Temporal lobe epilepsy (TLE) is present in 30% of epileptic patients and does not respond to conventional treatments. Bone marrow derived mesenchymal stem cells (BMSCs) induce endogenous neural stem cells, inhibit neurodegeneration, and promote brain self-repair mechanisms. The present study addresses the feasibility of BMSCs transplantation against pilocarpine-induced TLE experimentally. BMSCs were injected either intravenously (IV) or in hippocampus bilaterally (IC). Increased cell count of BMSCs was achieved via IC route. BMSCs treatment ameliorated the pilocarpine-induced neurochemical and histological changes, retained amino acid neurotransmitters to the normal level, downregulated the immunoreactivity to insulin growth factor-1 receptor, synaptophysin, and caspase-3 and reduced oxidative insult and inflammatory markers detected in epileptic model. It is worth noting that BMSCs IC-administered showed more pronounced effects than those administered via IV route. BMSCs transplantation presents a promise for TLE treatment that has to be elucidated clinically.

Silver and silver oxides are gaining interest in medical applications for their prominent antibacterial and antimicrobial potentials. Recent studies suggest that nanosilver oxide has remarkable anti-inflammatory effects and enhances wound healing. Nevertheless, its effect on gastric ulcer has not yet been illustrated. Thus the current study aimed to explore the prospect protective effect of nanosilver oxide against indomethacin-induced gastric ulcer. A new approach has been followed to synthesize nanosilver oxide. X-ray diffraction, UV-Vis spectroscopy and transition electron microscope techniques have been successfully used to characterize the synthesized nanoparticles. Treatment of ulcerated rats with different doses of nanosilver oxide especially (175 and 350 ppm/p.o.) alleviated adverse effects of indomethacin-induced gastric injury as demonstrated by decreasing ulcer index and elevating % of ulcer inhibition. These positive effects excelled those exerted by the reference antiulcer drug omeprazole. Nanosilver oxide suppressed gastric inflammation by reducing myeloperoxidase, tumor necrosis alpha, interleukin 1beta and interferon gamma. Moreover, nanosilver oxide halted gastric oxidative stress via inhibiting lipid  peroxidation and enhancing glutathione and paraoxonase-1. Regarding gastric apoptosis, nanosilver oxide down regulated the expression of caspase 9, tumor protein 53, and nuclear factor kappa B and allograft inflammatory factor-1 genes. These findings emphasize the antiulcerogenic potential of nanosilver oxide against indomethacin-induced gastric ulcers which are multi-factorial including anti-inflammatory, antioxidant and antiapoptotic effects.

No abstract

No abstract

No abstract