Turkish Journal of Biochemistry最新文献_第3页

LncRNA MALAT1 regulates the inflammatory response of dry eye disease via sponging miR-302d LncRNA MALAT1通过海绵化miR-302d调节干眼病的炎症反应

Turkish Journal of Biochemistry Pub Date : 2025-07-10 DOI: 10.1515/tjb-2025-0029

Yuling Bai, Xingshuang Li, Qingjie Gai, Yue Hao, Xilan Chen, Yuhua Du

{"title":"LncRNA MALAT1 regulates the inflammatory response of dry eye disease via sponging miR-302d","authors":"Yuling Bai, Xingshuang Li, Qingjie Gai, Yue Hao, Xilan Chen, Yuhua Du","doi":"10.1515/tjb-2025-0029","DOIUrl":"https://doi.org/10.1515/tjb-2025-0029","url":null,"abstract":"Abstract Objectives Dry eye disease (DED) is a prevalent ocular surface, and its pathogenesis remains inadequately elucidated. This research examined the possible regulatory mechanisms of lncRNA MALAT1 in DED to provide biomarkers for DED treatment. Methods qPCR was employed to assess the expression levels of MALAT1 and miR-302d in DED patients’ serum and HCECs cells. ELISA was utilized to measure the levels of IL-1β, IL-6, IL-8, and IFN-γ in DED patients’ serum and in various cell transfection groups. The effects of different cell transfection groups on the proliferation and apoptosis of HCECs were analyzed using the CCK-8 assay and flow cytometry. Furthermore, potential regulatory pathways were explored through GO and KEGG enrichment analyses of the target genes of miR-302d. Results MALAT1 exhibited a significant up-regulation in DED patients’ serum, while miR-302d was notable down-regulation, with a significant negative correlation between two molecules. MALAT1 was positively correlated with the Ocular Surface Disease Index (OSDI) and Symptom Assessment in Dry Eye (SANDE), suggesting its potential utility in evaluating the severity of DED. MALAT1 inhibited the proliferation of TNF-α-induced HCECs, promoted apoptosis, and enhanced the release of inflammatory factors. However, the suppression of miR-302d mitigated the impact of MALAT1 silencing on the function of HCECs. Enrichment analysis revealed that the target gene of miR-302d played a role in regulating cellular homeostasis and growth in HCECs. Conclusions The sponging effect of MALAT1 on miR-302d caused changes in HCECs cell function, and led to DED. MALAT1 was an important parameter reflecting the severity of DED patients.","PeriodicalId":23344,"journal":{"name":"Turkish Journal of Biochemistry","volume":"50 6","pages":"896-907"},"PeriodicalIF":0.0,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.degruyterbrill.com/document/doi/10.1515/tjb-2025-0029/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147894284","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

To investigate the action mechanism of lncRNA CDKN2B-AS1/hsa-miR-134-5p/CCND1 axis in cervical cancer based on bioinformatics 基于生物信息学研究lncRNA CDKN2B-AS1/hsa-miR-134-5p/CCND1轴在宫颈癌中的作用机制

Turkish Journal of Biochemistry Pub Date : 2025-05-22 DOI: 10.1515/tjb-2024-0320

Weiwei Xiong, M Wang, Xiaohua Wen, X B Wang, Ye Guo, Xingmei Ma, Yanru Liu

{"title":"To investigate the action mechanism of lncRNA CDKN2B-AS1/hsa-miR-134-5p/CCND1 axis in cervical cancer based on bioinformatics","authors":"Weiwei Xiong, M Wang, Xiaohua Wen, X B Wang, Ye Guo, Xingmei Ma, Yanru Liu","doi":"10.1515/tjb-2024-0320","DOIUrl":"https://doi.org/10.1515/tjb-2024-0320","url":null,"abstract":"Abstract Objectives Cervical cancer (CC) is a malignant tumor that poses a serious threat to women’s lives and has a complex pathogenesis. This study aims to investigate the mechanism underlying the lncRNA CDKN2B-AS1 in CC. Methods The expression of CDKN2B-AS1, hsa-miR-134-5p, and CCND1 was detected by RT-qPCR and western blotting, and their targeted regulatory relationships were verified by dual-luciferase reporter assay and overexpression/knockdown assay. CCK-8, Transwell, and Annexin V-FITC/PI staining experiments were used to assess the proliferation, migration, invasion and apoptosis of CC cells (HeLa and SiHa), respectively. The Kaplan-Meier survival curve was used to evaluate the clinical value of CDKN2B-AS1 in CC. Results CDKN2B-AS1, CCND1 were high-expressed, and hsa-miR-134-5p was low-expressed in CC cells and tissues. Silencing CDKN2B-AS1 significantly inhibited the growth and metastasis of HeLa and SiHa cells, and induced their apoptosis. The overall survival time of CC patients with high CDKN2B-AS1 was shorter (log rank p<0.05). Hsa-miR-134-5p mimic attenuated the luciferase activity of cells transfected with wild-type CDKN2B/CCND1 luciferase vector. Overexpression of CDKN2B-AS1 decreased the intracellular level of hsa-miR-134-5p, while its knockdown was inverse. The inhibition of hsa-miR-134-5p promoted CCND1 expression. Conclusions High CDKN2B-AS1 level predicted a poor prognosis of CC patients, and it promoted CC development by down-regulating hsa-miR-134-5p to enhance CCND1 expression.","PeriodicalId":23344,"journal":{"name":"Turkish Journal of Biochemistry","volume":"50 6","pages":"835-843"},"PeriodicalIF":0.0,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.degruyterbrill.com/document/doi/10.1515/tjb-2024-0320/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147897782","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

miR-199a-5p inhibits proliferation and migration of burn-denatured fibroblasts by targeting VEGFA in burn patients miR-199a-5p通过靶向烧伤患者的VEGFA抑制烧伤变性成纤维细胞的增殖和迁移

Turkish Journal of Biochemistry Pub Date : 2025-05-02 DOI: 10.1515/tjb-2025-0014

Qinghua Wu, Wenna Li

{"title":"miR-199a-5p inhibits proliferation and migration of burn-denatured fibroblasts by targeting VEGFA in burn patients","authors":"Qinghua Wu, Wenna Li","doi":"10.1515/tjb-2025-0014","DOIUrl":"https://doi.org/10.1515/tjb-2025-0014","url":null,"abstract":"Abstract Objectives The skin altered by burn injury has the capacity to revert to its normal function and structure. Nonetheless, the exact mechanism behind this restoration remains unclear. This study was to examine the function of miR-199a-5p in the migration and proliferation of fibroblasts affected by burn injury. Methods The miR-199a-5p expression was assessed using quantitative real-time polymerase chain reaction (qRT-PCR). The proliferation and migration capacity of human skin fibroblast (HSF) cells were measured by CCK-8 and Transwell assay. The protein levels of vascular endothelial growth factor A (VEGFA), phosphorylated phosphoinositide 3-kinases (p-PI3K), phosphorylated protein kinase B (p-AKT), and phosphorylated endothelial nitric oxide synthase (p-eNOS) were assessed via western blot assay. Results The miR-199a-5p levels were decreased in individuals with burn injuries as well as in burn-denatured HSF cells, at the same time, there was an increase in the VEGFA mRNA levels. miR-199a-5p negatively regulated VEGFA, which in turn suppressed the migration and proliferation of HSF cells. Additionally, miR-199a-5p inhibited the PI3K/AKT/eNOS signaling pathway through the regulation of VEGFA. Conclusions miR-199a-5p regulates proliferation and migration of burn degenerated fibroblasts by targeting VEGFA.","PeriodicalId":23344,"journal":{"name":"Turkish Journal of Biochemistry","volume":"50 5","pages":"724-730"},"PeriodicalIF":0.0,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.degruyterbrill.com/document/doi/10.1515/tjb-2025-0014/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147903872","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Notoginsenoside R1 inhibits Ang II-induced VSMCs migration by upregulating Sirt1 expression 三七皂苷R1通过上调Sirt1表达抑制Ang ii诱导的VSMCs迁移

Turkish Journal of Biochemistry Pub Date : 2025-04-29 DOI: 10.1515/tjb-2024-0278

Pinghong Ming, Yongwu Xia, Yunhong Liu, Rong Zhu, Litao Pan, Ting Cai

{"title":"Notoginsenoside R1 inhibits Ang II-induced VSMCs migration by upregulating Sirt1 expression","authors":"Pinghong Ming, Yongwu Xia, Yunhong Liu, Rong Zhu, Litao Pan, Ting Cai","doi":"10.1515/tjb-2024-0278","DOIUrl":"https://doi.org/10.1515/tjb-2024-0278","url":null,"abstract":"Abstract Objectives To investigate whether Notoginsenoside R1 (NGR1) inhibits angiotensin II (Ang II)-induced vascular smooth muscle cells (VSMCs) migration and to elucidate the underlying mechanisms. Methods VSMCs migration model were established using 1 μM Ang II treatment. Subsequently, the migration VSMCs were treated with varying concentrations of NGR1 (0, 10, 20, and 40 μM), respectively. A scratch wound assay was performed to assess the migration area of VSMCs, and western blotting assay was used to evaluate the levels of matrix metalloproteinases (MMP-2, MMP-9), p38 MAPK, phosphorylated p38 MAPK, and silent information regulator 1 (Sirt1) proteins. Results NGR1 inhibited Ang II-induced VSMCs migration, downregulated migration-related proteins MMP-2, MMP-9, and p38 MAPK phosphorylation, while upregulating Sirt1 in a dose-dependent manner. Furthermore, upregulation Sirt1 effectively inhibited Ang II-induced VSMCs migration and reduced p38 MAPK phosphorylation proteins expression. Notably, upregulation Sirt1 also further enhanced the inhibitory effects of NGR1 on VSMCs migration and decreased MMP-2, MMP-9, and p38 MAPK phosphorylation proteins expression. Conversely, Sirt1 silencing attenuated these effects. Conclusions NGR1 inhibits Ang II-induced migration of VSMCs by upregulating Sirt1, which suppresses p38 MAPK phosphorylation, MMP-2 and MMP-9 levels. These findings suggest that NGR1 may serve as a potential therapeutic agent for atherosclerosis.","PeriodicalId":23344,"journal":{"name":"Turkish Journal of Biochemistry","volume":"50 4","pages":"512-519"},"PeriodicalIF":0.0,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.degruyterbrill.com/document/doi/10.1515/tjb-2024-0278/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147879503","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Comprehensive analysis of KRT15 in pan-cancer and verification in lung adenocarcinoma KRT15在泛癌中的综合分析及在肺腺癌中的验证

Turkish Journal of Biochemistry Pub Date : 2025-03-05 DOI: 10.1515/tjb-2024-0076

Hong-Zhu Tao, Rong Li, Fang Yu, Linjie Luo, Shengwen Liu, Qilin Zhao, Bo-Jiang Chen, Jin Zhu

{"title":"Comprehensive analysis of KRT15 in pan-cancer and verification in lung adenocarcinoma","authors":"Hong-Zhu Tao, Rong Li, Fang Yu, Linjie Luo, Shengwen Liu, Qilin Zhao, Bo-Jiang Chen, Jin Zhu","doi":"10.1515/tjb-2024-0076","DOIUrl":"https://doi.org/10.1515/tjb-2024-0076","url":null,"abstract":"Abstract Objectives Evidence from previous documents points to the involvement of the keratin 15 (KRT15) gene in the modulation of signaling networks governing cancer cell death, survival, proliferation, migration, invasion, and metastasis. Nonetheless, its relevance in pan-cancer studies and the precise molecular mechanisms involved in lung cancer remain poorly understood. To comprehensively investigate the clinical relevance of the KRT15 gene in human lung cancer and a diverse array of cancers. Methods A comprehensive investigation of the clinical relevance of the KRT15 gene in a diverse array of human tumors was conducted. In light of this, the study also examined the possible link between the KRT15 gene and tumor immunogenic features. Based on the outcomes of pan-cancer analysis, we selected lung adenocarcinoma (LUAD) as the specific tumor type for an in-depth investigation into KRT15-induced signaling pathways and intercellular communications contributing to tumor progression. Results According to our study, KRT15 may hold significance as a newly identified biomarker, potentially contributing to both prognostic evaluation and immunotherapeutic targeting across various cancer types. Significantly, KRT15 was hypothesized to function as a guiding marker gene, holding potential for clinical prognostication and personalized tumor-specific therapies in LUAD. Suppression of KRT15 significantly impaired lung cancer cells’ growth, migration, invasion, and survival. Conclusions KRT15 possesses the potential to be an innovative biomarker and therapeutic target, playing a role in predicting the prognosis and treatment response of LUAD patients.","PeriodicalId":23344,"journal":{"name":"Turkish Journal of Biochemistry","volume":"50 2","pages":"256-270"},"PeriodicalIF":0.0,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.degruyter.com/document/doi/10.1515/tjb-2024-0076/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147902709","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The promotive role of reticulocalbin 3 (RCN3) in the pathogenesis of keloid via TGFβ1/Smad2/Smad7 signaling pathway in vitro 网状定位蛋白3 （RCN3）在体外通过tgf - β1/Smad2/Smad7信号通路促进瘢痕疙瘩发病中的作用

Turkish Journal of Biochemistry Pub Date : 2024-12-02 DOI: 10.1515/tjb-2024-0093

H. Wang, Zhen Zhang, Jie Mi, Zhaojun Liu, Z H Liu, Haiyan Wu

{"title":"The promotive role of reticulocalbin 3 (RCN3) in the pathogenesis of keloid <i>via</i> TGFβ1/Smad2/Smad7 signaling pathway <i>in vitro</i>","authors":"H. Wang, Zhen Zhang, Jie Mi, Zhaojun Liu, Z H Liu, Haiyan Wu","doi":"10.1515/tjb-2024-0093","DOIUrl":"https://doi.org/10.1515/tjb-2024-0093","url":null,"abstract":"Abstract Objectives Keloids, characterized by an excessive accumulation of fibrous tissue, remain a significant dermatological challenge. This study elucidates the role of Reticulocalbin 3 (RCN3) in modulating keloid fibroblasts (KFs) in vitro . Methods The RCN3 expression levels in human KFs and normal dermal fibroblast cells were examined using RT-qPCR and Western blot methods. RCN3 expression was knocked down in keloid fibroblasts after cells were transfected with shRNA targeting RCN3. On the other hand, recombinant RCN3 was added to treat the cells. RT-qPCR, Western blot, flow cytometry, CCK8 assays, and wound healing assays were performed to analyze the fibrotic markers (collagen I, III, MMP2, α-SMA) and TGFβ1/Smad2/6/7 pathway, apoptosis, proliferation and migration. Results RCN3 was upregulated in KFs. Its knockdown reduced fibrotic marker expression (collagen I, III, MMP2, α-SMA), cell proliferation, and migration, while increasing apoptosis. Conversely, recombinant RCN3 treatment enhanced the fibrotic responses. Changes in TGFβ1/Smad2 pathway, especially in Smad2 phosphorylation and Smad7, were evident following RCN3 modulation. Conclusions The study reveals RCN3 as a regulator in keloid pathology, affecting fibrosis, cellular behavior through TGFβ1/Smad2/Smad7 signaling.","PeriodicalId":23344,"journal":{"name":"Turkish Journal of Biochemistry","volume":"50 2","pages":"190-197"},"PeriodicalIF":0.0,"publicationDate":"2024-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.degruyterbrill.com/document/doi/10.1515/tjb-2024-0093/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147904083","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Ethanol inhibited growth hormone receptor-mediated endocytosis in primary mouse hepatocytes 乙醇抑制小鼠原代肝细胞生长激素受体介导的内吞作用

Turkish Journal of Biochemistry Pub Date : 2024-11-14 DOI: 10.1515/tjb-2024-0128

Zihan Ge, Xingjie Liu, Yang Yu, Hainan Lan, Yawen Zhang, Wei Zhang, Li Xian, Ruonan Li

{"title":"Ethanol inhibited growth hormone receptor-mediated endocytosis in primary mouse hepatocytes","authors":"Zihan Ge, Xingjie Liu, Yang Yu, Hainan Lan, Yawen Zhang, Wei Zhang, Li Xian, Ruonan Li","doi":"10.1515/tjb-2024-0128","DOIUrl":"https://doi.org/10.1515/tjb-2024-0128","url":null,"abstract":"Abstract Objectives Growth hormone (GH) exhibits various essential physiological functions, which are exerted by its binding to growth hormone receptor (GHR). Ethanol has been demonstrated to have an impact on GH’s biological activity. Nevertheless, mechanism underlying the regulation of the biological activity of GH by ethanol have yet to be fully elucidated. Methods This study utilized an indirect immunofluorescence assay to identify GHR expression in mouse hepatocytes. Western blot was used to determine the impact of ethanol on GH-induced intracellular signalling. Indirect immunofluorescence and colocalization experiments were used to determine the effect of ethanol on GH-GHR’s nuclear localization and endocytosis. Results GHR was primarily localized in the cell membrane and cytoplasm. The phosphorylation levels of JAK2 and STAT1/3/5 were markedly lowered after treatment with ethanol. On this basis, we further explored the mechanism underlying the regulation of GH biological activity by ethanol from the perspective of cell internalization. We found that the nuclear translocation of GH-GHR was inhibited when treated with ethanol. In addition, the results of colocalization analyses revealed that ethanol inhibited GHR-mediated nuclear translocation may mainly by inhibiting caveolin-dependent endocytosis. Conclusions Our study showed that ethanol inhibits GH signaling ability in a time-dependent manner. Ethanol could inhibit the nuclear localization of GH-GHR, which may be linked to the inhibition of the interaction between GHR and caveolin. The combined effect of these factors downregulated the GH-GHR signal. This study laid a foundation for further exploring the mechanism that the effects of ethanol on GH biological activity.","PeriodicalId":23344,"journal":{"name":"Turkish Journal of Biochemistry","volume":"50 1","pages":"126-133"},"PeriodicalIF":0.0,"publicationDate":"2024-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.degruyterbrill.com/document/doi/10.1515/tjb-2024-0128/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147892610","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The diagnostic value of serum exosomal miRNA-587 combined with hypersensitive C-reactive protein as noninvasive biomarker in early-stage non-small cell lung cancer 血清外泌体miRNA-587联合超敏c反应蛋白作为无创生物标志物对早期非小细胞肺癌的诊断价值

Turkish Journal of Biochemistry Pub Date : 2024-09-23 DOI: 10.1515/tjb-2023-0281

Jiefei Peng, Xianfen Ma, Luolin Shao, Zhigang Xin, Zhijun Zhang

{"title":"The diagnostic value of serum exosomal miRNA-587 combined with hypersensitive C-reactive protein as noninvasive biomarker in early-stage non-small cell lung cancer","authors":"Jiefei Peng, Xianfen Ma, Luolin Shao, Zhigang Xin, Zhijun Zhang","doi":"10.1515/tjb-2023-0281","DOIUrl":"https://doi.org/10.1515/tjb-2023-0281","url":null,"abstract":"Abstract Objectives Lung cancer is a highly prevalent and life-threatening disease worldwide, with non-small cell lung cancer (NSLC) accounting for around 80 % of all cases. Exosomes contain important genetic information for humans that could be employed, especially for early screening of tumors. Accordingly, we aimed to use exosomal miRNA (ex-miRNA) in early NSCLC diagnosis. Methods The extracted ex-miRNAs were validated through transmission electron microscopy, particle size potentiometer, and western blot analyses. Microarray was used to verify ex-miRNAs, and 20 miRNAs were selected. Herein, we obtained 240 blood samples from NSCLC patients (101 in the early stage) and 234 from healthy donors. Our study deployed real-time fluorescence quantitative PCR (qRT-PCR) for detecting significantly down-regulated miR-587 expression. In addition, the hypersensitive C-reactive protein (Hs-CRP) levels were measured in patient samples. Results The results of calculating the area under the curve (AUC) revealed that the diagnostic efficiency of miR-587 and Hs-CRP were 0.771 and 0.863, respectively. Meanwhile, the combined diagnostic efficiency of both increased to 0.901. In patients with early NSCLC, the diagnostic efficiency of miR-587, Hs-CRP, and combined AUC were 0.726, 0.873, and 0.899, respectively. This indicates that the accuracy of early NSCLC diagnosis is very high. Finally, we combined miR-587 and Hs-CRP with CEA and NSE for NSCLC (AUC=0.956) and early-stage patients (AUC=0.921). Conclusions In this study, miR-587 and Hs-CRP have significant diagnostic efficiency for NSCLC, especially the combination of CEA and NSE that could indicate early NSCLC diagnosis.","PeriodicalId":23344,"journal":{"name":"Turkish Journal of Biochemistry","volume":"49 5","pages":"674-684"},"PeriodicalIF":0.0,"publicationDate":"2024-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.degruyterbrill.com/document/doi/10.1515/tjb-2023-0281/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147886235","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Isoquercitrin attenuates neuroinflammation in LPS-stimulated BV2 microglia cells via p38MAPK/NF-κB pathway 异槲皮苷通过p38MAPK/NF-κB通路减轻lps刺激的BV2小胶质细胞的神经炎症

Turkish Journal of Biochemistry Pub Date : 2024-08-01 DOI: 10.1515/tjb-2023-0108

Shiyi Chang, Yan Chang, Jiajia Wang, Xuelian Huang

{"title":"Isoquercitrin attenuates neuroinflammation in LPS-stimulated BV2 microglia cells via p38MAPK/NF-κB pathway","authors":"Shiyi Chang, Yan Chang, Jiajia Wang, Xuelian Huang","doi":"10.1515/tjb-2023-0108","DOIUrl":"https://doi.org/10.1515/tjb-2023-0108","url":null,"abstract":"Abstract Objectives Microglia mediated neuronal inflammation has been reported to be responsible for neurodegenerative disease. Isoquercitrin (IQC), widely found in fruits, vegetables and foods, has high bioavailability and offers many benefits of humans. Although IQC has been shown to possess pleiotropic biological activities, but its anti-inflammatory mechanism in microglia at molecular level remains largely unclear. Therefore, this study aimed to investigate IQC’s inhibition on inflammation within BV2 microglia cells induced by lipopolysaccharide (LPS) and the underlying mechanism. Methods The cell viability was tested by using the MTT assay and the NO production was measured by Griess reagent. Inflammatory cytokines expression was determined by RT-qPCR and the expression of iNOS、COX2 and correlation factor of NF-κB and MAPK pathway were determined by RT-qPCR and western blotting. Results IQC does not affect the viability of LPS-stimulated microglia. IQC treatment inhibited LPS-triggered NO and PGE2 production, iNOS and COX2 expression and affected the mRNA levels of relative inflammatory cytokines. Moreover, IQC inhibited nuclear factor kappa B(NF-κB) and MAPK pathway activation mediated by LPS, thereby inhibiting the levels of inflammatory cytokines. Conclusions IQC exhibited remarkable anti-inflammatory effects and promised therapeutic potential for neural inflammation associated diseases.","PeriodicalId":23344,"journal":{"name":"Turkish Journal of Biochemistry","volume":"49 4","pages":"525-532"},"PeriodicalIF":0.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.degruyter.com/document/doi/10.1515/tjb-2023-0108/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147891864","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

CXCL12/CXCR4 as a potential axis in diagnosis and predicting disease severity in COVID-19 patients: a new perspective CXCL12/CXCR4作为诊断和预测COVID-19患者疾病严重程度的潜在轴心：一个新视角

Turkish Journal of Biochemistry Pub Date : 2024-07-22 DOI: 10.1515/tjb-2023-0193

Alev Lazoğlu Ozkaya, Esra Laloğlu, Albulhakim Hasan Gul, N. Çelik

{"title":"CXCL12/CXCR4 as a potential axis in diagnosis and predicting disease severity in COVID-19 patients: a new perspective","authors":"Alev Lazoğlu Ozkaya, Esra Laloğlu, Albulhakim Hasan Gul, N. Çelik","doi":"10.1515/tjb-2023-0193","DOIUrl":"https://doi.org/10.1515/tjb-2023-0193","url":null,"abstract":"\u0000 \u0000 \u0000 Coronavirus disease 2019 (COVID-19) exhibits variations in terms of patients’ clinical symptoms and levels of routinely employed biochemical markers. The aim of the current study was to determine the correlation between serum levels of the C-X-C chemokine ligand type 12 (CXCL12) and C-X-C chemokine receptor type 4 (CXCR4), one of its specific receptors, and disease severity in COVID-19 patients.\u0000 \u0000 \u0000 \u0000 Sixty-nine patients were diagnosed with COVID-19 from February to July 2021, and a healthy control group of 39 individuals were enrolled in the study. Patients were divided into subgroups: mild-moderate and severe. Serum CXCL12 and CXCR4 levels were measured using the enzyme-linked immunosorbent assay method.\u0000 \u0000 \u0000 \u0000 CXCL12 and CXCR4 concentrations were both significantly higher in the clinically severe disease group compared to the mild-moderate disease group (p<0.05 in both groups). CXCL12 and CXCR4 levels were also significantly higher in the patients with clinically mild-moderate disease compared to the control group (p<0.001 and p<0.05, respectively). Both CXCL12 and CXCR4 levels were correlated with clinical severity. Serum CXCL12 and CXCR4 levels were significantly positively correlated. Assuming a cut-off value of 1.44 ng/mL, serum CXCL12 levels showed 98 % sensitivity and 84 % specificity to distinguish between COVID-19 patients and healthy individuals (AUC=0.98, p<0.001, 95 % CI=0.95–1.0). Serum CXCR4 levels distinguished individuals with COVID-19 from healthy controls with 88 % sensitivity and 72 % specificity at a cut-off value of 69.7 pg/mL (AUC=0.82, p<0.001, 95 % CI=0.74–0.9).\u0000 \u0000 \u0000 \u0000 Serum CXCL12 and CXCR4 levels may be included among the biomarkers used to differentiate patients with COVID-19 and determine the clinical severity of the disease.\u0000","PeriodicalId":23344,"journal":{"name":"Turkish Journal of Biochemistry","volume":"28 10","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141816835","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0