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Purpose: The present study investigates the effects of myricitrin and solid lipid nanoparticle (SLN) containing myricitrin on the reproductive system of type 2 diabetic male mice. Materials and Methods: In this experimental study, SLN containing myricitrin was prepared by the cold homogenization method. Then, 90 adult male Naval Medical Research Institute mice were divided into 9 groups (n=10): control, vehicle, diabetic, diabetic+myricitrin or SLN containing myricitrin 1, 3, and 10 mg/kg. Diabetes was induced by streptozotocin (65 mg/kg) 15 minutes after nicotinamide (120 mg/kg) injection. Myricitrin and SLN containing myricitrin administered during 1 month. At the 34th days of the experiment, plasma and tissue samples were taken for experimental assessments. Results: Testis weight and volume decreased in the diabetic group. These variables increased in diabetic treated mice by a high dose of myricitrin or all doses of SLN containing myricitrin (p<0.05). Total antioxidant capacity and superoxide dismutase levels decreased in diabetic mice, and administration of myricitrin 10 mg/kg or all doses of SLN containing myricitrin increased them (p<0.05). Luteinizing hormone, Follicle-stimulating hormone, testosterone, and sperm count decreased in the diabetic group, treatment with a high dose of myricitrin or all doses of SLN containing myricitrin recovered them (p<0.05). Diabetes induced vacuoles and apoptosis in testicular cells, meanwhile myricitrin and SLN containing myricitrin improved them (p<0.05). Conclusions: Diabetes induced reproductive problem via increased oxidative stress and decrease antioxidant capacity, administration of myricitrin or SLN containing myricitrin improved them. Further, SLN containing myricitrin was more potent than myricitrin.

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Specific GABAergic interneurons in the hilus are lost in animal models with temporal-lobe epilepsy (TLE). Some preclinical evidence has indicated that GABAergic cells may provide relief from seizures in these models. This study was aimed to examine the ability of ethosuximide, an anticonvulsant drug, to promote neurogenesis in 3-day-old rat forebrain cortex stem cells. Most of the cells were found to be nestin-positive undifferentiated neural stem cells prior to their exposure to ethosuximide. It was noted that the number and percentage of tubulin β-III immunopositive neurons were increased after 6 days treatment with ethosuximide. Upon bFGF withdrawal, exposure to ethosuximide differentiated the stem cells to MAP2 positive neural cells (7.18 ± 0.43, 21.766 ± 0.55 and 41.57 ± 0.5 for control, 0.1 and 1 μM, respectively). GABA immunofluorescence images illustrated that ethosuximide increased GABAergic neurons (7.19 ± 0.32, 23.23 ± 0.55, and 46.30 ± 0.44 for control, 0.1 and 1 μM, respectively). Additionally, BrdU immunofluorescence assay showed that ethosuximide-enhanced nucleus proliferation in the neuronal stem cells. Therefore, the results of this study suggest that ethosuximide may compensate damage caused by seizure attacks and possibly other neuronal loss disorders.