Background: Silver nanoparticles (AgNPs) can accumulate in various organs after oral exposure. The main objective of the current study is to evaluate the renal toxicity induced by AgNPs after repeated oral exposure and to determine the relevant molecular mechanisms. Methods: In this study, 40 male Wistar rats were treated with solutions containing 30, 125, 300, and 700 mg/kg of AgNPs. After 28 days of exposure, histopathological changes were assessed using hematoxylin-eosin (H&E), Masson’s trichrome, and periodic acid-Schiff (PAS) staining. Apoptosis was quantified by TUNEL and immunohistochemistry of caspase-3, and the level of expression of the mRNAs of growth factors was determined using RT-PCR. Results: Histopathologic examination revealed degenerative changes in the glomeruli, loss of tubular architecture, loss of brush border, and interrupted tubular basal laminae. These changes were more noticeable in groups treated with 30 and 125 mg/kg. The collagen intensity increased in the group treated with 30 mg/kg in both the cortex and the medulla. Apoptosis was much more evident in middle-dose groups (i.e., 125 and 300 mg/kg). The results of RT-PCR indicated that Bcl-2 and Bax mRNAs upregulated in the treated groups (p < 0.05). Moreover, the data related to EGF, TNF-α, and TGF-β1 revealed that AgNPs induced significant changes in gene expression in the groups treated with 30 and 700 mg/kg compared to the control group. Conclusion: Our observations showed that AgNPs played a critical role in in vivo renal toxicity.
The aim of this study was to determine the effect of a high-fat diet (HFD) on oocyte maturation and quality in a mouse model. Female BALB/c mice were allocated to one of the following groups: (a) control group (n = 40), which received a controlled diet; or (b) HFD group (n = 40), which received an HFD for 12 weeks. Sections of the ovary were examined histologically. The number of follicles and corpora lutea were counted. In vitro maturation and in vitro fertilisation (IVF) were assessed in germinal vesicle (GV) and metaphase II (MII) oocytes, respectively. The expression of bone morphogenetic protein 15 (BMP15) and leptin receptor genes in GV and MII oocytes was evaluated using reverse transcription real-time polymerase chain reactions. In the HFD group, there was a decreased number of primordial and Graafian follicles, as well as corpora lutea (p < 0.05). The rate of oocyte development to the MII stage was also reduced (p < 0.001). Cumulus expansion was observed more frequently in the control group than the HFD group (p < 0.05). The IVF rate in the HFD group was lower than that in the control group (p < 0.05). In the HFD group, BMP15 and leptin receptor genes were upregulated in the GV stage (p > 0.05) and MII stage (p < 0.05), compared to the control group. An HFD reduces folliculogenesis in the primordial and Graafian stages, in vitro maturation and in vitro fertilisation rates, as well as oocyte quality in mice.
1 January 2016 in Clinical and Experimental Reproductive Medicine
The stroma is one of the 5 layers of the cornea that comprises more than 90% of the corneal thickness, and is the most important layer for the transparency of cornea and refractive function critical for vision. Any significant damage to this layer may lead to corneal blindness. Corneal blindness refers to loss of vision or blindness caused by corneal diseases or damage, which is the 4th most common cause of blindness worldwide. Different approaches are used to treat these patients. Severe corneal damage is traditionally treated by transplantation of a donor cornea or implantation of an artificial cornea. Other alternative approaches, such as cell/stem cell therapy, drug/gene delivery and tissue engineering, are currently promising in the regeneration of damaged cornea. The aim of tissue engineering is to functionally repair and regenerate damaged cornea using scaffolds with or without cells and growth factors. Among the different types of scaffolds, polymer-based scaffolds have shown great potential for corneal stromal regeneration. In this paper, the most recent findings of corneal stromal tissue engineering are reviewed.