General physiology and biophysics最新文献

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The effect of 12 week-maximum fat oxidation intensity (FATmax) exercise on microvascular function in obese patients with nonalcoholic fatty liver disease and its mechanism. 12周最大脂肪氧化强度(FATmax)运动对肥胖非酒精性脂肪肝患者微血管功能的影响及其机制
IF 1.5 4区 生物学
General physiology and biophysics Pub Date : 2023-05-01 DOI: 10.4149/gpb_2023004
Ruiqi Yang, Li Wan, Huan Zhu, Yong Peng
{"title":"The effect of 12 week-maximum fat oxidation intensity (FATmax) exercise on microvascular function in obese patients with nonalcoholic fatty liver disease and its mechanism.","authors":"Ruiqi Yang,&nbsp;Li Wan,&nbsp;Huan Zhu,&nbsp;Yong Peng","doi":"10.4149/gpb_2023004","DOIUrl":"https://doi.org/10.4149/gpb_2023004","url":null,"abstract":"<p><p>Fifty-four obese patients with non-alcoholic fatty liver disease (NAFLD) were selected for this study were randomly divided into an exercise group (16 men and 11 women, mean age 21.3 ± 1.0) and control group (16 men and 11 women, mean age 21.8 ± 0.8). The exercise group underwent a 12-week FATmax exercise intervention, while the control group did not engage in any type of systematic physical activity. The controlled diet was given to both groups. After the test, the microvascular reactivity of the exercise group was significantly higher than that of the control group (p < 0.05). After the experiment, the concentration of malondialdehyde (MDA), the activity of catalase (CAT) and the activity of exercise group were significantly lower than those of the control group (p < 0.05); and in contrast the activities of total superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) were significantly higher than those of the control group (p< 0.05). The change in microcirculation function caused by 12-week FATmax intensity exercise may have an interaction mechanism with oxidative stress and antioxidant system function, and may improve the microvascular reactivity of obese NAFLD patients. In addition, also may improve of oxidative stress and antioxidant system functions.</p>","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"42 3","pages":"251-262"},"PeriodicalIF":1.5,"publicationDate":"2023-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9352004","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}
引用次数: 1
The protective effects of glutamine against bronchopulmonary dysplasia are associated with MKP-1/MAPK/cPLA2 signalingmediated NF-kappaB pathway. 谷氨酰胺对支气管肺发育不良的保护作用与MKP-1/MAPK/cPLA2信号介导的NF-kappaB通路有关。
IF 1.5 4区 生物学
General physiology and biophysics Pub Date : 2023-05-01 DOI: 10.4149/gpb_2023006
Chouhui Xuan, Can Jin, Zhengyong Jin, Yongxue Chi
{"title":"The protective effects of glutamine against bronchopulmonary dysplasia are associated with MKP-1/MAPK/cPLA2 signalingmediated NF-kappaB pathway.","authors":"Chouhui Xuan,&nbsp;Can Jin,&nbsp;Zhengyong Jin,&nbsp;Yongxue Chi","doi":"10.4149/gpb_2023006","DOIUrl":"https://doi.org/10.4149/gpb_2023006","url":null,"abstract":"<p><p>Glutamine is proven to have potential therapeutic effects on decreasing hyperoxia-induced acute pulmonary injury. The aim of this study is to investigate the effects and mechanism of glutamine on bronchopulmonary dysplasia (BPD) induced by hyperoxia in rat alveolar type II epithelial cells (AECIIs) RLE-6TN. Following hyperoxia induction and glutamine treatment, ROS levels were detected by DCFH-DA assay and TUNEL staining was performed to detect cell apoptosis. The levels of inflammatory indicators and expression of apoptosis-related proteins were detected through ELISA and Western blot, respectively. Besides, the expression of related proteins in mitogen-activated protein kinase phosphatase-1 (MKP-1)/mitogen-activated protein kinases (MAPK)/cytoplasmic phospholipase A2 (cPLA2) signaling was also detected by Western blot. To further analyze the role of MKP-1/MAPK/cPLA2 signaling, MKP-1 was silenced and anisomycin was used to treat cells, respectively. It was shown that glutamine significantly decreased inflammation, oxidative stress and apoptosis in hyperoxia-induced cells while MKP-1 interference and anisomycin were able to reverse these effects, suggesting that the protective effects of glutamine on BPD induced by hypoxia were related to MKP-1/MAPK/cPLA2 signaling. To sum up, glutamine protected against BPD by decreasing inflammation, oxidative stress and apoptosis via MKP-1/MAPK/cPLA2 signaling.</p>","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"42 3","pages":"229-239"},"PeriodicalIF":1.5,"publicationDate":"2023-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9356781","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}
引用次数: 0
Hypoxic cardiomyocyte-derived exosomes regulate cardiac fibroblast activation, apoptosis, migration and ferroptosis through miR-208a/b. 缺氧心肌细胞来源的外泌体通过miR-208a/b调控心肌成纤维细胞活化、凋亡、迁移和铁下垂。
IF 1.5 4区 生物学
General physiology and biophysics Pub Date : 2023-03-01 DOI: 10.4149/gpb_2022061
Ying Guo, Zi-Dong Bie, Xi Li
{"title":"Hypoxic cardiomyocyte-derived exosomes regulate cardiac fibroblast activation, apoptosis, migration and ferroptosis through miR-208a/b.","authors":"Ying Guo,&nbsp;Zi-Dong Bie,&nbsp;Xi Li","doi":"10.4149/gpb_2022061","DOIUrl":"https://doi.org/10.4149/gpb_2022061","url":null,"abstract":"<p><p>Studies have found that cardiomyocytes and cardiac fibroblasts (CFs) can communicate through exosomes, thereby affecting each other's biological functions, but there are few studies on the mechanism. miR-208a/b are specifically expressed in the heart and highly expressed in exosomes derived from various myocardial diseases. Hypoxia induced cardiomyocytes to secrete exosomes (H-Exo) with high expression of miR-208a/b. When H-Exo were added to CFs for co-culture, it was found that CFs took up exosomes, thereby upregulating the expression of miR-208a/b. H-Exo significantly promoted the viability and migration of CFs, enhanced the expression of α-SMA, collagen I and III, and promoted the secretion of collagen I and III. miR-208a or/and miR-208b inhibitors significantly attenuated the effects of H-Exo on CF biological functions. miR-208a/b inhibitors significantly enhanced the levels of apoptosis and caspase-3 activity in CFs, while H-Exo significantly attenuated the pro-apoptotic effects of miR-208a/b inhibitors. Further treatment of CFs with ferroptosis inducer Erastin found that H-Exo further enhanced the accumulation of ROS, MDA and Fe2+, the main indicators of ferroptosis, and inhibited the expression of GPX4, a key regulator of ferroptosis. miR-208a or/and miR-208b inhibitors significantly attenuated the effects of Erastin and H-Exo on ferroptosis. In conclusion, hypoxic cardiomyocyte-derived exosomes can regulate the biological functions of CFs through highly expressed miR-208a/b.</p>","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"42 2","pages":"149-158"},"PeriodicalIF":1.5,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9256564","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}
引用次数: 1
Bioinformatic analysis and validation of cardiac hypertrophy-related genes. 心脏肥大相关基因的生物信息学分析和验证。
IF 1.5 4区 生物学
General physiology and biophysics Pub Date : 2023-03-01 DOI: 10.4149/gpb_2022059
Ai Meng, Siang Wei, Lihuan Yan, Yao Xiao, Zhiwen Ding, Yan Feng
{"title":"Bioinformatic analysis and validation of cardiac hypertrophy-related genes.","authors":"Ai Meng,&nbsp;Siang Wei,&nbsp;Lihuan Yan,&nbsp;Yao Xiao,&nbsp;Zhiwen Ding,&nbsp;Yan Feng","doi":"10.4149/gpb_2022059","DOIUrl":"https://doi.org/10.4149/gpb_2022059","url":null,"abstract":"<p><p>In this study, we have screened genes involved in myocardial hypertrophy (MH) using a mice model for compensatory stress overload (transverse aortic constriction, TAC) and bioinformatics. Microarrays were downloaded, and according to the Venn diagram, three groups of data intersections were obtained. Gene function was analyzed by Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG), whereas protein-protein interactions (PPI) were analyzed using the STRING database. A mouse aortic arch ligation model was established to verify and screen the expression of hub genes. A total of 53 (DEGs) and 32 PPI genes were screened out. GO analysis showed DEGs mainly involved in cytokine and peptide inhibitor activity. KEGG analysis focused on ECM receptor interaction and osteoclast differentiation. Expedia co-expression gene network analysis showed that Serpina3n, Cdkn1a, Fos, Col5a2, Fn1 and Timp1 participated in the occurrence and development of MH. RT-qPCR verified that all the other 9 hub genes except Lox were highly expressed in TAC mice. This study lays a foundation for further study on the molecular mechanism of MH and for screening of molecular markers.</p>","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"42 2","pages":"159-167"},"PeriodicalIF":1.5,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9089299","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}
引用次数: 0
The role of NOS3 (rs2070744) and GNB3 (rs5443) genes' polymorphisms in endothelial dysfunction pathway and carotid intima-media thickness in hypertensive patients. NOS3 (rs2070744)和GNB3 (rs5443)基因多态性在高血压患者内皮功能障碍通路和颈动脉内膜-中膜厚度中的作用
IF 1.5 4区 生物学
General physiology and biophysics Pub Date : 2023-03-01 DOI: 10.4149/gpb_2022060
Andrii Sydorchuk, Larysa Sydorchuk, Adelina Gutnitska, Valentina Vasyuk, Oleksii Tkachuk, Valentina Dzhuryak, Yuriy Myshkovskii, Petro Kyfiak, Ruslan Sydorchuk, Oksana Iftoda
{"title":"The role of NOS3 (rs2070744) and GNB3 (rs5443) genes' polymorphisms in endothelial dysfunction pathway and carotid intima-media thickness in hypertensive patients.","authors":"Andrii Sydorchuk,&nbsp;Larysa Sydorchuk,&nbsp;Adelina Gutnitska,&nbsp;Valentina Vasyuk,&nbsp;Oleksii Tkachuk,&nbsp;Valentina Dzhuryak,&nbsp;Yuriy Myshkovskii,&nbsp;Petro Kyfiak,&nbsp;Ruslan Sydorchuk,&nbsp;Oksana Iftoda","doi":"10.4149/gpb_2022060","DOIUrl":"https://doi.org/10.4149/gpb_2022060","url":null,"abstract":"<p><p>The mechanisms orchestrating the balance between nitric oxide and endothelium-derived contracting factors, and genetic predisposition to endothelial dysfunction in hypertensive patients remain to be determined. One-hundred hypertensive patients participated in the case-control study to clarify the risk of endothelial dysfunction and carotid \"intima media\" thickness (IMT) changes depending on NOS3 (rs2070744) and GNB3 (rs5443) genes' polymorphisms. It is found that presence of NOS3 gene's С-allele significantly elevates the risk of atherosclerotic plaques on carotid arteries (OR95%CI: 1.24-11.20; р = 0.019) and the probability of low NOS3 gene expression (OR95%CI: 17.72-520.0; р < 0.001). Homozygous carriage of С-allele of GNB3 gene is protective and corresponds to the lowest chances of the carotid IMT increase, atherosclerotic plaques formation and sVCAM-1 elevation (OR = 0.10-0.34; OR95%CI: 0.03-0.95; р ≤ 0.035-0.001). Vice versa, Т-allele of GNB3 gene significantly augments the risk of the carotid IMT increase (OR95%CI: 1.09-7.74; р = 0.027) including development of atherosclerotic plaques, associating GNB3 (rs5443) with cardiovascular pathology.</p>","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"42 2","pages":"179-190"},"PeriodicalIF":1.5,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9089301","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}
引用次数: 1
Protective effects of NF-κB inhibitor and continuous perfusion of pulmonary arteries on pulmonary injury in piglet models of deep hypothermia low flow. NF-κB抑制剂和肺动脉持续灌注对仔猪深低温低流量肺损伤的保护作用。
IF 1.5 4区 生物学
General physiology and biophysics Pub Date : 2023-03-01 DOI: 10.4149/gpb_2022058
Yewei Xie, Rufang Zhang, Jia Li
{"title":"Protective effects of NF-κB inhibitor and continuous perfusion of pulmonary arteries on pulmonary injury in piglet models of deep hypothermia low flow.","authors":"Yewei Xie,&nbsp;Rufang Zhang,&nbsp;Jia Li","doi":"10.4149/gpb_2022058","DOIUrl":"https://doi.org/10.4149/gpb_2022058","url":null,"abstract":"<p><p>Deep hypothermia with low flow perfusion (DHLF) is a common cardiopulmonary bypass (CPB) technique. The associated lung ischemia/reperfusion injury is a major cause of postoperative morbidity and mortality in patients undergoing DHLP; we aimed to investigate the effects of nuclear factor-κB (NF-κB) inhibitor pyrrolidine dithiocarbamate (PDTC) with continuous perfusion of pulmonary arteries (CPP) on DHLF-induced lung injury and the related molecular mechanisms. Twenty-four piglets were randomly divided into the DHLF (control), CPP (with DHLF), or CPP+PDTC (intravenous PDTC before CPP with DHLF) groups. Lung injury was evaluated by respiratory function measurement, lung immunohistochemistry, and serum levels of TNF, IL-8, IL-6, and NF-κB before CPB, at CPB completion, and at 1 h post-CPB. Western blot was used to detect NF-κB protein expression in lung tissues. After CPB, decreased parcial pressure of oxygen (PaO2) and increased parcial pressure of carbon dioxide (PaCO2) and serum levels of TNF, IL-8, IL-6, and NF-κB were observed in the DHLF group. Both CPP and CPP+PDTC groups showed better indices of lung function, decreased levels of TNF, IL-8, and IL-6, and less severe pulmonary edemas and injuries. PDTC with CPP further improved pulmonary function and mitigated pulmonary injury than did CPP alone. PDTC with CPP better attenuates DHLF-induced lung injury than does CPP alone.</p>","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"42 2","pages":"169-177"},"PeriodicalIF":1.5,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9152582","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}
引用次数: 0
Stress, depression, and hippocampus: from biochemistry to electrophysiology. 压力、抑郁和海马体:从生物化学到电生理学。
IF 1.5 4区 生物学
General physiology and biophysics Pub Date : 2023-03-01 DOI: 10.4149/gpb_2023001
Alzbeta Idunkova, Lubica Lacinova, Lucia Dubiel-Hoppanova
{"title":"Stress, depression, and hippocampus: from biochemistry to electrophysiology.","authors":"Alzbeta Idunkova,&nbsp;Lubica Lacinova,&nbsp;Lucia Dubiel-Hoppanova","doi":"10.4149/gpb_2023001","DOIUrl":"https://doi.org/10.4149/gpb_2023001","url":null,"abstract":"<p><p>Major depressive disorder is a very common serious mental illness with increasing prevalence in the population. Its pathology includes biochemical, morphological, and electrophysiological changes in various brain areas. In spite of decades of extensive research pathophysiology of depression is still not sufficiently understood. When depression occurs just before or during pregnancy, it may have a detrimental effect on perinatal and/or postnatal brain development, affecting the offspring's behavior. An important role in the pathology of depression is the hippocampus as a center for cognition and memory. Here we review changes in morphology, biochemical, and electrical signaling caused by depression in first and second generation identified in various animal models.</p>","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"42 2","pages":"107-122"},"PeriodicalIF":1.5,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9089302","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}
引用次数: 2
Silencing of long non-coding RNA SOX2-overlapping transcript relieves myocardial ischemia/reperfusion injury through up-regulating miRNA-146a-5p. 长链非编码RNA sox2重叠转录物的沉默通过上调miRNA-146a-5p减轻心肌缺血/再灌注损伤。
IF 1.5 4区 生物学
General physiology and biophysics Pub Date : 2023-03-01 DOI: 10.4149/gpb_2022065
Zhongxin Li, Guangdong Liu, Hua Huang
{"title":"Silencing of long non-coding RNA SOX2-overlapping transcript relieves myocardial ischemia/reperfusion injury through up-regulating miRNA-146a-5p.","authors":"Zhongxin Li,&nbsp;Guangdong Liu,&nbsp;Hua Huang","doi":"10.4149/gpb_2022065","DOIUrl":"https://doi.org/10.4149/gpb_2022065","url":null,"abstract":"<p><p>Long non-coding RNAs (lncRNAs) are involved in the development of myocardial ischemia/reperfusion injury (MIRI). In this study, we aimed to explore the regulatory effect and mechanism of lncRNA SOX2-overlapping transcript (SOX2-OT) in MIRI. The viability of oxygen and glucose deprivation/reperfusion (OGD/R)-treated H9c2 cells was detected by MTT assay. The levels of interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, malondialdehyde (MDA), and superoxide dismutase (SOD) were measured by ELISA. The target relationship between SOX2-OT and miR-146a-5p was predicted by LncBase, and subsequently confirmed by Dual luciferase reporter assay. The effects of SOX2-OT silencing on myocardial apoptosis and function were further validated in MIRI rats. The expression of SOX2-OT was increased in OGD/R-treated H9c2 cells and myocardial tissues of MIRI rats. Silencing of SOX2-OT increased the viability and inhibited the inflammation and oxidative stress of OGD/R-treated H9c2 cells. SOX2-OT negatively regulated its target miR-146a-5p. Silencing of miR-146a-5p reversed the effects of sh-SOX2-OT on OGD/R-treated H9c2 cells. In addition, silencing of SOX2-OT also alleviated myocardial apoptosis and improved myocardial function in MIRI rats. Silencing of SOX2-OT relieved the apoptosis, inflammation, and oxidative stress of myocardial cells via up-regulating miR-146a-5p, contributing to the remission of MIRI.</p>","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"42 2","pages":"191-199"},"PeriodicalIF":1.5,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9089303","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}
引用次数: 4
Construction of a novel lncRNA-miRNA-mRNA competing endogenous RNA network in muscle in response to exercise training. 运动训练后肌肉中lncRNA-miRNA-mRNA竞争内源性RNA网络的构建
IF 1.5 4区 生物学
General physiology and biophysics Pub Date : 2023-03-01 DOI: 10.4149/gpb_2022062
Mingkun Nie, Qingling Liu, Cheng Yan
{"title":"Construction of a novel lncRNA-miRNA-mRNA competing endogenous RNA network in muscle in response to exercise training.","authors":"Mingkun Nie,&nbsp;Qingling Liu,&nbsp;Cheng Yan","doi":"10.4149/gpb_2022062","DOIUrl":"https://doi.org/10.4149/gpb_2022062","url":null,"abstract":"<p><p>Physical inactivity has evidently been a hazard factor for many diseases, including cardiovascular disease, diabetes, cancer, etc. Rising evidence indicates that RNA, as competitive endogenous RNA (ceRNA), plays an important role in adaptive changes in skeletal muscle in response to exercise training. Although the effects of exercise-induced fitness on skeletal muscle have been well established, the mechanisms underlying are not fully understood. The purpose of this study is to construct a novel ceRNA network in skeletal muscle in response to exercise training. Skeletal muscle gene expression profiles were downloaded from the GEO database. Then, we identified differentially expressed lncRNAs, miRNAs, and mRNAs between the pre-exercise and post-exercise samples. Subsequently, we constructed lncRNA-miRNA-mRNA regulatory networks based on the ceRNA theory. 1153 mRNAs (687 upregulated and 466 downregulated), 7 miRNAs (3 upregulated and 4 downregulated), and 5 lncRNAs (3 upregulated and 2 downregulated) were identified as differentially expressed genes. 3 lncRNAs, 5 miRNAs and 227 mRNAs were obtained to build miRNA-mediated ceRNA networks. We constructed a novel ceRNA regulatory network in muscle in response to exercise training, which provides insights into molecular mechanisms underlying the health benefits brought by physical activity.</p>","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"42 2","pages":"123-133"},"PeriodicalIF":1.5,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9089300","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}
引用次数: 0
Ivabradine curbs isoproterenol-induced kidney fibrosis. 伊伐布雷定抑制异丙肾上腺素诱导的肾纤维化。
IF 1.5 4区 生物学
General physiology and biophysics Pub Date : 2023-03-01 DOI: 10.4149/gpb_2022057
Tomas Baka, Peter Stanko, Kristina Repova, Silvia Aziriova, Kristina Krajcirovicova, Andrej Barta, Stefan Zorad, Fedor Simko
{"title":"Ivabradine curbs isoproterenol-induced kidney fibrosis.","authors":"Tomas Baka,&nbsp;Peter Stanko,&nbsp;Kristina Repova,&nbsp;Silvia Aziriova,&nbsp;Kristina Krajcirovicova,&nbsp;Andrej Barta,&nbsp;Stefan Zorad,&nbsp;Fedor Simko","doi":"10.4149/gpb_2022057","DOIUrl":"https://doi.org/10.4149/gpb_2022057","url":null,"abstract":"<p><p>This study investigated whether chronic isoproterenol administration could induce kidney alterations and whether ivabradine, a heart rate (HR)-reducing substance exerting cardiovascular protection, is able to attenuate potential kidney damage. Twenty-eight Wistar rats were divided into non-diseased controls, rats treated with ivabradine, rats treated with isoproterenol, and rats treated with isoproterenol plus ivabradine. Six weeks of isoproterenol administration was associated with decreased systolic blood pressure (SBP) (by 25%) and glomerular, tubulointerstitial and vascular/perivascular fibrosis due to enhanced type I collagen volume (7-, 8-, and 4-fold, respectively). Ivabradine reduced HR (by 15%), partly prevented SBP decline (by 10%) and site-specifically mitigated kidney fibrosis by decreasing type I collagen volume in all three sites investigated (by 69, 58, and 67%, respectively) and the ratio of type I collagen-to-type III collagen in glomerular and vascular/perivascular sites (by 79 and 73%, respectively). We conclude that ivabradine exerts protection against kidney remodelling in isoproterenol-induced kidney damage.</p>","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"42 2","pages":"209-215"},"PeriodicalIF":1.5,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9458852","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}
引用次数: 0
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