Cell Journal最新文献

Objective: Dysregulation of lipid and carbohydrate/fatty acid (FA) balance in Sertoli and germ cells alters the NADP+/ NADPH ratio, resulting in metabolic autophagy in testicles. Tramadol (TRA) adversely affects spermatogenesis development, and it is not reversed within short periods of time after withdrawal. Therefore, the present study aimed to examine the boosting effect of different exercise training protocols (ETPs) on TRA-induced detrimental effects after withdrawal.

Materials and methods: In this experimental study, 36 mature Wistar rats were separated into control and TRAsole (administered 40 mg/kg of TRA and euthanized 60 days after TRA administration), Con-TRA (stopped TRA administration after 60 days, and continued for additional 60 days after withdrawal), TRA+low-intensity (TRA+LICT), TRA+ moderate-intensity (TRA+MICT), and TRA+high-intensity continuous (TRA+HICT) ETPs-induced groups (n=6/ group, ETPs were initiated for 60 days after stopping TRA administration). Next, the intracytoplasmic carbohydrate and lipids/FAs content, testicular lactate and lactate dehydrogenase (LDH) levels, relative ratios of NADP+/NADPH, serum testosterone levels, and the Leydig cells steroidogenic activity, the mRNA levels of Beclin-1, p62, LC3-I, and Atg7 as well as the LC3-I/II+ germ and somatic cells mean distributions were analyzed.

Results: The LICT and MICT could ameliorate the TRA-induced carbohydrates/lipids, FAs imbalance, increase lactate, LDH and testosterone levels, re-balance the NADP+/NADPH ratio, and reregulate the autophagy and steroidogenic activities in the Leydig and Sertoli cells.

Conclusion: Collectively, LICT and MICT can ameliorate the TRA-induced metabolic-oxidative autophagy by rebalancing energy survey in testicles and down-regulating autophagy reactions in Sertoli cells and rebalancing it in the Leydig cells.

Among the various manifestations of oral cavity cancer, tongue squamous cell carcinoma (TSCC), is the most common form of this condition. TSCC represents a major challenge in the field of cancer treatment. The emergence of small interfering RNAs (siRNAs) has opened new avenues for therapeutic intervention in TSCC. This research provides an overview of siRNA-mediated mechanisms and emphasizes their complex involvement in modulating key signaling pathways associated with TSCC progression. Relevant articles from 2004 to 2023 were conducted by using different keywords, such as "Interfering RNA " and "Small Interfering ". The search was following the Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) guidelines based on inclusion and exclusion criteria. The quality of the studies was assessed using the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) criteria. The selected studies (n=17) were subjected to perform comprehensive analysis. We concluded that the PI3K/AKT and ERK pathways, one of oncogenic signaling cascades in TSCC is notable. siRNAs and their role in targeting specific signaling pathways help us understand the molecular mechanisms underlying TSCC that may lead to the development promising therapies for TSCC. These therapies have the advantage of personalization and precision, targeted delivery, and the potential to overcome drug resistance. Therefore, the study enhances our comprehension of siRNA-based interventions' clinical potential in TSCC.

Objective: There are ethical and technical challenges in studying human germ cell development. Therefore, the aim of the study is in vitro differentiation of human embryonic stem cells (hESCs), as pluripotent cells, to the germ cells which is a valuable tool for studying molecular and cellular aspects of gametogenesis and understanding causes of infertility.

Materials and methods: In this experimental study, two different complete media [Dulbecco's Modified Eagle Medium (DMEM)+20% fetal bovine serum (FBS) and embryoid bodies (EBs) medium; KOSR/HES without basic fibroblast growth factor (bFGF)] were used in the both of test groups using testicular cells derived conditioned medium (TCCM) and control groups spontaneously differentiated (SD). Thereby, EBs from hESCs (Yazd2; 46XY) were cultured in different conditions EB medium; EB medium and conditioned EB medium; EB medium, DMEM, and FBS without conditioning; EB medium, conditioned DMEM, and FBS medium. EBs were collected after 4, 7, and 14 days and their gene expression profiles were assessed and compared to hESCs, as day 0, using IF and relative reverse transcription quantitative polymerase chain reaction (RT-qPCR).

Results: An increase in the gametogenesis gene expression level in TCCM groups was showed in comparison with SD groups. Additionally, immunostaining of differentiated cells in all groups showed in vitro gametogenesis (IVG).

Conclusion: Our findings showed that human TCCM could be used as a natural niche for in vitro male and female germ cell development. However, further studies are needed to define the factors and metabolites within the human TCCM.

Objective: Trimethyltin (TMT) chloride is an organotin compound used in industry. It has been linked to generating reactive oxygen species (ROS), inflammatory processes, and neuronal death. Carvacrol is a monoterpene phenol found in the Lamiaceae plant family, modulating inflammatory conditions and necroptosis in neural tissue. This study aimed to investigate the neuroprotective effects of carvacrol in a rat model of hippocampal neuronal injury induced by TMT.

Materials and methods: In this experimental study, sixty male Wistar rats were randomly divided into five groups (n=12): group 1 receiving saline, group 2 received dimethyl sulfoxide (DMSO) as a vehicle for 21 days, group 3 receiving a single dose of TMT (8 mg/kg) and groups 4 and 5 receiving carvacrol 40 and 70 mg/kg daily for 21 days after a single dose of TMT. All injections were intraperitoneal (I.P.). Caspase-3, Bax, Bcl-2, and Bdnf gene expression and the number of pyknotic neurons in the hippocampus were quantified. Spatial memory was assessed with a radial arm maze.

Results: Statistical analysis of histological data revealed the carvacrol significantly attenuated cognitive dysfunction and the number of pyknotic neurons in the hippocampal CA1 region of rats treated with TMT. Based on real-time polymerase chain reaction (PCR), carvacrol modulated the expression of genes involved in apoptosis (Bax and Caspase-3) and upregulated anti-apoptotic (Bcl-2) and brain derived neurotrophic factor (Bdnf) genes in the hippocampal tissue.

Conclusion: These findings revealed neuroprotective effects of carvacrol which might be mediated by apoptotic and anti-apopetotic factors.

In this article published in Cell J, Vol 24, No 12, 2022, on pages 741-747, the authors found that there was some mistakes in the Table 1 and we have corrected them in the following table. The authors would like to apologize for any inconvenience.

In this article published in Cell J, Vol 17, No 1, 2015, on pages 159-162, the authors found that the affiliation of second author in address 2 was missed during the formatting of the paper. Therefore, we corrected it. The authors would like to apologize for any inconvenience.

Objective: In Parkinson's disease (PD), mitochondrial defects and oxidative stress cause an increase in free radicals and the death of dopaminergic neurons in the substantia nigra. By preventing lipid peroxidation and protecting against peroxide radicals, vitamin E is the most important antioxidant of biological membranes that can neutralize free radicals. Also, the improvement of the functional status of mitochondria can be influenced by exercise, which can be partially the result of changes in the mitochondrial mitophagy and dynamics system. This study aimed to investigate the interactive effects of six weeks of vitamin E (VE) consumption and training on the mitochondrial function [Cytochrome C (Cyt-C), Adenosine triphosphate (Atp) synthase, optical atrophy1 mitochondrial dynamics like guanosine triphosphatase (GTPase), 8-Oxodequanosin and Pten induced kinase 1 (Pink1) is a protein coding gene] in the hippocampus tissue of PD rats.

Materials and methods: In this experimental study, 4-6-month-old Sprague-Dawley rats (mean weight 250 ± 30 g) were given parkinsonism with reserpine (2 mg/kg) and were categorized into different groups, including healthy (H), PD, VE solvent+PD (Sham), aerobic exercise+PD (AE+PD), VE+PD, AE+VE+PD. The aerobic training program was carried out for six weeks and 5 sessions per week and each session lasted 15-22 minutes. VE was also taken orally at 30 mg/kg daily.

Results: A six-week regimen of VE supplement along with the AE significantly reduced the Cyt-C gene expression level, also we observed a significant increase in gene expression level of the Pink1, Atp synthase and Opa1 (P<0.05). There is no significant difference was found in the level of 8-Oxog detected in hippocampal tissue samples (P>0.05).

Conclusion: The consumption of VE along with AE may provide therapeutic effects on mitochondrial damage in PD rats.

Objective: The prevalence of neurological disorders often varies by sex, with conditions such as Alzheimer's disease and autism spectrum disorder (ASD) demonstrating notable differences in incidence. The aim of this study is to understand the molecular basis for these divergences in order to facilitate the creation of sex-specific therapeutic strategies.

Materials and methods: This study is a bioinformatic analysis of publicly available RNA sequencing datasets involving autism patients. The study utilized RNA sequencing data from postmortem human brains' prefrontal cortex, including 38 neurotypical controls and 34 individuals with ASD. The sequencing data was obtained from previously published papers, and we downloaded the raw data from SRA. We investigated the molecular basis of sex-biased presentation in ASD through comprehensive transcriptomic analysis.

Results: Comparative analysis of gene expression between male and female subjects, both autistic and unaffected, was conducted, using a significance level of ≤0.01. In autistic individuals, 136 genes demonstrated differential expression between sexes, predominantly upregulated in males, indicating a bias in male gene expression. Among these, 12 genes were identified as risk factors in the SFARI dataset. While most sex-biased genes were autosomal, expression differences on sex chromosomes were also observed in neurotypical subjects. Notable genes included TCF7L2, collagen family genes, and solute carrier family genes. In ASD males, extracellular matrix (ECM) organization emerged as a significant pathway, while immune-related processes were prominent in unaffected individuals.

Conclusion: Our study highlights the impact of the ECM pathway in ASD, with notable differences between sexes, particularly in males. MIR424 shows promise as a potential biomarker for ASD in males. Recognizing the importance of sex differences in ASD transcriptomic research is crucial, as these variances provide insights into the disorder's pathophysiology and may guide the development of more personalized treatments for both sexes.

Objective: Despite the advances in treatment, breast cancer (BC) remains a major cause of death in women. This study aims to evaluate the prognostic significance of detecting circulating tumor cells (CTCs) and disseminated tumor cells (DTCs) in paired peripheral blood (PB) and bone marrow (BM) samples obtained both before and after adjuvant chemotherapy from patients with operable BC.

Materials and methods: In this experimental study, from 160 patients with primary BC, we collected 160 PB and BM samples before and we could be able to collect PB and BM samples from 100 of them after adjuvant chemotherapy. The expression level of cytokeratin 19 (CK19), carcinoembryonic antigen (CEA), mammaglobin 1 (MGB1), mucin 2 (MUC2) and trefoil factor 1 (TFF1) mRNAs in the PB/BM samples were analyzed by quantitative real-time polymerase chain reaction (PCR).

Results: Multivariate Cox regression analyses indicated that the detection of CK19 mRNA-positive CTCs/DTCs either before or after adjuvant chemotherapy was an independent factor for prognosis associated with decreased diseasefree survival (DFS). Patients with tumor cells detected in both PB and BM and patients with persistent detection of tumor cells before and after chemotherapy had worse outcomes compared to those with tumor cells detected in one or neither of the compartments.

Conclusion: This study suggests that the detection of CK19 mRNA-positive CTCs/DTCs either before or after adjuvant chemotherapy could be an independent predictor of DFS in operable BC patients.

Objective: The objective of this study was to assess whether Spen paralogue and orthologue C-terminal domain containing 1 (SPOCD1) gene expression could serve as a valuable prognostic and diagnostic biomarker in common cancers, drawing from insights in recent literature. We sought to verify this concept by utilizing data sourced from The Cancer Genome Atlas (TCGA) alongside clinical samples.

Materials and methods: In this bioinformatics and experimental study, SPOCD1 RNA-seq data from 12 common cancers were collected from TCGA Pan-Cancer Atlas using the R package "TCGA BIOLINKS" and normalized for analysis. Various analytical tools, including receiver operating characteristic (ROC) curves, Kaplan-Meier and Coxregression analyses, and pathway enrichment analysis via the molecular signatures database (MSigDB), were applied. Drug resistance/sensitivity correlations with SPOCD1 expression were explored using the Gene Expression Omnibus (GEO) database. Clinical colorectal cancer (CRC) samples, including both colon and rectal malignant samples, were also evaluated.

Results: The results showed elevated SPOCD1 expression in most cancers (9/12), with notable prognostic value in COAD, HNSC, KICH, and LIHC, and a correlation with poor prognosis in COAD for disease-free survival. ROC curve analysis suggested SPOCD1 as a diagnostic biomarker in the majority of cases (7/12), although this pattern was inconsistent in clinical CRC samples. Pathway enrichment analysis revealed a strong correlation between SPOCD1 expression and critical molecular pathways. Unlike former results, we found that SPOCD1 upregulated when interacting with PD-0325901. However, treating with Panobinostat led to downregulation. Both are as anticancer reagents.

Conclusion: This study confirms the potential of SPOCD1 as a diagnostic and prognostic biomarker in prevalent cancers. However, extensive clinical data, particularly for CRC, are required to validate its reliability. Different COAD subtypes may exhibit varying correlations with SPOCD1 expression levels, underscoring the need for further investigation to fully understand its diagnostic and prognostic value.