Methamphetamine (METH) can potentially disrupt neurotransmitters activities in the central nervous system (CNS) and cause neurotoxicity through various pathways. These pathways include increased ...production of reactive nitrogen and oxygen species, hypothermia, and induction of mitochondrial apoptosis. In this study, we investigated the long-term effects of METH addiction on the structural changes in the amygdala of postmortem human brains and the involvement of the brain- cAMP response element-binding protein/brain-derived neurotrophic factor (
) and
signaling pathways. We examined ten male postmortem brains, comparing control subjects with chronic METH users, using immunohistochemistry, real-time polymerase chain reaction (to measure levels of
, and tumor necrosis factor-α
), Tunnel assay, stereology, and assays for reactive oxygen species (ROS), glutathione disulfide (GSSG), and glutathione peroxidase (GPX). The findings revealed that METH significantly reduced the expression of
, and GPX while increasing the levels of GSSG, ROS, RIPK3,
, and
. Furthermore, METH-induced inflammation and neurodegeneration in the amygdala, with ROS production mediated by the
and
signaling pathways.
In men, several factors cause infertility, among which we can mention damage to sperm due to high temperature. So far, various treatments have been proposed for it, but they have not been highly ...effective. The current study aimed to evaluate the effect of exosome therapy (EXO) and photobiomodulation therapy (PBMT) on spermatogenesis arrest in male mice after scrotum hyperthermia.
In this experimental study, the animals were divided into four groups: control, scrotal hyperthermia, scrotal hyperthermia+EXO (100 μL/d) (mice were treated for 30 days), scrotal hyperthermia+PBMT (laser of 0.03 J/cm2 for 30 seconds/for 30 days). Hyperthermia was induced by exposure to the temperature of 43 °C for 20 minute every day for 5 times. After 6 weeks, the animals were sacrificed.
The treated groups showed a significant increase in sperm parameters, as compared to the hyperthermic groups. Moreover, these favorable effects were observed in relation to the volume of testicular tissue, the number of germ cells, Leydig cells and Sertoli cells, and the level of testosterone. Research on antioxidants showed a significant reduction in oxidized glutathione (GSSG) and reactive oxygen species (ROS) in the treatment groups in comparison to the hyperthermia group (
<0.001). Also, there has been a significant increase in the amount of hydrogen peroxide enzyme observed in the hyperthermia group as opposed to the treatment group (
<0.001).
These findings show that EXO and PBMT can improve spermatogenesis caused by hyperthermia, reduce ROS and GSSG, and increase glutathione (GSH) and sperm quality.
Spinal cord injury is a significant cause of motor dysfunctions. There is no definite cure for it, and most of the therapeutic modalities are only symptomatic treatment. In this systematic review and ...meta-analysis, the effectiveness of stem cell therapy in the treatment of the spinal cord injuries in animal models was studied and evaluated. A systematic search through medical databases by using appropriate keywords was conducted. The relevant reports were reviewed in order to find out cases in which inclusion and exclusion criteria had been fulfilled. Finally, 89 articles have been considered, from which 28 had sufficient data for performing statistical analyses. The findings showed a significant improvement in motor functions after cell therapy. The outcome was strongly related to the number of transplanted cells, site of injury, chronicity of the injury, type of the damage, and the induction of immune-suppression. According to our data, improvements in functional recovery after stem cell therapy in the treatment of spinal cord injury in animal models was noticeable, but its outcome is strongly related to the site of injury, number of transplanted cells, and type of transplanted cells.
Bone marrow stromal stem cells (BMSCs) play a significant role in cell therapy. These cells quickly die after transplantation to the affected area due to oxidative stress. The natural disaccharide, ...trehalose which can be known as autophagy inducer. The present study aimed to investigate the role of trehalose in preventing BMSCs from oxidative stress caused by H
O
. BMSCs were isolated from the adult rats. The cells were divided into three groups: (a) control; (b) 100 µM H
O
; (c) 100 µM H
O
and trehalose 3%. The morality rate was analyzed by viability test. Immunocytochemistry and Western blot was used in order to evaluate p62 protein and LC3II/LC3I ratio, respectively. In order to evaluate apoptosis, cleaved caspase-3 protein was used. In viability test, the survival rate for BMSCs after 8 h were 82%, 72%, 49%, and 39% (for groups who received 50, 100, 200, and 400 µM H
O
, respectively) compared to the control group. Pre-treatment with the use of trehalose 3% increased cell survivals. The levels of p62 protein, were increased in the cells under H
O
treatment, while the levels of p62 protein in the cytoplasm, as autophagy inclusions, reduced for the group with trehalose pre-treatment. In addition, trehalose caused to increase LC3II/LC3I ratio and decreased the expression of cleaved caspase-3. Trehalose decreased apoptosis and increased the autophagy and survival levels of the cells against H
O
. Due to the unique properties of trehalose and its low toxicity, it can be used as a pharmaceutical agent in cellular transplantation to reduce oxidative stress.
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•Chronic METH exposure induces ATG5 and LC3 overexpression.•Chronic METH exposure induces neuronal cell death in the prefrontal cortex.•METH can produce ROS which is detrimental for ...cells.
Methamphetamine (METH) abuse is accompanied by oxidative stress, METH-induced neurotoxicity, and apoptosis. Oxidative stress has devastating effects on the structure of proteins and cells. Autophagy is an evolutionarily conserved intracellular regulated mechanism for orderly degradation of dysfunctional proteins or removing damaged organelles. The precise role of autophagy in oxidative stress-induced apoptosis of dopaminergic neuronal cells caused by METH has not clarified completely. In this study, we sought to evaluate the effects of METH abuse on autophagy in the prefrontal cortex of postmortem users, mainly focusing on the ATG5 and LC3 during neuroinflammation. Postmortem molecular and histological examination was done for two groups containing 12 non-addicted and 14 METH addicted cases. ATG5 and LC3 expression were analyzed by real-time PCR and immunohistochemistry (IHC) methods. Histopathological analysis was performed by stereological cell counting of neuronal cells using Hematoxylin and Eosin (H & E) staining technique. In order to detect DNA damage in the prefrontal lobe, Tunnel staining was performed. Real-time PCR and IHC assay showed overexpression of ATG5 and LC3 protein in the prefrontal cortex of Meth users. The cell death and neuronal degeneration were increased significantly based on Tunel assay and the stereological analysis in the Prefrontal cortex. Chronic METH exposure probably induces ATG5 and LC3 overexpression and neuronal cell death in the Prefrontal cortex of the postmortem cases.
The purpose of this study is to investigate the effect of a low-power laser on the proliferation, migration, differentiation of different types of mesenchymal stem cells (MSCs) in different studies.
...The relevant articles that were published from 2004 to 2019 were collected from the sources of PubMed, Scopus, and only the articles specifically examining the effect of a lowpower laser on the proliferation, differentiation, and migration of the MSCs were investigated.
After reviewing the literature, only 42 articles were found relevant. Generally, most of the studies demonstrated that different laser parameters increased the proliferation, migration, and differentiation of the MSCs, except the results of two studies which were contradictory. In fact, changing the parameters of a low-power laser would affect the results. On the other hand, the source of the stem cells was reported as a key factor. In addition, the combination of lasers with other therapeutic approaches was found to be more effective.
The different parameters of lasers has been found to be effective in the proliferation, differentiation, and migration of the MSCs and in general, a low-power laser has a positive effect on the MSCs, helping to improve different disease models.
Autophagy is a mechanism disassembling the damaged organelles from the cell. This study attempted to examine the expression of several autophagy-related genes in Parkinson’s disease (PD) rat model.
...The male Wistar rats were divided into three groups as control, sham, and lesion. In the latter group, the PD rat model was induced by the injection of 6-hydroxydopamine in the striatum. The behavioral test was conducted one (baseline) and four weeks after the surgery through apomorphine hydrochloride. Then the RT-PCR technique was employed to evaluate the expressions of p62/SQSTM, autophagy-related genes (ATG)5, ATG12, ATG16L1, ATG10, as well as GAPDH and LC3.
By injecting apomorphine, the striatal lesion group showed a significant contralateral rotation at fourth week as compared to the baseline. The examination of p62, ATG5, ATG12, ATG16L1, and LC3 expressions using RT-PCR revealed that p62, ATG5, ATG12, LC3, and ATG16L1 were expressed in the substantia nigra of PD rat model, while ATG10 was not expressed.
ATG10 expression is necessary for the initiation of autophagy. Thus, these results show that autophagy deregulation occurs in the initiation stages of the process in the rat model of PD.
Abstract Regulatory T cells (Treg cells), defined as CD4+ CD25+ FoxP3+ T cells by expression of CD4, high-affinity IL-2 receptor and the transcription factor, forkhead box P3 (FoxP3). They play a ...pivotal role in protecting individuals from autoimmunity and a growing body of evidence suggests their role in the prevention of multiple sclerosis development. However, there are discrepancies about the type of defect in the Treg cells of multiple sclerosis patients and especially whether the Treg number alteration could be contributed to multiple sclerosis pathogenesis. Indeed, whether low number of Treg cells can be a risk factor contributing to multiple sclerosis pathogenesis is the matter of debate and there is not any comprehensive agreement on it. Thus, the objective of this systematic review and meta-analysis was to precisely quantify the nature and magnitude of the association between Treg cell number and the risk ratio/odds ratio (OR) of multiple sclerosis in the case-control studies. Hence, medical databases of Embase, PubMed/Medline, PubMed, PubMed Central and SCOPUS were searched for empirical papers using “Regulatory T cell frequency”, “Treg frequency” in combination with “multiple sclerosis”. In the case-control studies, papers were reviewed for inclusion/exclusion criteria and 8 publications were included. Under random-effect model meta-analysis the data showed that the frequency of Treg cells was not a risk factor in multiple sclerosis using current laboratory methods.
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