intraperitoneal injection of AgNPs adversely affected the structure of adult rat testes. The tissue damage was more manifested with increased dose and duration of exposure.

Myocardial infarction (MI), Isoproterenol (ISO), Nitric oxide (NO), Neuronal NOS (nNOs), Endothelial NOs (eNOs), Gold nanoparticle (GNPs), Diamiobenzidine (DAB), Serum Creatine Kinase-MB (CK-MB), Alanine aminotransferase (ALT), Cardiac troponin T (cTnT), Electrochemiluminiscence (ECLIA), Cardiomyocytes (CMC), Peroxisomal proliferator activated receptor (PPARs), Reactive oxygen species (ROS).

Exposure to nicotine in smoking contributes to most unexplained male infertility but the mechanisms remain to be fully elucidated. Zinc (Zn) is an essential trace element in normal growth, development and reproduction. Zinc oxide nanoparticles (ZnONPs) are well-known antioxidants. Therefore, this work was designed to investigate the potential ability of ZnONPs to protect testis and epididymis in nicotine-treated rats. Forty adult male Wistar albino rats were divided into control group and two experimental groups (treated and supplemented rats). In the treated group, rats received nicotine at a dose of 1 mg/kg/day orally for 30 days. Rats in the supplemented group received ZnONPs (10 mg/kg/day) with nicotine (1 mg/kg/day), orally for the same period. Testicular and epididymal sections were stained with H&E to assess the histological changes. Negrosin-eosin staining of epididymal sperms was performed to assess their viability and morphological changes. Serum testosterone, FSH and LH levels were assessed. Also, oxidative stress parameters and semiquantitative real-time PCR for steroidogenic enzymes were measured. Morphometric studies of both organs were statistically analyzed. Mild to severe testicular and epididymal structural changes together with sperm morphological abnormalities were detected in nicotine-treated rats. Biochemical results also showed a decrease in all measured parameters except for an increased malondialdehyde (MDA) level that meant deterioration of their reproductive function. On the other hand, ZnONP supplementation in the last group showed an obvious improvement in all investigated parameters.

Being one of the most debilitating complications among diabetic patients, diabetic polyneuropathy (DPN) is a paramount point of continuous research. Stem cell therapies have shown promising results. However, limited cell survival and paracrine activities hinder its transfer from bench to bedside. We designed this study to evaluate fluoxetine-pretreatment technique of mesenchymal stem cells (MSCs) as an approach to enhance their paracrine and immunomodulatory properties in DPN. Effects of fluoxetine treatment of MSCs were tested in vitro. Forty-two adult Wistar male albino rats were utilized, further subdivided into control, diabetic, MSC-treated and fluoxetine-pretreated MSC groups. Sciatic nerve sections were prepared for light and electron microscope examination and immunohistochemical detection of neurofilament (NF) protein. Also, we assessed in vitro survival and paracrine properties of fluoxetine-pretreated MSCs. Real time PCR of BDNF, VEGF, IL-1β, and IL-10 expression in tissue homogenate was performed. Our results showed restoration of normal neuronal histomorphology and ultrastructure, moreover, immunohistochemical expression of anti-neurofilament protein was significantly elevated in MSC-treated groups compared to the diabetic one. Fluoxetine enhanced the MSC survival and their paracrine properties of MSCs in vitro. Furthermore, the fluoxetine-pretreated MSC group revealed a significant elevation of mRNA expression of BDNF (neurotrophic factor) and VEGF (angiogenic factor), denoting ameliorated MSC paracrine properties. Similarly, improved immunomodulatory functions were evident by a significant reduction of interleukin-1β mRNA expression (pro-inflammatory) and a reciprocal significant increase of interleukin-10 (anti-inflammatory). We concluded that fluoxetine-pretreatment of MSCs boosts their survival, paracrine, and immunomodulatory traits and directly influenced neuronal histomorphology. Hence, it presents a promising intervention of diabetic polyneuropathy. Graphical Abstract.

Traumatic optic neuropathy is an important cause of severe vision loss. So, many attempts were performed to transplant stem cells systemically or locally to regenerate the injured retina. In this study, we investigated the effect of human umbilical cord blood mesenchymal stem cells (hUBMSCs) on histological structure, apoptotic, antiapoptotic, oxidant and antioxidant markers in an experimental model of cryo-induced retinal damage in mice. Forty-eight mice were included with 4 major groups; group I contained 18 mice as controls. The others included 30 mice exposed to cryo-induced retinal injury and were subdivided into three equal groups: group II received no treatment after injury. Group III was intravenously injected with hUCBMSCs after injury and group IV received an intravitreal injection with hUCBMSCs into both eyes. Retinal tissues were used for histopathological, immunological and gene expression studies. Real time-PCR was performed to assess B-cell lymphoma 2 (bcl2), Bcl2-associated X protein (bax), heme oxygenase-1 (hmox-1) and thioredoxin-2 (tnx-2) expression and to assess the differentiation of the stem cells into the retinal tissue. Immunohistochemical analysis was performed to assess caspase-3, 3-nitrotyrosine (3-NT) and basic fibroblast growth factor (bFGF). Disturbed retinal structure was seen in cryo-injured mice while hUCBMSCs treated groups showed nearly normal structure. By real time-PCR, significantly reduced mRNA expressions of Bax and notably enhanced mRNA expression of Bcl-2, hmox-1 and txn-2 were demonstrated in retinal injured mice with hUCBMSCs treatment compared to those without. In addition, immunohistochemical analysis confirmed downregulation of 3-NT and caspase-3 and upregulation of bFGF after hUCBMSCs injection in injured retina. Furthermore, there was no differentiation of transplanted stem cells into the retinal tissue. In conclusions, hUCBMSCs could improve the morphological retinal structure in cryo-induced retinal damage model by modulation of the oxidant-apoptotic status and by increased the expression of bFGF. © 2017 IUBMB Life, 69(3):188-201, 2017.