Ulcerative colitis (UC) is among the most challenging human diseases. Nanotechnology has incontestable promising outcomes in inflammatory bowel diseases. This study aimed to investigate the therapeutic effect of naked gold nanoparticles (AuNPs) on dextran sodium sulphate (DSS) induced ulcerative colitis in mice. We also examined the expression of interleukin-17 (IL-17) following AuNPs treatment. Mice were randomly divided into control, DSS and DSS+ AuNPs groups. Severity of colitis was assessed by disease activity index (DAI) measurement. At the end of the experiment, the final body weights were recorded. The colon was dissected and processed for histopathological examinations by light and electron microscopes. Colon homogenates were prepared for assay of tissue malondialdehyde (MDA) and real-time PCR analysis of IL-17A. Immunohistochemical localization of IL-17A was carried out. Scanning electron microscopy (SEM) and Energy Dispersive X-ray (EDX) detector were used to detect the presence of AuNPs in the colonic tissue of DSS+ AuNPs groups. Our results showed that AuNPs effectively targeted the colonic tissue, and reduced changes induced by DSS. The underlying mechanisms could be related to anti-oxidant effect (as evident by decreasing tissue MDA) and anti-inflammatory potential of AuNPs. Our study draws attention to as a novel therapeutic strategy for treating UC.

Serum miR-210 and miR-155 levels are independent diagnostic markers for RA, out-performing several routine indices and reflect disease activity. Thus, miR-210 and miR-155 might serve as non-invasive biomarkers for the diagnosis of RA.

Zinc oxide nanoparticles (ZnO NPs) therapy is a promising strategy for treatment of several diseases. We aimed to investigate the therapeutic potential of ZnO NPs in ameliorating the histopathological and functional alterations in the pancreas of a rat model of streptozotocin-induced diabetes. Rats were randomized into control, diabetic and ZnO NPs-treated diabetic groups. Biochemical assays of blood glucose and serum insulin were performed. Pancreas specimens were processed for light and electron microscope examinations. ZnO NPs effectively reversed diabetes-induced pancreatic injury, as evidenced by the structural and ultrastructural improvement and confirmed by biochemical normalization of blood glucose and serum insulin.

Atrazine (ATZ) is one of the most commonly used herbicides contaminating plants, soil and water resources. Several strategies have been used to counteract ATZ toxicity. Here, we tested the hypothesis that lycopene could ameliorate ATZ-induced toxicity in the adrenal cortex. For this purpose, 35 adult male albino rats were randomized into five equal groups: untreated control, vehicle control (received 0.5 mL corn oil/day), lycopene (treated with lycopene dissolved in 0.5 mL corn oil, 10 mg/kg b.w./day), ATZ (received ATZ dissolved in 0.5 mL corn oil 300 mg/kg b.w./day), and ATZ + lycopene (treated with ATZ and lycopene at the same previously mentioned doses). All treatments were given by oral gavage for 4 weeks. We found that ATZ exposure significantly increased relative adrenal weight, plasma ACTH levels, and adrenal oxidative stress as manifested by elevated malondialdehyde levels, decreased reduced glutathione content and depressed antioxidant enzyme activities in adrenal cortex tissues with respect to control groups. Furthermore, the transcription of adrenal cortex nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), nuclear factor kappa B, and caspase-3 genes was increased significantly compared with the control groups. This was accompanied with DNA fragmentation and structural and ultrastructural changes in zona glomerulosa and zona fasiculata of the adrenal cortex. Notably, all these changes were partially ameliorated in rats treated concomitantly with ATZ and lycopene. Our results showed that lycopene exerts protective effects against ATZ-induced toxicity in rat adrenal cortex. These effects may be attributed to the antioxidative property of lycopene and its ability to activate the Nrf2/HO-1 pathway.

SUMMARYPermethrin (PM), a synthetic pyrethroid insecticide, has broad toxicity spectra. We aimed to investigate the effects of PM on the testes of adult albino rats, examine the recovery response and evaluate the efficacy of naringenin (NG) supplementation. Adult male albino rats were randomly assigned to five groups of six each: control, NG (50 mg/kg), PM (70 mg/kg), recovery (after subsequent withdrawal of PM) and NG-PM group. All treatments were given by oral gavage for 6 weeks and another 3 weeks for the recovery group. At the time of sacrifice, each testis was weighed. Biochemical analysis of epididymal sperm count and serum testosterone level was performed. Testes were processed for histological, ultrastructural and c-Kit immunohistochemical study. PM toxicity was evidenced by a highly significant decrease in testicular weight, epididymal sperm count and serum testosterone level compared to control. Furthermore, testicular structure abnormalities and reduced c-Kit immunoreactions were observed. Stoppage of PM in the recovery group partially reversed PMinduced changes. There was a mild decrease in testicular weight and biochemical parameters compared to control. The structure of seminiferous tubules was partially retained. The NG-PM group showed an overall improvement in testicular weight and biochemical alterations which were confirmed by light and electron microscopic examination. In conclusion, PM induced testicular toxicity, which was ameliorated by NG co-administration. However, stoppage of PM exposure was associated with partial recovery.