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Abstract Background Innovative research highlighted the probable connection between autism spectrum disorder (ASD) and gut microbiota as many autistic individuals have gastrointestinal problems as co-morbidities. This review emphasizes the role of altered gut microbiota observed frequently in autistic patients, and the mechanisms through which such alterations may trigger leaky gut. Main body Different bacterial metabolite levels in the blood and urine of autistic children, such as short-chain fatty acids, lipopolysaccharides, beta-cresol, and bacterial toxins, were reviewed. Moreover, the importance of selected proteins, among which are calprotectin, zonulin, and lysozyme, were discussed as biomarkers for the early detection of leaky gut as an etiological mechanism of ASD through the less integrative gut–blood–brain barriers. Disrupted gut–blood–brain barriers can explain the leakage of bacterial metabolites in these patients. Conclusion Although the cause-to-effect relationship between ASD and altered gut microbiota is not yet well understood, this review shows that with the consumption of specific diets, definite probiotics may represent a noninvasive tool to reestablish healthy gut microbiota and stimulate gut health. The diagnostic and therapeutic value of intestinal proteins and bacterial-derived compounds as new possible biomarkers, as well as potential therapeutic targets, are discussed.

Abstract Background Neuroinflammation plays a major role in the pathogenesis of autism because the cytokine levels are typically disturbed in the brain in autistic patients. Prebiotics-rich diet maintains the healthy gut microbiota and hence can regulate the neuroinflammation indirectly. The study aimed to investigate the role of bee pollen and propolis in ameliorating neuroinflammation, including cytokine levels, in an animal model of autism. Methods Hamsters were classified as four groups: Group I, control; Group II, autistic model/animals treated with 250 mg propionic acid (PPA)/kg body weight (BW)/day for 3 days; Group III, animals treated with bee pollen at a dose of 250 mg/kg BW/day for 4 weeks; and Group IV, animals treated with propolis at a dose of 250 mg/kg BW/day for 4 weeks. Neuroinflammatory responses were evaluated using the levels of interferon γ (IFN-γ), interleukin 1 alpha (IL-1α), IL-6, IL-10, IL-12 (p70), vascular endothelial growth factor (VEGF), and tumor necrosis factor α (TNFα). Results Significant decrease of IL-10 (P

Alternative and complimentary usage of the natural compound has raised hopes of finding curative options for liver hepatocarcinogenesis. In the present study, the curative effect of bee honey against diethylnitrosamine (DEN) (50 mg/kg) and carbon tetrachloride (CCl4) (2 mg/Kg)–induced hepatocellular carcinoma (HCC) in male rats in the presence or absence of some chemotherapeutic drugs, Cisplatin (Cis), Cyclophosphamide (CY) and 5- Fluorouracil (5-FU) were investigated. The obtained results demonstrated that treatment with DEN/CCl4 caused oxidative stress as assigned by the increase in malondialdehyde (MDA) and fall in glutathione (GSH) content. Meantime detraction in the antioxidants, including superoxide dismutase (SOD), catalase (CAT), glutathione-s-transferase (GST) and glutathione peroxidase (GPx) was observed. Also, the results showed induction of inflammation as reflected by an increase in the levels of both α- fetoprotein and α- fucosidase in the liver. This was accompanied by changes in the hepatic function biomarkers which characterized by the increased levels of transaminases (AST, ALT), alkaline phosphatase (ALP) and γ-Glutamyl transferase (γ-GT) and decrease in total protein content in the serum. In conclusion, the combination of the selected drugs and bee honey may be an effective chemo- preventive and therapeutic strategy for treating DEN and CCl4-induced HCC. Keywords: Hepatocellular carcinoma, Diethyl nitrosamine, Carbon tetrachloride, Bee honey, Chemotherapy, Oxidative stress, Inflammatory markers