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Objectives The current study was aimed to investigate the effect of morpholin-4-ium 4 methoxyphenyl (morpholino) phosphinodithioate (GYY4137) on ipsilateral epididymis injury in a rat model of experimental varicocele (VC). Materials and Methods Sixty Wistar rats were randomly assigned to sham, sham plus GYY4137, VC and VC plus GYY4137 groups. Sperm quality parameters, including sperm count, motility and viability were evaluated after 4 weeks. Histological changes were measured by hematoxylin and eosin staining between the groups. The oxidative stress levels were estimated by determining epididymal superoxide dismutase (SOD) and malondialdehyde (MDA). The apoptosis status and the expression of phosphatidylinositol 3'-OH kinase (PI3K)/Akt were analyzed by immunohistochemical analysis, western blot and RT-qPCR. Results VC resulted in the decrease of sperm parameters, significant histological damage and higher levels of oxidative stress and apoptosis. Compared to the VC group, GYY4137 markedly ameliorated these observed changes. In addition, treatment with GYY4137 obviously reduced the levels of caspase-3 and Bax and increased the levels of the phosphorylation of PI3K p85 and Akt. Conclusion Our data demonstrated that GYY4137 may alleviate the sperm damage and epididymis injury in experimentally VC-induced rats by activation of the PI3K/Akt pathway.Objectives Exercise ameliorates the quality of life and reduces the risk of neurological derangements such as Alzheimer's (AD) and Parkinson's disease (PD). Irisin is a product of the physical activity and is a circulating hormone that regulates the energy metabolism in the body. In the nervous system, Irisin influences neurogenesis and neural differentiation in mice. We previously demonstrated that co-treatment of bone marrow stem cells (BMSCs) with a neurotrophic factor reduce Parkinson's symptoms. Our goal in this project was to evaluate whether Irisin with BMSCs can protect the dopaminergic (DA) neurons in PD. Materials and Methods 35 adult male Wistar rat weighing (200-250 g) were chosen. They were separated into five experimental groups (n=7). To create a Parkinson's model, intranasal (IN) administration of the MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) was used. The BMSCs (2×106) and Irisin (50 nm/ml) was used for 7 days for treatment after creation of the PD model. After completion of the tests (4 weeks), their brains were used for the TUNEL and immunohistochemical (IHC) assays. Results One of the important results of this study was that the Irisin induce BMSCs transport into the injured area of the brain. Co-treatment of the Irisin with BMSCs increased tyrosine hydroxylase-positive neurons (TH+) in substantia nigra (SN) and striatum of the PD mice brain. In this group, the number of TUNEL-positive cells significantly decreased. Behavioral symptoms were better in the combination group and Irisin simultaneously. Conclusion Co- treatment of Irisin with BMSCs protects the DA neurons from degeneration and apoptotic process after MPTP injection.Objectives Parkinson's disease (PD) is characterized by motor and cognitive dysfunctions. The progressive degeneration of dopamine-producing neurons that are present in the substantia nigra pars compacta (SNpc) has been the main focus of study and PD therapies since ages. Materials and Methods In this manuscript, a systematic revision of experimental and clinical evidence of PD-associated cell process was conducted. Results Classically, the damage in the dopaminergic neuronal circuits of SNpc is favored by reactive oxidative/nitrosative stress, leading to cell death. Interestingly, the therapy for PD has only focused on avoiding the symptom progression but not in finding a complete reversion of the disease. Recent evidence suggests that the renin-angiotensin system imbalance and neuroinflammation are the main keys in the progression of experimental PD. Conclusion The progression of neurodegeneration in SNpc is due to the complex interaction of multiple processes. In this review, we analyzed the main contribution of four cellular processes and discussed in the perspective of novel experimental approaches.Objectives The present paper aims to review the studies describing the interactions between HopQ and CEACAMs along with possible mechanisms responsible for pathogenicity of Helicobacter pylori. Materials and Methods The literature was searched on "PubMed" using different key words including Helicobacter pylori, CEACAM and gastric. Results HopQ is one of the outer membrane proteins of H. pylori and belongs to the family of adhesin proteins. In contrast to other adhesins, HopQ interacts with host cell surface molecules in a glycan independent manner. Human CEACAMs are the cell surface adhesion molecules mainly present on the epithelial cells, endothelial cells and leukocytes. Irbinitinib inhibitor The overexpression of these molecules may contribute to cancer progression and relapse. Recent studies have shown that HopQ may interact with human CEACAMs, particularly CEACAM1, CEACAM3, CEACAM5 and CEACAM6, but not CEACAM8. HopQ interacts with GFCC'C" interaction surface of IgV domain of N- terminal region of CEACAM1. Moreover, binding of HopQ to CEACAM1 prevent its trans-dimerization and stabilizes it in monomeric form. H. pylori may use these HopQ-CEACAM interactions to transfer its CagA oncoprotein into host gastric epithelial cells, which is followed by its phosphorylation and release of interleukin-8. HopQ-CEACAM interactions may also utilize T4SS, instead of CagA, to activate NF-κB signaling and trigger inflammation. Conclusion HopQ of H. pylori may interact with CEACAMs of the human gastric cells to induce the development of gastric ulcers and cancers by transferring CagA oncoprotein or inducing activation of T4SS to initiate and maintain inflammatory reactions.Retinal degeneration (RD) is one of the most common causes of visual impairment and blindness and is characterized by progressive degeneration of photoreceptors. Transplantation of neural stem/progenitor cells (NPCs) is a promising treatment for RD, although the mechanisms underlying the efficacy remain unclear. Accumulated evidence supports the notion that paracrine effects of transplanted stem cells is likely the major approach to rescuing early degeneration, rather than cell replacement. NPC-derived exosomes (NPC-exos), a type of extracellular vesicles (EVs) released from NPCs, are thought to carry functional molecules to recipient cells and play therapeutic roles. In present study, we found that grafted human NPCs (hNPCs) secreted EVs and exosomes in the subretinal space (SRS) of RCS rats, an RD model. And direct administration of mouse neural progenitor cell-derived exosomes (mNPC-exos) delayed photoreceptor degeneration, preserved visual function, prevented thinning of the outer nuclear layer (ONL), and decreased apoptosis of photoreceptors in RCS rats.
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