Biomolecules & biomedicine最新文献

{"title":"Piperine inhibits the proliferation of colorectal adenocarcinoma by regulating <i>ARL3-</i>mediated endoplasmic reticulum stress.","authors":"Chenqu Wu, Yanqing Qian, Jun Jiang, Deming Li, Li Feng","doi":"10.17305/bb.2024.10525","DOIUrl":"10.17305/bb.2024.10525","url":null,"abstract":"<p><p>Colorectal adenocarcinoma (COAD) is a significant cause of cancer-related mortality worldwide, necessitating the identification of novel therapeutic targets and treatments. This research aimed to investigate the role of ARL3 in COAD progression and to explore the effects of Piperine on ARL3 expression, cell proliferation, epithelial-mesenchymal transition (EMT), and endoplasmic reticulum (ER) stress. Bioinformatics analysis of The Cancer Genome Atlas (TCGA)-COAD, GSE39582, and GSE44861 datasets assessed ARL3 expression levels. Immunohistochemical data from the Human Protein Atlas (HPA) database confirmed ARL3 overexpression in COAD. The association of ARL3 with COAD clinical parameters and prognosis was also examined. COAD cells were treated with Piperine, and in vitro assays evaluated cell proliferation, apoptosis, EMT marker expression, and ER stress (ERS) responses. ARL3 overexpression in COAD correlated with poor prognosis and varied across pathological stages. Piperine treatment inhibited COAD cell proliferation in a concentration- and time-dependent manner, as indicated by reduced Ki-67 levels and decreased colony-forming ability. Piperine induced S-phase cell cycle arrest and facilitated apoptosis in COAD cells, evidenced by changes in Bax, Bcl-2, cleaved caspase-3, and cleaved Poly (ADP-ribose) polymerase (PARP) levels. Moreover, Piperine downregulated ARL3 expression in COAD cells, thereby suppressing transforming growth factor beta (TGF-β)-induced EMT. Additionally, Piperine attenuated the ARL3-mediated ER stress response, significantly reducing binding immunoglobulin protein (BiP), inositol-requiring enzyme 1 alpha (p-IRE1α), activating transcription factor 6 (ATF6), and C/EBP homologous protein (CHOP) levels. Piperine exerts anti-cancer effects in COAD by modulating ARL3 expression, disrupting cell cycle progression, inhibiting the EMT pathway, and regulating ERS. These findings suggest that Piperine holds promise as a therapeutic agent for COAD through its targeting of ARL3.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"391-405"},"PeriodicalIF":0.0,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11734826/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141556117","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}

{"title":"lncRNA CASC7 contributes to the progression of LPS-induced liver injury by targeting miRNA-217/TLR4 axis.","authors":"Chengqin Sun, Yan Chen, Zhonge Chen, He Wang, Weiwen Yang, Xiaoqian Zhou","doi":"10.17305/bb.2024.10543","DOIUrl":"10.17305/bb.2024.10543","url":null,"abstract":"<p><p>It has been reported that long non-coding RNAs (lncRNAs) are involved in sepsis-induced liver injury, while the role of cancer susceptibility candidate 7 (CASC7) in liver injury induced by sepsis remains elusive. In our study, 62 patients and 55 healthy controls were enrolled from our hospital, from whom CASC7 and microRNA-217 (miR-217) in serum samples were detected by quantitative real-time PCR (qRT-PCR). Then the sepsis-induced liver injury mice model was established by lipopolysaccharide (LPS). The effect of CASC7 on liver injury induced by sepsis was confirmed by hematoxylin and eosin (HE) staining, ELISA assay, TUNEL assay, Annexin V-FITC apoptosis assay and cell counting kit-8 (CCK-8) assay, respectively. Besides, RNA pull-down, luciferase reporter gene assay, qRT-PCR, and western blot were used to evaluate the underlying mechanisms. In this study, lncRNA CASC7 was significantly increased while miR-217 was significantly decreased in patients with sepsis-induced liver injury compared with that in healthy controls. There was a negative association of CASC7 and miR-217 in serum samples from patients with sepsis-induced liver injury and healthy controls. CASC7 was upregulated in a time-dependent manner in liver tissues of LPS-treated mice. It was found that knockdown of CASC7 reduced the liver injury induced by LPS in mice. In vitro, LPS treatment enhanced cell apoptosis, while knockdown of CASC7 inhibited the role of LPS in cell apoptosis. Moreover, knockdown of CASC7 suppressed the LPS-enhanced tumor necrosis factor alpha (TNF-α) and interleukin 1 beta (IL-1β) expression. In addition, miR-217 was found to be a target of CASC7, and miR-217 mimic could reverse CASC7-promoted liver injury. Furthermore, toll-like receptor 4 (TLR4) was identified as the target of miR-217, and both CASC7 and miR-217 could downregulate the mRNA and protein level of TLR4. Additionally, TLR4 overexpression could reverse miR-217-inhibited or CASC7-promoted liver injury. Taken together, CASC7 contributes to the progression of LPS-induced liver injury via the miR-217/TLR4 axis.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"493-504"},"PeriodicalIF":0.0,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11734829/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141790184","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}

{"title":"Inhibition of RUNX1 slows the progression of pulmonary hypertension by targeting CBX5.","authors":"Ximiao Ma, Yiqiu Cao, Dongpeng Yang, Zhu Dong, Xiaowu Wang","doi":"10.17305/bb.2024.10720","DOIUrl":"10.17305/bb.2024.10720","url":null,"abstract":"<p><p>Pulmonary artery smooth muscle cell (PASMC) dysfunction is the central pathogenic mechanism in pulmonary hypertension (PH). This study explored the mechanism of action of RUNX1, a potential therapeutic target for PH, in PASMCs. A PH mouse model was used to investigate the impacts of RUNX1 knockdown on hemodynamics, right ventricular hypertrophy (RVH), and pulmonary artery remodeling (hematoxylin-eosin [H&E] staining). Isolated PASMCs were transfected with RUNX1- or chromobox 5 (CBX5)-related vectors and then subjected to cell function assays. Immunoprecipitation was used to detect molecular binding and ubiquitination. RUNX1 knockdown reduced right ventricular systolic pressure (RVSP), RVH, and pulmonary artery remodeling in mice with PH. Knockdown of RUNX1 or CBX5 suppressed proliferation, invasion, and migration and stimulated apoptosis in PASMCs under hypoxia. RUNX1 enhanced ubiquitin-specific protease 15 (USP15) promoter activity. USP15 bound to CBX5 and reduced CBX5 ubiquitination, thereby promoting CBX5 expression. CBX5 overexpression promoted the proliferation and movement of hypoxic PASMCs with reduced RUNX1 expression and decreased their apoptosis. In conclusion, RUNX1 knockdown inhibits USP15 transcription to promote the ubiquitination and degradation of CBX5, thereby alleviating PH in mice and reducing hypoxia-induced PASMC dysfunction.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"472-481"},"PeriodicalIF":0.0,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11734815/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141992509","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}

{"title":"Molecular characterization and genotype of multi-drug resistant <i>Staphylococcus epidermidis</i> in nasal carriage of young population, Mahasarakham, Thailand.","authors":"Peechanika Chopjitt, Panita Tangthong, Jiranuch Kongkaem, Pritprapoan Wonkyai, Achira Charoenwattanamaneechai, Surasak Khankhum, Phitcharat Sunthamala, Anusak Kerdsin, Nuchsupha Sunthamala","doi":"10.17305/bb.2024.11116","DOIUrl":"10.17305/bb.2024.11116","url":null,"abstract":"<p><p>Staphylococcus epidermidis, a coagulase-negative staphylococcus, is a prevalent skin commensal that has increasingly been recognized as a significant pathogen, particularly in hospital environments, where it is associated with device-related infections. The emergence of multi-drug resistance and its ability to form biofilms complicate the clinical management of infections caused by this organism, posing a growing public health concern. This study aimed to investigate the nasal carriage of S. epidermidis among healthy young individuals and to analyze its antibiotic resistance patterns, resistance genes, and biofilm formation capabilities. Nasal swabs were collected from 40 undergraduate students at Mahasarakham University, Thailand, aged between 20 and 22 years. A total of 38 isolates were confirmed as S. epidermidis through both phenotypic and molecular characterization. Antibiotic susceptibility testing demonstrated resistance to various classes of antimicrobials, including beta-lactams, macrolides, and tetracyclines. Notably, five isolates exhibited methicillin resistance S. epidermidis (MRSE). Resistance genes, such as mecA, ermA, tetM, tetL, and tetK, were identified across the isolates, contributing to the observed resistance profiles. Biofilm formation assays revealed that most isolates displayed weak to moderate biofilm formation, with only one isolate demonstrating strong biofilm-forming capacity. Genetic analysis indicated a significant correlation between biofilm formation and the presence of the icaA gene, which is crucial for biofilm production. This study suggests the necessity for ongoing surveillance of nasal carriage of S. epidermidis to enhance understanding of its role in the dissemination of antimicrobial resistance and biofilm-associated infections, particularly within healthcare settings.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"461-471"},"PeriodicalIF":0.0,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11734814/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142402178","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}

{"title":"Diagnostic accuracy of two-dimensional shear wave elastography and point shear wave elastography in identifying different stages of liver fibrosis in patients with metabolic dysfunction-associated steatotic liver disease: A meta-analysis.","authors":"Xiangyi Xu, Yiqing Zhang, Qiwei Zhu, Yuchen Xie, Yuanyuan Zhou, Bingtian Dong, Chaoxue Zhang","doi":"10.17305/bb.2024.11577","DOIUrl":"https://doi.org/10.17305/bb.2024.11577","url":null,"abstract":"<p><p>To assess the diagnostic accuracy of two-dimensional shear wave elastography (2-D SWE) and point shear wave elastography (pSWE) in detecting liver fibrosis stages in patients with metabolic dysfunction-associated steatotic liver disease (MASLD), a comprehensive search was conducted across four databases up to February 9, 2024. A bivariate random-effects model was used to analyze the diagnostic accuracy of the methods. After screening, 13 studies involving pSWE included 1527 patients, while nine studies involving 2-D SWE included 1088 patients. The areas under the summary receiver operating characteristic (SROC) curves for diagnosing significant fibrosis (F ≥ 2), advanced fibrosis (F ≥ 3), and cirrhosis (F = 4) using pSWE and 2-D SWE were as follows: 0.84 (95% CI 0.80-0.87), 0.91 (95% CI 0.88-0.93), and 0.94 (95% CI 0.91-0.95) for pSWE; 0.83 (95% CI 0.79-0.86), 0.85 (95% CI 0.82-0.88), and 0.89 (95% CI 0.86-0.91) for 2-D SWE, respectively. The pooled sensitivity for pSWE and 2-D SWE for stages F ≥ 2, F ≥ 3, and F = 4 were 0.71 (95% CI 0.63-0.78), 0.81 (95% CI 0.72-0.88), and 0.81 (95% CI 0.63-0.91) for pSWE, and 0.77 (95% CI 0.68-0.84), 0.80 (95% CI 0.72-0.87), and 0.92 (95% CI 0.75-0.98) for 2-D SWE, respectively. The pooled specificity of pSWE and 2-D SWE for these stages were 0.83 (95% CI 0.76-0.88), 0.87 (95% CI 0.81-0.92), and 0.91 (95% CI 0.86-0.94) for pSWE, and 0.76 (95% CI 0.66-0.84), 0.76 (95% CI 0.69-0.82), and 0.83 (95% CI 0.78-0.85) for 2-D SWE, respectively. In conclusion, both 2-D SWE and pSWE demonstrated high diagnostic performance in identifying various stages of liver fibrosis in MASLD patients.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143017204","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}

{"title":"Alleviating the IL-1β-stimulated extracellular matrix degradation in osteoarthritis, and chondrocyte inflammation by <i>Morinda officinalis</i> polysaccharide via the SIRT6/NF-κB pathway.","authors":"Dongfang Zhao, Shuqin Xing, Jiao Qi, Zhiqiang Wei, Jianghai Huang, Jigao Sun, Xinzhu Wen, Yafei Wang","doi":"10.17305/bb.2024.11437","DOIUrl":"https://doi.org/10.17305/bb.2024.11437","url":null,"abstract":"<p><p>Morinda officinalis polysaccharide (MOP) is a major active component of Morinda officinalis, known for its roles in supporting bone health and reducing oxidation and inflammation. However, no studies to date have specifically examined the effects of MOP on interleukin-1β (IL-1β)-stimulated chondrocyte inflammation or the progression of osteoarthritis (OA). To investigate, cell counting kit-8 assays were performed to evaluate MOP's impact on the viability of human chondrocytes (C28/I2 c...</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143017212","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}

{"title":"L-theanine promotes angiogenesis in limb ischemic mice by modulating NRP1/VEGFR2 signaling.","authors":"Jingyi Wang, Yinghui Xu, Yating Ruan, Xinyang Hu","doi":"10.17305/bb.2024.11256","DOIUrl":"https://doi.org/10.17305/bb.2024.11256","url":null,"abstract":"<p><p>Peripheral artery disease (PAD), primarily caused by atherosclerosis, leads to the narrowing or blockage of arteries that supply blood to the limbs. This study explores the pro-angiogenic effects of L-theanine and its underlying mechanisms in a mouse model of hindlimb ischemia (HLI). To evaluate L-theanine's pro-angiogenic effects, human umbilical vein endothelial cells (HUVECs) were subjected to tube formation, migration, sprouting, and proliferation assays. In vivo, C57BL/6 mice with induced HLI were treated with L-theanine. Blood flow recovery was measured via Doppler ultrasound, and vascular density was analyzed using immunofluorescence staining. RNA sequencing identified neuropilin-1 (NRP1) as a key regulator, and the expression levels of NRP1 and VEGFR2 were examined through qPCR and Western blotting. L-theanine significantly enhanced angiogenesis in HUVECs, as demonstrated by improved tube formation, migration, sprouting, and proliferation. In mice, L-theanine treatment resulted in increased vessel density and improved blood flow recovery. Furthermore, L-theanine was found to activate the NRP1/VEGFR2 signaling pathway in both HUVECs and the HLI mouse model. These findings indicate that L-theanine can promote angiogenesis and activate key pathways involved in vascular repair, suggesting its potential as a therapeutic agent for treating vascular defects associated with PAD.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142973625","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}

{"title":"Pathological roles of ubiquitination and deubiquitination systems in sepsis-induced myocardial dysfunction.","authors":"Zhiping Wang, Simiao Sun, Lili Huang, Xinlong Chen, Huifen Xu, Hongwei Ma, Mingbing Xiao, Linhua Wang","doi":"10.17305/bb.2024.11738","DOIUrl":"https://doi.org/10.17305/bb.2024.11738","url":null,"abstract":"<p><p>Sepsis-induced myocardial dysfunction (SIMD) is a severe complication of sepsis, characterized by impaired cardiac function and high mortality rates. Despite significant advances in understanding sepsis pathophysiology, the molecular mechanisms underlying SIMD remain incompletely elucidated. Ubiquitination and deubiquitination, critical post-translational modifications (PTMs) regulating protein stability, localization, and activity, play pivotal roles in cellular processes, such as inflammation, apoptosis, mitochondrial function, and calcium handling. Dysregulation of these systems has been increasingly implicated in the pathogenesis of SIMD. This review provides a comprehensive overview of the pathological mechanisms driving SIMD, with a focus on the classification and functions of E3 ubiquitin ligases and deubiquitinating enzymes (DUBs), their regulatory systems, and their involvement in SIMD. Dysfunction of the ubiquitin-proteasome system (UPS), often driven by altered activity of E3 ligases, accelerates the degradation of critical regulatory proteins, thereby exacerbating cardiac inflammation, oxidative stress, and apoptosis. Concurrently, imbalances in DUB activity disrupt protein homeostasis, further amplifying myocardial injury. Emerging research underscores the therapeutic potential of targeting these systems. Strategies aimed at modulating E3 ligase activity or restoring DUB balance have shown promise in preclinical studies. This review summarizes current findings on the roles of ubiquitination and deubiquitination in SIMD pathogenesis, highlights the key challenges in advancing this field, and proposes directions for future research.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142973647","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}

{"title":"Prediction of post-insertion infections related to totally implantable subcutaneous venous access ports in tumor patients using a nomogram.","authors":"Sen Wang, Heng Zong, Lei Tang, Yuandong Wei","doi":"10.17305/bb.2024.11583","DOIUrl":"https://doi.org/10.17305/bb.2024.11583","url":null,"abstract":"<p><p>Totally implantable subcutaneous venous access ports (TISVAPs) are essential for long-term central venous chemotherapy, delivering medication directly into the central veins of patients. While they play a critical role in reducing patient discomfort, TISVAPs pose a notable risk of post-insertion infections-particularly concerning for oncology patients with compromised immune systems due to aggressive treatment regimens. Our research addresses this issue by developing a predictive nomogram to estimate the risk of TISVAP-associated infections. The model is based on independent risk factors identified in our study: a history of diabetes, the type of chemotherapy, peripheral blood leukocyte count (WBC), and serum albumin levels. Using retrospective clinical data from 309 oncology patients who underwent TISVAP implantation at a tertiary A-grade comprehensive hospital, we divided the dataset into training (n=246) and validation (n=63) subsets. Through logistic and Lasso regression analyses, we identified the independent risk factors associated with infections. The resulting interactive nomogram demonstrated strong accuracy and reliability, with C-indexes of 0.82 and 0.835 for the training and validation sets, respectively. This tool equips healthcare providers to proactively identify high-risk patients and tailor preventive strategies accordingly. Ultimately, our research aims to enhance patient outcomes and improve the quality of life for those undergoing long-term venous chemotherapy.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142959717","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}

{"title":"Therapeutic effects of chlorogenic acid on allergic rhinitis through TLR4/MAPK/NF-κB pathway modulation.","authors":"Xiaoyan Xu, Lei Wang, Guangyao Wu, Xixia Li","doi":"10.17305/bb.2024.11582","DOIUrl":"https://doi.org/10.17305/bb.2024.11582","url":null,"abstract":"<p><p>Chlorogenic acid (CGA) exhibits promising anti-inflammatory properties, making it a potential therapeutic agent for inflammatory conditions and allergic rhinitis (AR). This study aimed to evaluate the therapeutic effects of CGA on inflammation in RAW264.7 macrophage cells and on AR in mice. RAW264.7 cells were treated with lipopolysaccharide (LPS) to induce inflammation and cultured with varying concentrations of CGA, a Tlr4-silenced gene (shTlr4) transfection, and the MAPK/NF-κB pathway activator diprovocim. Cell viability was assessed using the CCK8 assay, while levels of nitric oxide (NO), TNF-α, and IL-6 were measured by Griess colorimetry, immunofluorescence, and ELISA. Expression and phosphorylation levels of the MAPK/NF-κB pathway were evaluated using qPCR and western blotting. Additionally, ovalbumin (OVA)-induced AR mice received different doses of CGA, and Toll-like receptor-4 (Tlr4) overexpression was induced. In vitro, CGA treatment significantly reduced LPS-induced cell activity, NO, TNF-α, and IL-6 secretion, and downregulated Tlr4, p-p38, p-p65, and p-IκB expression. Tlr4 inhibition suppressed cell activity and inflammation by blocking MAPK/NF-κB pathway activation. Conversely, Tlr4 overexpression counteracted the effects of CGA, increasing cell activity and inflammatory factor concentration. In OVA-induced AR mice, CGA effectively alleviated allergic symptoms, reduced inflammatory factor secretion, and inhibited TLR4/MAPK/NF-κB pathway activity. These findings suggest CGA's potential as an anti-inflammatory agent in RAW264.7 cells and AR models through modulation of the TLR4/MAPK/NF-κB pathway.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142933952","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}