No abstract

In ovo injection of nano‐selenium (Se) produced by lactic acid bacteria (LAB–nano‐Se) was investigated on the hatchability, immune responses and the histopathological alterations in hatched chicks. The eggs (18 day age) were injected with 0.5 ml of 0.9% NaCl (normal saline, NS), while the control group was kept without injection. In the third, fourth and fifth groups, the eggs were injected with 0.5 ml of NS and LAB–nano‐Se at 10, 20 and 30 μg/egg. The results revealed improved growth performance in groups injected with LAB–nano‐Se when compared to the control treatment. The highest final weight and weight gain were noticed in 20 μg LAB–nano‐Se/egg group (p < .05). The feed conversion ratio was reduced in all treated groups when compared to the control group (p < .05). Groups injected with LAB–nano‐Se showed enhanced hatchability of the whole incubated eggs (p < .05). Total lipids and cholesterol levels were decreased significantly in groups treated with LAB–nano‐Se at 10 and 20 μg/egg when compared to the non‐treated group. At the same time, globulin was increased by LAB–nano‐Se in ovo injection. Furthermore, the total antioxidant capacity, catalase, glutathione peroxidase, superoxide dismutase increased in groups treated with LAB–nano‐Se at 10 and 20 μg/egg with insignificant (p > .05) differences with those treated with LAB–nano‐Se at 30 μg/egg using in ovo injection technique. Also, higher total blood protein and phagocytosis were significantly observed in groups treated with at 10, 20 and 30 μg LAB–nano‐Se/egg. The histopathological images of hatched chicks revealed that nano‐Se presented normal effects on liver and kidney tissues and restored the parameters as mentioned earlier. To conclude, LAB–nano‐Se exhibited beneficial effects in hatched chicks through improving immune and antioxidant activities as well as histopathological effects by using in ovo technique.

This study examined if wheat germ oil (WGO) has gastroprotective impacts against ethanol-induced gastric ulcer in rats. Rats were assigned into control, WGO, ethanol, omeprazole + ethanol, and WGO + ethanol. WGO prevented gastric ulceration and damage induced by ethanol, the same effect induced by omeprazole, a widely known medication used for gastric ulcer treatment. WGO reduced gastric ulcer index, nitric oxide, and malondialdehyde levels in the stomach. WGO boosted the expression of nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), Bcl2, and the antioxidants. WGO showed inflammatory and anti-inflammatory impacts through the control of interleukin (IL)-1β, Tumor necrosis factor alpha (TNF-α), and IL-10 that were altered in ethanol-administered rats. Ethanol up-regulated caspase-3 and nuclear factor-kappa B (NF-kB) expression and showed histopathological changes such as necrosis and mucosal degeneration that were mitigated by pre-administration of WGO. Moreover, WGO decreased gastric immunoreactivity of NF-kB and increased transforming growth factor beta-1 (TGF-β1) that were associated with upregulation of Nrf2, heme oxygenase-1 (HO-1), and antioxidant expression and production. In conclusion, WGO reduced ethanol-induced stomach toxicity by regulating genes involved in oxidative stress, inflammation, and apoptotic/antiapoptotic pathways.

Based on data from perfused rat livers, high biliary concentrations of 5-OH-FX might also be observed in our patients explaining why LDH, bilirubin, and alkaline phosphatase were elevated in up to 8/12 patients after repeated infusion of flucloxacillin. Liver toxicity of flucloxacillin might therefore be observed in patients with renal impairment after continuously elevated 5-OH-FX levels.
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This study aimed to investigate the oxidative neurotoxicity induced by silver nanoparticles (AgNPs) and assess the neuroprotective effects of quercetin against this toxicity. Forty adult male rats were divided into four equal groups: control, AgNPs (50 mg/kg intraperitoneally), quercetin (50 mg/kg orally), and quercetin + AgNPs. After 30 days, blood and brain tissue samples were collected for further studies. AgNP exposure increased lipid peroxidation and decreased glutathione peroxidase, catalase, and superoxide dismutase activities in brain tissue. AgNPs decreased serum acetylcholine esterase activity and γ-aminobutyric acid concentrations. AgNPs upregulated tumor necrosis factor-α, interleukin-1β, and Bax transcript levels. AgNPs reduced the transcripts of claudin-5, brain-derived neurotrophic factor, paraoxonase, nuclear factor-erythroid factor 2 (Nrf2), and Bcl-2. Histopathologically, AgNPs caused various degenerative changes and neuronal necrosis associated with glial cell reactions. AgNPs increased the immunohistochemical staining of glial fibrillary acidic protein (GFAP) in the cerebrum and cerebellum. Oral treatment with quercetin efficiently counteracted the opposing effects of AgNPs on brain tissue via modulation of tight junction proteins, Nrf2, and paraoxonase, and its positive mechanism in modulating pro-inflammatory cytokines and the downregulation of GFAP expression, and the apoptotic pathway. AgNPs also altered the severity of histopathological lesions and modulated GFAP immunostaining in the examined tissue.