Biocell最新文献

{"title":"Machine learning and bioinformatics to identify biomarkers in response to <i>Burkholderia pseudomallei</i> infection in mice","authors":"Yao Fang, Fei Xia, FEIFEI TIAN, Lei Qu, FANG YANG, Juan Fang, ZHENHONG HU, H.T. Liu","doi":"10.32604/biocell.2024.031539","DOIUrl":"https://doi.org/10.32604/biocell.2024.031539","url":null,"abstract":"Objective: In the realm of Class I pathogens, Burkholderia pseudomallei (BP) stands out for its propensity to induce severe pathogenicity. Investigating the intricate interactions between BP and host cells is imperative for comprehending the dynamics of BP infection and discerning biomarkers indicative of the host cell response process. Methods: mRNA extraction from BP-infected mouse macrophages constituted the initial step of our study. Employing gene expression arrays, the extracted RNA underwent conversion into digital signals. The percentile shift method facilitated data processing, with the identification of genes manifesting significant differences accomplished through the application of the t-test. Subsequently, a comprehensive analysis involving Gene Ontology enrichment and Kyoto Encyclopedia of Genes and Genomes pathway was conducted on the differentially expressed genes (DEGs). Leveraging the ESTIMATE algorithm, gene signatures were utilized to compute risk scores for gene expression data. Support vector machine analysis and gene enrichment scores were instrumental in establishing correlations between biomarkers and macrophages, followed by an evaluation of the predictive power of the identified biomarkers. Results: The functional and pathway associations of the DEGs predominantly centered around G protein-coupled receptors. A noteworthy positive correlation emerged between the blue module, consisting of 416 genes, and the StromaScore. FZD4, identified through support vector machine analysis among intersecting genes, indicated a robust interaction with macrophages, suggesting its potential as a robust biomarker. FZD4 exhibited commendable predictive efficacy, with BP infection inducing its expression in both macrophages and mouse lung tissue. Western blotting in macrophages confirmed a significant upregulation of FZD4 expression from 0.5 to 24 h post-infection. In mouse lung tissue, FZD4 manifested higher expression in the cytoplasm of pulmonary epithelial cells in BP-infected lungs than in the control group. Conclusion: These findings underscore the upregulation of FZD4 expression by BP in both macrophages and lung tissue, pointing to its prospective role as a biomarker in the pathogenesis of BP infection.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"48 4","pages":"613-621"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.techscience.com/biocell/online/detail/20164/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147898297","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"miR-30a-5p/PHTF2 axis regulates the tumorigenesis and metastasis of lung adenocarcinoma","authors":"Lijuan Zhang, QINGYIN MENG, Li Zhuang, Quan Gong, XIANDA HUANG, XUEQIN LI, SHIJUAN LI, GUOQIN WANG, Xicai Wang","doi":"10.32604/biocell.2024.047260","DOIUrl":"https://doi.org/10.32604/biocell.2024.047260","url":null,"abstract":"Background: Lung adenocarcinoma is a very pervasive histological form of lung cancers, and inhibiting metastasis is crucial for effective treatment. In this investigation, we explored the functional interaction of miR-30a-5p and the putative transcription factor 2 of the homeodomain (PHTF2) in dictating the aggressiveness and metastasis of lung adenocarcinoma. Method: We collected clinical samples to evaluate the expression patterns of miR-30a-5p and PHTF2 in lung adenocarcinoma along with normal tissues. Cellular experiments including cell count kit (CCK)-8 growth assay, apoptosis analysis, migration and invasion examinations were performed to assess the aggressiveness of lung adenocarcinoma cells. Furthermore, we examined tumorigenesis and metastasis in a nude mouse model. Results: MiR-30a-5p exhibited downregulation pattern in lung adenocarcinoma samples. Transfection of miR-30a-5p mimic in lung adenocarcinoma cells resulted in the suppression of malignant characteristics. Notably, the administration of miR-30a-5p mimic also curbed tumorigenesis and metastasis of lung adenocarcinoma cells in animal model. Moreover, PHTF2 was found to be a molecular target of miR-30a-5p. Upregulating PHTF2 counteracted the tumor-suppressive effect of the miR-30a-5p mimic. Conclusion: miR-30a-5p functions as a tumor-suppressive molecule while PHTF2 acts as an oncogenic factor in the development and metastasis of lung adenocarcinoma. Therefore, targeting miR-30a-5p and PHTF2 could be developed into a promising therapeutic approach for inhibiting metastasis in lung adenocarcinoma.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"48 4","pages":"581-590"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.techscience.com/biocell/online/detail/20094/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147907580","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CircR-ZC3HC1 mediates MiR-384-5p/SIRT1 axis to promote neuronal autophagy and relieves ischemic stroke","authors":"Min Shen, XIAOMAN XU, GUANGLING SUN, L.I.A. Wang, TAO YING, HANG SU, Wei Wang, QINGHUA CAO, ZHEZHE SUN","doi":"10.32604/biocell.2023.047640","DOIUrl":"https://doi.org/10.32604/biocell.2023.047640","url":null,"abstract":"Objective: Circular RNAs (circRNAs) have been shown to involve in pathological processes of ischemic stroke (IS), including autophagy. This study was designed to explore the effect of circR-ZC3HC1 on neuronal autophagy in IS and the related mechanisms. Methods: Expression of circR-ZC3HC1 in blood samples of IS patients and healthy controls was detected. Hippocampal neurons were treated with oxygen and glucose deprivation (OGD) to establish IS in vitro model. The expression of LC3 and p62 and the number of autophagosomes were examined to evaluate the autophagy level of OGD induced neurons using western blotting and transmission electron microscope. Cell apoptosis rate and the expression of cleaved caspase-3, Bax, and Bcl-2 were assessed by flow cytometry and western blotting. The binding relationships among circR-ZC3HC1, miR-384-5p, and SIRT1 were predicted and verified. Results: Low expression of circR-ZC3HC1 was found in blood samples of IS patients and OGD-treated neurons. Overexpressed circR-ZC3HC1 or inhibited miR-384-5p expression promoted autophagy and inhibited apoptosis of OGD-treated neurons, which could be reversed by further 3-MA treatment. Mechanistically, circR-ZC3HC1 targeted miR-384-5p to mediate SIRT1 expression. miR-384-5p overexpression or SIRT1 knockdown in the presence of circR-ZC3HC1 overexpression in OGD-treated neurons lead to reduced autophagy and enhanced apoptosis. Conclusion: Collectively, circR-ZC3HC1 promoted neuronal autophagy to attenuate IS via miR-384-5p/SIRT1 axis.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"48 3","pages":"491-499"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.techscience.com/biocell/online/detail/19895/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147908308","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Overexpression of RUNX1 mitigates dexamethasone-induced impairment of osteogenic differentiation and oxidative stress injury in bone marrow mesenchymal stem cells by promoting alpha-2 macroglobulin transcription","authors":"QINGJIAN HE, HUIXIN ZHU, Shanhong Fang","doi":"10.32604/biocell.2023.045109","DOIUrl":"https://doi.org/10.32604/biocell.2023.045109","url":null,"abstract":"Introduction: Dexamethasone (Dex) caused impaired osteoblast differentiation and oxidative stress (OS) in bone marrow mesenchymal stem cells (BMSCs). This work sought to elucidate the precise molecular pathway through which Dex influences osteogenic differentiation (OD) and OS in BMSCs. Methods: The expression of Runt-related transcription factor 1 (RUNX1) and alpha-2 macroglobulin (A2M) was assessed in Dex-treated BMSCs using qRT-PCR and Western Blot. Following the functional rescue experiments, cell proliferation was determined by MTT assay, reactive oxygen species (ROS) expression by DCFH-DA fluorescent probe, lactate dehydrogenase (LDH), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (Gpx) expression by kits, OD by alkaline phosphatase (ALP) staining and activity quantification, and the expression of OD-related proteins RUNX2, collagen type 1 alpha 1 (COL1A1), and osteocalcin (OCN) by qRT-PCR and Western Blot. The binding of RUNX1 to A2M was initially analyzed through Jaspar website and subsequently verified by dual-luciferase reporter and ChIP assays. Results: Dex-treated BMSCs had low RUNX1 and A2M expression. Dex treatment apparently elevated ROS and LDH levels, diminished cell proliferation rate and SOD, CAT, and Gpx expression, lightened intensity of ALP staining, and declined calcified nodules, ALP activity, and RUNX2, COL1A1, and OCN expression in BMSCs, which was counterweighed by RUNX1 or A2M overexpression. RUNX1 positively targeted A2M. A2M knockdown effectively nullified the ameliorative effects of RUNX1 overexpression on impaired OD and OS injury in Dex-induced BMSCs. Conclusions: Overexpression of RUNX1 attenuated Dex-induced impaired OD and OS injury in BMSCs by promoting A2M transcription.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"48 2","pages":"205-216"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.techscience.com/biocell/online/detail/19914/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147909383","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CARD11 serves as a therapeutic biomarker for the drug therapies of ccRCC","authors":"KAIWEN TIAN, Hanzhong Chen, Qianqian Wang, FENGLIAN JIANG, CHUNXIANG FENG, Li Teng, XIAOYONG PU, YANLIN TANG, JIUMIN LIU","doi":"10.32604/biocell.2024.048737","DOIUrl":"https://doi.org/10.32604/biocell.2024.048737","url":null,"abstract":"Background: The incidence of clear cell renal cell carcinoma (ccRCC) is globally high; however, despite the introduction of innovative drug therapies, there remains a lack of effective biomarkers for evaluating treatment response. Recently, Caspase recruiting domain-containing protein 11 (CARD11) has garnered attention due to its significant association with tumor development and the immune system. Methods: The expression of CARD11 mRNA and protein in ccRCC were analyzed by public database and immunohistochemistry. The focus of this study is on the epigenomic modifications of CARD11, its expression of ccRCC immunophenotype, and its correlation with response to immunotherapy and targeted therapy. Furthermore, to investigate the mechanism of this molecule’s influence on different biological behaviors of cells, cell tests in vitro have been conducted to observe the impact of its expression level. Results: CARD11 expression was upregulated which may be mainly modified by body methylation and was correlated with poor prognosis in ccRCC. In the tumor microenvironment of ccRCC, CARD11 expression was positively correlated with increased T lymphocyte infiltration and increased expression of inhibitory immune checkpoints. Moreover, ccRCC patients with high CARD11 expression had a better response to immunotherapy and targeted therapy. The knockdown of CARD11 ultimately suppressed the proliferation, migration, and invasion capabilities of ccRCC cells while simultaneously enhancing tumor cell apoptosis. Conclusion: We identified CARD11 as a novel therapeutic biomarker for immunotherapy and targeted therapy in ccRCC.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"48 5","pages":"817-834"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.techscience.com/biocell/online/detail/20156/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147912010","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Galectin 2 regulates JAK/STAT3 signaling activity to modulate oral squamous cell carcinoma proliferation and migration <i>in vitro</i>","authors":"XINRU FENG, Luyi Xiao","doi":"10.32604/biocell.2024.048395","DOIUrl":"https://doi.org/10.32604/biocell.2024.048395","url":null,"abstract":"Background: Galectin 2 (LGALS2) is a protein previously reported to serve as a mediator of disease progression in a range of cancers. The function of LGALS2 in oral squamous cell carcinoma (OSCC), however, has yet to be explored, prompting the present study to address this literature gap. Methods: Overall, 144 paired malignant tumor tissues and paracancerous OSCC patient samples were harvested and the LGALS2 expression levels were examined through qPCR and western immunoblotting. The LGALS2 coding sequence was introduced into the pcDNA3.0 vector, to enable the overexpression of this gene, while an LGALS2-specific shRNA and corresponding controls were also obtained. The functionality of LGALS2 as a regulator of the ability of OSCC cells to grow and undergo apoptotic death in vitro was assessed through EdU uptake and CCK-8 assays, and flow cytometer, whereas a Transwell system was used to assess migratory activity and invasivity. An agonist of the Janus Kinase 2 (JAK2)/Signal Transducer and Activator of Transcription 3 (STAT3) pathway was also used to assess the role of this pathway in the context of LGALS2 signaling. Results: Here, we found that lower LGALS2 protein and mRNA expression were evident in OSCC tumor tissue samples, and these expression levels were associated with clinicopathological characteristics and patient survival outcomes. Silencing LGALS2 enhanced proliferation in OSCC cells while rendering these cells better able to resist apoptosis. The opposite was instead observed after LGALS2 was overexpressed. Mechanistically, the ability of LGALS2 to suppress the progression of OSCC was related to its ability to activate the JAK/STAT3 signaling axis. Conclusion: Those results suggest a role for LGALS2 as a suppressor of OSCC progression through its ability to modulate JAK/ STAT3 signaling, supporting the potential utility of LGALS2 as a target for efforts aimed at treating OSCC patients.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"48 5","pages":"793-801"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.techscience.com/biocell/online/detail/20135/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147913705","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of TMEM159 as a biomarker of glioblastoma progression based on immune characteristics","authors":"JI SHI, Ye Zhang, Yi Chen, TANGJUN GUO, Haozhe Piao","doi":"10.32604/biocell.2024.051049","DOIUrl":"https://doi.org/10.32604/biocell.2024.051049","url":null,"abstract":"<b>Background:</b> Glioblastoma multiforme (GBM) is the most general malignancy of the primary central nervous system that is characterized by high aggressiveness and lethality. Transmembrane protein 159 (TMEM159) is an endoplasmic reticulum protein that can form oligomers with seipin. The TMEM159-seipin complex decides the site of lipid droplet (LD) formation, and the formation of LDs is a marker of GBM. However, the role of TMEM159 in the progression of GBM has not been investigated to date. <b>Methods:</b> In this study, we examined the genes that may be associated with patient prognosis in GBM by bioinformatics analyses, and identified the key genes that affect the development of GBM using single-cell RNA sequencing technology. The biological functions of TMEM159 in GBM cells were additionally assessed by clone formation and transwell assays as well as using a model of chick embryo chorioallantois membrane (CAM) and western blotting. The association between TMEM159 and epidermal growth factor receptor (EGFR) was finally analyzed in GBM cells. <b>Results:</b> A prognostic model was established and validated for predicting the prognosis. Survival curve analysis showed a critical difference in the prognosis of the high- and low-risk groups predicted by the prognostic model. The results demonstrated that TMEM159 affected the proliferation and invasion of GBM cells. The chick embryo CAM assays demonstrated that the inhibition of TMEM159 expression reduced angiogenesis in the CAM model. <b>Conclusions:</b> The prognostic model achieved good predictive potential for high-risk patients. The findings also revealed that TMEM159 might be an important prognostic factor for GBM, indicating that the protein may be a promising therapeutic target for suppressing the development of GBM.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"48 8","pages":"1241-1263"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147890889","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cholic acid mitigates osteoarthritis by inhibiting the NF-κB/PERK/SIRT1 signaling pathway","authors":"JIAOE SHENG, ZUMIN YI, SANSHAN HE, QINGCHAO WU, XIA HUANG, GUOQING YAN, YUFANG DAI, LINCHONG SU","doi":"10.32604/biocell.2024.028421","DOIUrl":"https://doi.org/10.32604/biocell.2024.028421","url":null,"abstract":"Introduction: Cholic acid (CA) is a natural steroid useful in treating chronic bronchitis and cholecystitis. On the other hand, its potential impact on osteoarthritis (OA) is unknown. Objective: Using an in vitro and in vivo osteoarthritis model, we sought to assess the chondroprotective properties of CA. Methods: We employed the Cell Counting Kit-8 to measure the impact of CA on chondrocyte activity to assess the toxicity of the cells. Multiple molecular biology experimental techniques were used to investigate potential signaling pathways that CA may use to prevent inflammation and give chondrocytes protection. Furthermore, how CA affects the OA model in Sprague-Dawley (SD) rats was evaluated. Results: CA significantly suppressed the up-regulation of the interleukin-1 β (IL-1β), cyclooxygenase-2 (COX-2), and matrix metalloproteinase 13 (MMP-13) and the downregulation of aggrecan and type II collagen A1 (COL2A) in chondrocytes treated tumor necrosis factor-alpha (TNF-α). Differentially expressed genes (DEG) enrichment revealed IL-17, TNF, chemokine, cytokine-cytokine receptor, toll-like receptor, and nucleotide oligomerization domain-like receptor were the primary signaling pathways. The enriched DEGs included CXCL6, CCL20, MMP3, CXCL3, CXCL11, CCL5, CXCL10, MMP9, MMP13, and CXCL2; these DEGs are involved in inflammatory responses and their expression induced by TNF-α was reversed by CA treatment. CA inhibits p65 nuclear translocation and inhibitory subunit kappa B alpha (IκBα) phosphorylation induced by TNF-α. Furthermore, CA attenuated protein expression of protein kinase RNA-like endoplasmic reticulum kinase (PERK), inositol-requiring transmembrane kinase/endoribonuclease 1α (IRE1α), glucose regulatory protein 78 (GRP78), and sirtuin 1 (SIRT1), and down-regulation of phosphorylation of AMP-activated protein kinase-α (p-AMPKα) in TNF-α-treated chondrocytes. Conclusions: CA significantly ameliorated cartilage degradation in the OA rat model. CA alleviated the inflammatory response through the nuclear factor kappa B/PERK/SIRT1 axis and ameliorated cartilage degradation.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"48 7","pages":"1095-1104"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.techscience.com/biocell/online/detail/20734/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147892059","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sciadopitysin exerts anticancer effects on HepG2 hepatocellular carcinoma cells by regulating reactive oxygen species-mediated signaling pathways","authors":"YAN-NAN LI, Yun-Hong Xiu, YAN-JUN TANG, Jing‐Long Cao, WEN-SHUANG HOU, AN-QI WANG, Tian‐Zhu Li, Cheng‐Hao Jin","doi":"10.32604/biocell.2024.050515","DOIUrl":"https://doi.org/10.32604/biocell.2024.050515","url":null,"abstract":"Objectives: Sciadopitysin (SP) is a flavonoid in Ginkgo biloba that exhibits various pharmacological activities. This study aimed to investigate its antitumor effects and the underlying molecular mechanism of SP in hepatocellular carcinoma (HCC) cells. Methods: Network pharmacology was used for target prediction analysis. Cell Counting Kit-8 (CCK-8) assay was used to test the cell viability. Flow cytometry was used to test the cell cycle distribution, apoptosis status, and reactive oxygen species (ROS) levels. Transwell and wound-healing assay was used to test the migration effect of SP on HepG2 cells. Western Blot assay was used to test the expression levels of proteins. Results: Network pharmacology analysis results showed that the mitogen-activated protein kinase (MAPK) and other signaling pathways are involved in the SP anti-HCC biological process. CCK-8 assay results demonstrated that SP showed an obvious killing effect on three types of HCC cells and low cytotoxic effect on normal cells. Western Blot and flow cytometry results showed that SP regulated MAPK/signal transducer and activator of transcription 3 (STAT3)/nuclear factor kappa-B (NF-κB) signaling pathway to induce mitochondrion-dependent apoptosis in HepG2 cells. Additionally, SP can arrest the G0/G1 phase cell cycle via the protein kinase B (AKT)/p21/p27/cyclin-dependent kinase (CDK)/Cyclin signaling pathway. Wound healing and transwell assays showed that SP inhibited cell motility and invasion through the AKT/glycogen synthase kinase3β (GSK-3β)/vimentin/β-catenin signaling pathway. Conclusion: These findings demonstrated that SP induced mitochondrion-dependent apoptosis, arrested cell cycle in the G0/G1 phase, and inhibited cell migration by regulating the ROS-mediated signaling pathway in HepG2 cells. Thus, SP could serve as a therapeutic agent for the treatment of human HCC.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"48 7","pages":"1055-1069"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.techscience.com/biocell/online/detail/20621/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147900286","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anemarsaponin B mitigates acute pancreatitis damage in mice through apoptosis reduction and MAPK pathway modulation","authors":"Yi Hu, ZHONGYANG REN, ZHENGZHONG ZHAO, YONGJIA HUANG, WANTING HUANG, Jie Liu, LING DING","doi":"10.32604/biocell.2024.049140","DOIUrl":"https://doi.org/10.32604/biocell.2024.049140","url":null,"abstract":"Background: Acute pancreatitis (AP), known for its rapid onset and significant incidence and mortality rates, presents a clinical challenge due to the limited availability of effective treatments and preventive measures. Anemarsaponin B (ASB) has emerged as a potential therapeutic agent, demonstrating capabilities in reducing immune inflammation, positioning it as a promising candidate for AP treatment. Methods: We investigated the effects of ASB on AP in mice, induced by caerulein and lipopolysaccharide (LPS). Peripheral blood samples were collected 24 h post-induction with caerulein to assess of key biomarkers including lipase, amylase, TNF-α, IL-1β, IL-6, SOD, and GSH-Px. A range of techniques such as immunohistochemistry staining, immunofluorescence staining, Western blotting, and quantitative Polymerase Chain Reaction (q-PCR), were employed to measure the expression of critical genes. Additionally, pancreas samples from the mice were harvested for microbiome and metabolome sequencing, with the data analyzed to understand the impact of ASB on AP. Results: Our study revealed that, compared to the sham group, the AP group exhibited significantly higher serum levels of lipase, amylase, and cytokines, while levels of SOD and GSH Px were notably lower. Treatment with ASB led to a substantial decrease in the levels of lipase, amylase, and cytokines, and an increase in SOD and GSH-Px levels. q-PCR analysis of pancreatic histiocytes corroborated these serum findings. Hematoxylin and Eosin (H&E) staining indicated significant alterations in the pathological changes in the pancreas, lungs, and small intestine of the AP model due to ASB. Immunofluorescence assays demonstrated that ASB alleviated the apoptosis of pancreatic histiocytes in the AP model. Western Blot and histological analyses showed that ASB reduced the phosphorylation of TAK, p38, JNK, and ERK proteins, as well as the levels of TRAF6 protein in the AP model. Furthermore, metabolomic and gut microbiota analysis identified 27 differential metabolites and 34 differential species. The combined metabolome and microbiome analysis suggested an association between certain microbes (e.g., unclassified-Saprospiraceae and unclassified-Micavibrionales) and metabolites (e.g., LysoPE (0:0/20:0), PC (DiMe(13,5)/PGJ2)), and Heptanoic acid, indicating potential pathways through which ASB may exert its therapeutic effects in AP. Conclusions: ASB exhibits therapeutic efficacy in treating AP induced by caerulein combined with lipopolysaccharide (LPS), primarily through modulating the mitogen-activated protein kinase (MAPK) signaling pathway. This discovery offers fresh perspectives for AP drug development, underscoring the potential of targeting specific cellular pathways. Additionally, the intricate interplay observed between the gut microbiota and metabolites following ASB treatment highlights novel therapeutic targets, suggesting that manipulating the gut microbiome and metabolome could be a viable strate","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"48 5","pages":"745-758"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.techscience.com/biocell/online/detail/20410/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147903817","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}