni -infected mice liver. Inoculation of mice with 100 μL AuNPs at different doses (0.25, 0.5, and 1 mg/kg mice body weight) twice on day 46 and day 49 postinfection reduced the total worm burden, the egg load in the liver, and the granuloma size. AuNPs also appeared to decrease the activities of malondialdehyde and nitric oxide significantly, and increase the level of glutathione compared to the infected untreated group. Concomitantly, AuNPs ameliorated the inflammatory response by decreasing the mRNA expression of interleukin-1β, interleukin-6, tumor necrosis factor-α, interferon-γ, and inducible nitric oxide synthase. These consistent molecular, histopathological, and biochemical data suggest that AuNPs could ameliorate infection-induced damage in the livers of mice. Our results indicated that AuNPs are effective anti-schistosomal and antioxidant agents. Further confirmation of the role of nanogold as an anti-schistosomal agent, as well as its mechanism of action, requires further studies to be undertaken in the future.

Schistosomiasis is still one of the main parasitic diseases that affect human health in tropical regions. Whilst praziquantel (PZQ) is the main classic antischistosomal drug, the need for new drugs is still a must due to the low effectiveness of the drug on the schistosome young worms, and the evolving of PZQ resistant strains. Nanotechnology is one of the most important recent and current methods used to treat human diseases including parasitic ones. Therefore, the present study aimed to examine the curative role of gold nanoparticles (GNPs) on splenic tissue of mice infected with Sambon, 1907. High-resolution transmission electron microscopy was used for characterization of nanoparticles (NP). GNPs of 1 mg/kg mice body weight were inoculated into mice infected with. The parasite caused deteriorations in histological architecture of the spleen tissue, and splenomegaly. Additionally, the parasite induced a significant reduction in splenic tissue glutathione levels; however, the concentrations of nitric oxide and malondialdehyde were significantly increased. Treatment of mice with GNPs reduced the extent of histological impairment and oxidative stress in spleen tissue. Therefore, our results demonstrate the protective role of GNPs against splenic damage in mice infected with

Nanoparticles are now widely used in various aspects of life, especially zinc oxide nanoparticles (ZnNPs) that used in mouth washing, cosmetics, sunscreens, toothpaste and root canal flings. This research aims to determine the impact of ZnNPs on healthy mice's brain tissue. ZnNPs have caused major changes in the brain monoamines (dopamine, norepinephrine and serotonin) and ions such as Ca 2+ , Na + , K + and Zn 2+ . Concerning the histological picture, administration of ZnNPs caused some histopathological impairment in brain tissue. In addition, ZnNPs reduced the level of glutathione and catalase in brain tissue, although an increase in the level of nitrite / nitrate and ROS was observed, while the level of malondialdhyde was not significantly altered. Moreover, ZnNPs induced DNA fragmentation in brain of mice. Collectively, the obtained results revealed that ZnNPs affected the brain levels of investigated monamines, ions, enzymatic and non-enzymatic antioxidants thus they may have potential influence on central nervous system.

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