Fish are a source of high-quality protein with low cholesterol, but they are susceptible to parasitic infections, which have a significant impact on aquaculture, in addition to their zoonotic potential. The present study estimated parasitic infections and evaluated the diversity of zoonotic parasites in freshwater Nile tilapia (Oreochromis niloticus) in Assiut Governorate, Upper Egypt. A total of 300 samples were randomly collected from the Assiut Governorate. These fish were examined for both ectoparasites and endoparasites, followed by the experimental infection of mice with encysted metacercariae (EMC) for the retrieval of the adult worms. The overall prevalence of the variable parasites was 82% (246 of 300). Both ecto- and endoparasites were detected in 41% (123 of 300) of the examined fish. The identified ectoparasites were Gyrodactylus, Dactylogrus, Cichlidogyrus, Trichodina and Icthyophthirius multifiliis, in 5%, 4%, 22%, 6% and 4% of the fish, respectively. The endoparasites were trematodes (Orientocreadium batrachoides 3%), nematodes (Contracaecum. 2%), acanthocephala (Acanthosentis tilapiae 25%) and protozoa that included Isospora and Eimeria spp., in 1% and 8% of fish, respectively. Myxobolus was detected in 2% of the examined fish. The overall prevalence of encysted metacercariae (EMC) was 95% (285 of 300), while infection with macroscopic EMC had a prevalence of 37% and microscopic EMC had a prevalence of 58%. The adult worms recovered from the experimental infections were Prohemistomum vivax and Mesostephanus spp., which belong to the family Cyathocotylidae. Collectively, these findings reflect the relatively high occurrence of parasites among the studied fish, confirming the necessity of strict measures to control infection.

Multiple sclerosis (MS) is an autoimmune demyelinating neurodegenerative disease of the central nervous system (CNS) due to injury of the myelin sheath by immune cells. The clotting factor fibrinogen is involved in the pathogenesis of MS by triggering microglia and the progress of neuroinflammation. Fibrinogen level is correlated with MS severity; consequently, inhibition of the fibrinogen cascade may reduce MS neuropathology. Thus, this review aimed to clarify the potential role of fibrinogen in the pathogenesis of MS and how targeting of fibrinogen affects MS neuropathology. Accumulation of fibrinogen in the CNS may occur independently or due to disruption of blood–brain barrier (BBB) integrity in MS. Fibrinogen acts as transduction and increases microglia activation which induces the progression of inflammation, oxidative stress, and neuronal injury. Besides, brain fibrinogen impairs the remyelination process by inhibiting the differentiation of oligodendrocyte precursor cells. These findings proposed that fibrinogen is associated with MS neuropathology through interruption of BBB integrity, induction of neuroinflammation, and demyelination with inhibition of the remyelination process by suppressing oligodendrocytes. Therefore, targeting of fibrinogen and/or CD11b/CD18 receptors by metformin and statins might decrease MS neuropathology. In conclusion, inhibiting the expression of CD11b/CD18 receptors by metformin and statins may decrease the pro-inflammatory effect of fibrinogen on microglia which is involved in the progression of MS.

Several negative outcomes are associated with current anti-epileptic medications. Epigallocatechin gallate (EGCG) is a plant-derived compound called catechin and has many medicinal activities, such as anti-inflammatory and antioxidant activities. Biosynthesized selenium nanoparticles are also showing their neuroprotective effect. The anti-epileptic effect of EGCG, alone or with SeNPs, is still debated. Here, we aimed to investigate the potential anti-seizure effect of biosynthesized SeNPs using EGCG (EGCG-SeNPs) against epileptic seizures and hippocampal damage, which is enhanced by pentylenetetrazole (PTZ) injection in mice. Mice were grouped as follows: control; PTZ-exposed group (epileptic model); EGCG + PTZ-treated group; sodium selenite (Na₂SeO₃) + PTZ-treated group; EGCG-SeNPs + PTZ-treated group; and valproic acid (VPA) + PTZ-treated group. EGCG-SeNPs administration showed anti-epileptic activity by increasing the latency time and reducing the seizure duration following the PTZ injection. Additionally, EGCG-SeNPs counteracted the PTZ-induced changes in oxidants and antioxidants. Moreover, EGCG-SeNPs inhibited the inflammatory response by suppressing the release of pro-inflammatory cytokines and decreasing the immunoreactivity of the glial fibrillary acidic protein and mRNA expression of glutamate receptor subunit zeta-1 (NMDAR; Grin1), showing their inhibitory effect on epilepsy-associated inflammation. Moreover, EGCG-SeNPs reduced PTZ-induced neuronal apoptosis, as indicated by a reduction in the levels of pro-apoptotic proteins and an elevation of the anti-apoptotic protein. Moreover, EGCG-SeNPs administration significantly modulated the PTZ-induced changes in monoamine levels and acetylcholinesterase activity in the hippocampal tissue. The obtained findings suggest the anti-seizure activity of EGCG-SeNPs via their antioxidant, anti-inflammatory, and anti-apoptotic effects, along with their neuromodulatory effect.

Due to bleomycin's cytotoxic characteristics, which include cardiotoxicity, this investigation looked at the effectiveness of costus ethanolic extract in reducing cardiotoxicity in male rats receiving bleomycin therapy. Forty adult male rats (160-200 g) were evenly allocated into four groups: group (1) included normal rats serving as the control; group (2) included normal rats administered 200 mg/kg of costus ethanolic extract (CEE) orally for 6 weeks; group (3) consisted of rats receiving bleomycin (15 mg/kg twice weekly, ip) for 6 weeks; and group (4) involved rats treated orally with CEE (200 mg/kg/day) for 6 weeks following bleomycin intoxication. The results indicated that the CEE significantly reversed the cardiological deteriorations brought on by bleomycin; this was demonstrated by a considerable increase in cardiac SOD, GPx, GSH, and CAT, along with a substantial decrease in cardiac MDA, NO, and DNA fragmentation. Also, serum, LDH, CK-MB, CK- total, TNF-α, IL-4, IL-6 IL-10, IL-1β, triglycerides, cholesterol, and LDL were significantly reduced, while CD4 levels increased, and HDL declined significantly. The results of the histological and immunohistochemical analyses revealed a notable regeneration. In conclusion, CEE's anti-cardiotoxic, anti-inflammatory, and antioxidant properties prove its ability to be a cardio-protective supplement. This may be mediated by its active constituents' radical scavenging and antioxidant properties, particularly high phenolic content.

The current study aimed to evaluate the chemical, phytochemical, and sensory properties; the nutritional value; and the antioxidant properties resulting from the incorporation of yogurt fortified with the aqueous extract of Hawthorn leaves in Sprague Dawley rats. The results revealed that the yogurt containing the aqueous extract from Hawthorn leaves exhibited no significant differences in terms of its protein, fat, and ash contents compared to control samples. Moreover, the highest total phenolic content (62.00 ± 1.70) and antioxidant activity (20.60 ± 0.74%) were detected in the yogurt containing 0.4% Hawthorn leaf extract compared to the other samples. The consumption of yogurt fortified with the aqueous extract from Hawthorn leaves by rats experiencing oxidative stress resulted in a significant decrease (p ≤ 0.05) in the triglyceride, total cholesterol, low-density lipoprotein, aspartate aminotransferase, alanine aminotransferase, creatinine, urea, and malondialdehyde levels and a remarkable increase (p ≤ 0.05) in the high-density lipoprotein, total protein, and albumin levels as well as in the total antioxidant potentials of serum compared to the positive control group, indicating that the extract from Hawthorn leaves can play a preventive role against oxidative stress. Collectively, our study concluded that the extract from Hawthorn leaves can provide health benefits to yogurt on the basis of its high bioactive components and can exert protective effects against oxidative stress in rats.

Diabetes is one of the most common chronic metabolic diseases, and its occurrence rate has increased in recent decades. Sidr (Ziziphus spina-christi L.) is a traditional herbaceous medicinal plant. In addition to its good flavor, sidr has antidiabetic, anti-inflammatory, sedative, analgesic, and hypoglycemic activities. Camel milk has a high nutritional and health value, but its salty taste remains the main drawback in relation to its organoleptic properties. The production of flavored or fortified camel milk products to mask the salty taste can be very beneficial. This study aimed to investigate the effects of sidr fruit pulp (SFP) on the functional and nutritional properties of fermented camel milk. SFP was added to camel milk at rates of 5%, 10%, and 15%, followed by the selection of the best-fermented product in terms of functional and nutritional properties (camel milk supplemented with 15% SFP), and an evaluation of its hypoglycemic activity in streptozotocin (STZ)-induced diabetic rats. Thirty-two male adult albino rats (weighing 150–185 g) were divided into four groups: Group 1, nontreated nondiabetic rats (negative control); Group 2, diabetic rats given STZ (60 mg/kg body weight; positive control); Group 3, diabetic rats fed a basal diet with fermented camel milk (10 g/day); and Group 4, diabetic rats fed a basal diet with fermented camel milk supplemented with 15% SFP (10 g/day). The results revealed that supplementation of camel milk with SFP increased its total solids, protein, ash, fiber, viscosity, phenolic content, and antioxidant activity, which was proportional to the supplementation ratio. Fermented camel milk supplemented with 15% SFP had the highest scores for sensory properties compared to other treatments. Fermented camel milk supplemented with 15% SFP showed significantly decreased (p < 0.05) blood glucose, malondialdehyde, low-density lipoprotein-cholesterol, cholesterol, triglycerides, aspartate aminotransferase, alanine aminotransferase, creatinine, and urea, and a significantly increased (p < 0.05) high-density lipoprotein-cholesterol, total protein content, and albumin compared to diabetic rats. The administration of fermented camel milk supplemented with 15% SFP in diabetic rats restored a series of histopathological changes alonsgside an improvement in various enzyme and liver function tests compared to the untreated group, indicating that fermented camel milk supplemented with 15% SFP might play a preventive role in such patients.