Çiğdem Gökçek-Saraç, Tuğçe Şimşek, Serdar Karakurt
{"title":"Cytoprotective effects of low-frequency pulsed electromagnetic field against oxidative stress in glioblastoma cells.","authors":"Çiğdem Gökçek-Saraç, Tuğçe Şimşek, Serdar Karakurt","doi":"10.4149/gpb_2022056","DOIUrl":"https://doi.org/10.4149/gpb_2022056","url":null,"abstract":"<p><p>The low-frequency pulsed electromagnetic field (PEMF) may have possible cytoprotective effects against the destructive effects of oxidative stress. The goal was to investigate if shortterm low-frequency PEMF has cytoprotective effects in glioblastoma cell line following high-dose hydrogen peroxide (H2O2) treatment. U87-MG cells were divided into four groups: Sham-control group; PEMF group (cells exposed to PEMF); H2O2 group (cells treated with H2O2 at time intervals 30 min and 48 h, respectively); H2O2+PEMF group (cells exposed to PEMF after H2O2 treatment at time intervals 30 min and 48 h, respectively). The cell viability, levels of reactive oxygen species, glutathione peroxidase activity, and the amount of glutathione were measured. The cytoprotective effect of PEMF against deleterious effects of oxidative stress triggered by different time interval of H2O2 treatment might be mediated by the increase in the cell viability, the elevation in the antioxidant enzyme activity/amount, and the decrease in the reactive oxygen species level. In addition, the cytoprotective effect of PEMF varies depending on different time intervals of H2O2 treatment. In the light of these findings, further in vivo and/or in vitro studies on neurophysiological effects of PEMFs and their underlying molecular mechanisms are needed to elucidate neurotoxic or neuroprotective role against antioxidant defense mechanisms.</p>","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10632238","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Effect on hypoxia/reoxygenation-induced cardiomyocyte injury and Pink1/Parkin pathway.","authors":"Xiyang Lu, Guangwei Huang, Hailong Bao, Zonggang Duan, Chao Li, Muzhi Lin, Haiyan Zhou, Zhenhua Luo, Wei Li","doi":"10.4149/gpb_2022045","DOIUrl":"https://doi.org/10.4149/gpb_2022045","url":null,"abstract":"<p><p>Our study aimed to detect the effects of proprotein convertase subtilisin/kexin type 9 (PCSK9) on exacerbating cardiomyocyte hypoxia/reoxygenation (H/R) injury and the possible mechanism. A cell model of H/R was constructed. PCSK9 mRNA and protein levels were significantly upregulated during AC16 cardiomyocyte H/R. Flowmetry detection of apoptosis, as well as JC-1, confirmed that PCSK9 upregulation of autophagy levels was accompanied by apoptosis. Furthermore, in the H/R+si-PCSK9 group, the expression of autophagy-related protein LC3 decreased and P62 increased. At the same time, the presentation of the autophagic pathway Pink1/Parkin was also downregulated. In conclusion, in AC16 cardiomyocytes treated with H/R, PCSK9 expression and autophagy levels were increased; a possible molecular mechanism was the activation of the Pink1/Parkin pathway.</p>","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10632239","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Zdenka Gasparova, Euridika Ruskova, Dominika Seckarova Michalikova, Zuzana Brnoliakova, Karol Svik, Lukas Slovak, Stefan Bezek, Vladimir Knezl, Ruzena Sotnikova
{"title":"High-fructose intake-induced dyslipidemia and oxidative stress accompanied by hippocampal dysfunctions in hypertensive but not hypertriacylglycerolemic rats.","authors":"Zdenka Gasparova, Euridika Ruskova, Dominika Seckarova Michalikova, Zuzana Brnoliakova, Karol Svik, Lukas Slovak, Stefan Bezek, Vladimir Knezl, Ruzena Sotnikova","doi":"10.4149/gpb_2022053","DOIUrl":"https://doi.org/10.4149/gpb_2022053","url":null,"abstract":"<p><p>A high-fructose intake is metabolically analogous to a high-fat diet. The impact of highfructose intake was investigated in spontaneously hypertensive (SHR) and hypertriacylglycerolemic (HTG) rats to find out the impact of which risk factor of metabolic syndrome - hypertension or hypertriacylglycerolemia - will cause more complications. Rats were fed a standard or a fructose diet (F60) with 60% of added fructose for 5 weeks. The F60 diet increased the total serum cholesterol content of both HTG-F60 and SHR-F60 rats. Further, in SHR-F60 it increased serum triacylglycerols, TBARS in the liver, a specific activity of NAGA in the kidney, aggravated glucose tolerance, deteriorated synaptic plasticity, and reduced somatic and dendritic responses in the hippocampus. SHR rats were more sensitive to the F60 diet, suggesting that hypertension along with a high-fructose intake result in a more pronounced disorder compared to hypertriacylglycerolemia. This work wants to draw attention to fructose-induced health risks associated with hypertension.</p>","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10639612","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Teng Ma, Changliang Peng, Dongjin Wu, Song Yang, Li Ji, Zhang Cheng, Chunzheng Gao
{"title":"Immune-based prognostic biomarkers associated with metastasis of osteosarcoma.","authors":"Teng Ma, Changliang Peng, Dongjin Wu, Song Yang, Li Ji, Zhang Cheng, Chunzheng Gao","doi":"10.4149/gpb_2022050","DOIUrl":"https://doi.org/10.4149/gpb_2022050","url":null,"abstract":"<p><p>This study aimed to identify immune-based prognostic biomarkers associated with metastasis of osteosarcoma. Based on the GEO and TCGA databases, 437 differentially expressed genes were screened between primary and metastatic osteosarcoma. Weighted gene co-expression network analysis (WGCNA) revealed 496 genes in turquoise module which had the highest correlation with osteosarcoma metastasis. Within these two group genes, 122 common genes involved in osteosarcoma metastasis were identified. These genes were enriched in chemokine activity, chemokine receptor binding, TNF signaling pathway, etc. Survival analysis revealed 8 prognostic genes (ANK3, EGR1, FBP1, FOS, KIFC3, MAOB, ISLR and MFAP4) from the 122 genes. RT-qPCR showed that all of these eight genes were differentially expressed between 143B and MNNG/HOS Cl cells. Various infiltrating immune cells showed significant differences between primary and metastatic osteosarcoma. Expression of all the 8 prognostic genes was correlated with infiltration abundance of multiple immune cells, such as follicular helper T cells, activated dendritic cells. In addition, 10 microRNAs and 7 transcription factors that targeted these prognostic genes were predicted. In conclusion, 8 immune-based prognostic genes associated with osteosarcoma metastasis were identified.</p>","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10640049","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Milan Grofik, Michal Cibulka, Jana Oleksakova, Stefan Sivak, Daniel Cierny, Zuzana Tatarkova, Marian Grendar, Vladimir Nosal, Robert Ruzinak, Egon Kurca, Martin Kolisek
{"title":"Oxidative stress parameters and their relation to motor subtype of Parkinson's disease and levodopa treatment status.","authors":"Milan Grofik, Michal Cibulka, Jana Oleksakova, Stefan Sivak, Daniel Cierny, Zuzana Tatarkova, Marian Grendar, Vladimir Nosal, Robert Ruzinak, Egon Kurca, Martin Kolisek","doi":"10.4149/gpb_2022051","DOIUrl":"https://doi.org/10.4149/gpb_2022051","url":null,"abstract":"<p><p>Parkinson's disease (PD) is an oxidative stress-linked neurodegenerative disorder, with the highest prevalence among seniors. The objective of this study were: (1) to analyse levels of following oxidative stress parameters: total antioxidant capacity (TAC), uric acid (UA), total glutathione (tGSH), bilirubin (Bil) and albumin (Alb), in blood of PD patients and healthy controls; (2) to find possible associations of examined oxidative stress parameters with PD subtypes and levodopa treatment status; and (3) to evaluate power and relevance of the aforementioned oxidative stress parameter for the prediction of onset and progression of PD by utilizing Random Forest machine learning (RFML). Oxidative stress parameters were determined in 125 PD patients and 55 healthy controls. Evaluated with frequentist statistics, our data revealed that UA is the only oxidative stress parameter associated with PD. However, when the PD cohort was divided in gender-dependent manner, tGSH and Bil were also significantly associated with PD in subgroup of female patients. RFML rendered no predictive power of any of the tested oxidative stress parameters in respect to PD, its subtypes, and/or status of levodopa treatment. In conclusion, despite the positive association of UA with PD (in complete cohort of PD patients) and of tGSH and Bil with PD but only in female patients, these oxidative stress parameters are of no use in clinical practice due to the lack of the predictive/diagnostic power.</p>","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10640052","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Oleksandr Ivankov, Dina R Badreeva, Elena V Ermakova, Tomáš Kondela, Tatiana N Murugova, Norbert Kučerka
{"title":"Anionic lipids modulate little the reorganization effect of amyloid-beta peptides on membranes.","authors":"Oleksandr Ivankov, Dina R Badreeva, Elena V Ermakova, Tomáš Kondela, Tatiana N Murugova, Norbert Kučerka","doi":"10.4149/gpb_2022052","DOIUrl":"https://doi.org/10.4149/gpb_2022052","url":null,"abstract":"<p><p>Amyloid-β peptide interactions with model lipid membranes have been studied by means of small angle neutron scattering and molecular dynamics simulations. These interactions had been indicated recently as an origin of the membrane structure reorganizations between spherical small unilamellar vesicles and planar bicelle-like structures. In present work, we investigate the influence of charge on the peptide-triggered morphological changes by introducing the anionic lipid DMPS to the underlying DMPC membrane. Changes to the membrane thickness and the overall membrane structure with and without Aβ25-35 incorporated have been investigated over a wide range of temperatures. Our results document the previously reported morphological reformations between bicelle-like structures present in gel phase and small unilamellar vesicles present in fluid phase to be independent from the charge existence in the system.</p>","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10640051","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Xiao-Hui Liu, Yi-Ming Yang, Ming-Ming Zhang, Hao-Yu Fu
{"title":"Five glycosylation-related gene signatures predict the prognostic risks of lung adenocarcinoma","authors":"Xiao-Hui Liu, Yi-Ming Yang, Ming-Ming Zhang, Hao-Yu Fu","doi":"10.4149/gpb_2023025","DOIUrl":"https://doi.org/10.4149/gpb_2023025","url":null,"abstract":"This study aimed to identify glycosylation-related genes associated with lung adenocarcinoma (LUAD) prognosis through comprehensive bioinformatic analysis. Glycosylation-related genes were identified from the Human Gene Nomenclature Committee, and LUAD prognostic genes were screened from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO)-GSE68465 datasets. Glycosylation risk score (GLRS) was calculated to predict LUAD prognostic risk. Samples were grouped into GLRS-high and GLRS-low and compared. The Tumor Immune Dysfunction and Exclusion (TIDE) score was computed to assess the antitumor immune escape possibility after immunotherapy. From 213 glycosylation-related genes, five gene signatures served as prognostic LUAD predictors using univariate and stepwise Cox regression analyses. GLRS-based models were constructed using TCGA and GSE68465 samples; their sensitivity and specificity in predicting LUAD prognosis were confirmed. GLRS was an independent LUAD prognostic factor and contributed to the nomogram to predict patient survival. High GLRS was associated with advanced tumor stage and higher mutation frequencies, estimate scores, and TIDE scores. GLRS-high and GLRS-low patients differed in immune cell infiltration and epithelial-mesenchymal transition (EMT)-related gene expression. Thus, we propose five glycosylation-related gene signatures to predict overall survival and prognostic risks of LUAD. Their regulatory roles may be related to immune invasion, immunotherapy response, mutation, and EMT.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135704112","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Polydatin inhibited TNF-α-induced apoptosis of skeletal muscle cells through AKT-mediated p38 MAPK and NF-κB pathways","authors":"Yongli Liu, Fang Xie, Changhuai Lu, Zongbo Zhou, Shudong Li, Jia Zhong, Qian Li, Xianfang Shao","doi":"10.4149/gpb_2023027","DOIUrl":"https://doi.org/10.4149/gpb_2023027","url":null,"abstract":"Skeletal muscle atrophy severely impacts one's quality of life. The effects and mechanism of polydatin on skeletal muscle atrophy are unclear. This study investigated the effects and mechanism of polydatin on TNF-α-induced skeletal muscle cells. The skeletal muscle cell atrophy model was established by inducing C2C12 cells with TNF-α. Cell viability, IL-1β levels and cell apoptosis were assessed. The mRNA and protein expression levels of apoptosis-related proteins were measured. Meanwhile, the binding of polydatin to AKT was analyzed by molecular docking. TNF-α reduced cell fusion and viability while up-regulated IL-1β level and promoted cell apoptosis. TNF-α activated AKT, NF-κB, and p38 MAPK signaling pathways. Polydatin reversed these effects induced by TNF-α, with a low concentration being more effective. Polydatin was predicted to bind to GLY162, PHE161, GLU198, THR195 and GLU191 sites of AKT protein through van der Waals force and conventional hydrogen bonds. Overexpression of AKT led to increased phosphorylation levels of AKT, p38, and p65 proteins, as well as IL-1β levels and cell apoptosis. Polydatin inhibited TNF-α-induced apoptosis of C2C12 cells by regulating NF-κB and p38 MAPK signaling pathways through AKT. This suggests that polydatin shows promise as a new drug for the treatment of skeletal muscle atrophy.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135667601","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The effects of the pulsed magnetic field on sepsis-induced liver tissue injury in rats","authors":"Fikret Gevrek, Serkan Yelliand, Serkan Gürgül","doi":"10.4149/gpb_2023026","DOIUrl":"https://doi.org/10.4149/gpb_2023026","url":null,"abstract":"Sepsis is the host's response to infection and can lead to severe and life-threatening cases. We aimed to investigate the effects of pulsed magnetic field (PMF) on septic liver tissue injury. A total of 28 adult Wistar albino rats were divided equally into four study groups: Sham, PMF-1, PMF-2, and Sepsis, with seven rats in each. Sepsis was performed using the CLP method. PMF-1 and PMF-2 were exposed to 7.5 Hz and 15 Hz PMF, respectively, for 24 hours. After having their livers removed, liver tissues were analysed using histological techniques. We observed remarkable healing in PMF groups. Apoptotic cells decreased in the PMF-treated groups compared with the Sepsis group (p < 0.05). Immune expressions of Acas-3, Bax, and HIF-1 increased in the Sepsis group, while Bcl-2 expression decreased (p < 0.05). The results imply that PMF application has anti-apoptotic, antiinflammatory, and therapeutic effects on septic liver tissue injury.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135667657","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Effects of novel mRNA-VEGF@USPIO nanoparticles on human brain microvascular endothelial cell injury","authors":"Jiang Zhao, Zhiyuan Qian","doi":"10.4149/gpb_2023032","DOIUrl":"https://doi.org/10.4149/gpb_2023032","url":null,"abstract":"We investigated the effect of mRNA-VEGF@ultrasmall superparamagnetic iron oxide (USPIO) nanoparticles on the repair of human brain microvascular endothelial cell (HBMECs) injury and its related mechanisms. mRNA-VEGF@USPIO nanoparticles were designed, prepared, and characterized using NTA and UV spectrophotometry. Cell viability was determined using the CCK-8. Cells in the control, TNF-α, and mRNA-VEGF@USPIO groups were sequenced and the differentially expressed genes (DEGs) were identified. Finally, a functional analysis of the DEGs was performed. Both NTA and spectrophotometry results indicated that mRNA-VEGF@USPIO was successfully constructed. TNF-α significantly reduced cell viability and promoted apoptosis compared with the control group (p < 0.05), whereas mRNA-VEGF@USPIO nanoparticles reversed the changes caused by TNF-α. Via sequencing, 9063 DEGs were identified between the control and TNF-α groups, 9125 DEGs were identified between the control and mRNA-VEGF@USPIO groups, and 211 DEGs were identified between the TNF-α and mRNA-VEGF@USPIO groups. Additionally, 71 overlapping DEGs were identified in the three groups using Venn diagrams. These overlapping DEGs were mainly enriched in cytokine-cytokine receptor interactions and the TNF signaling pathway, NF-κB signaling pathway, and NOD-like receptor signaling pathway. This study shows that mRNA-VEGF@USPIO nanoparticles can repair HBMECs injury.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135703840","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}