Biomolecules & Therapeutics最新文献_第4页

The Anti-Inflammatory Activities of Benzylideneacetophenone Derivatives in LPS Stimulated BV2 Microglia Cells and Mice. 苯亚甲基苯乙酮衍生物在 LPS 刺激的 BV2 小胶质细胞和小鼠中的抗炎活性

IF 3 3区医学

Biomolecules & Therapeutics Pub Date : 2024-10-11 DOI: 10.4062/biomolther.2024.049

Mijin Kim, Seungmin Kang, Seikwan Oh

{"title":"The Anti-Inflammatory Activities of Benzylideneacetophenone Derivatives in LPS Stimulated BV2 Microglia Cells and Mice.","authors":"Mijin Kim, Seungmin Kang, Seikwan Oh","doi":"10.4062/biomolther.2024.049","DOIUrl":"https://doi.org/10.4062/biomolther.2024.049","url":null,"abstract":"A previously reported study highlighted the neuroprotective potential of the novel benzylideneacetophenone derivative, JC3, in mice. In pursuit of compounds with even more robust neuroprotective and anti-inflammatory properties compared to JC3, we synthesized substituted 1,3-diphenyl-2-propen-1-ones based on chalcones. Molecular modeling studies aimed at discerning the chemical structural features conducive to heightened biological activity revealed that JCII-8,10,11 exhibited the widest HOMOLUMO gap within this category, indicating facile electron and radical transfer between HOMO and LUMO in model assessments. From the pool of synthesized compounds, JCII-8,10,11 were selected for the present investigation. The biological assays involving JCII-8,10,11 demonstrated their concentration-dependent suppression of iNOS and COX-2 protein levels, alongside various cytokine mRNA expressions in LPS-induced murine microglial BV2 cells. Furthermore, western blot analyses were conducted to investigate the MAPK pathways and NF-κB/p65 nuclear translocation. These evaluations conclusively confirmed the inflammatory inhibition effects in both in vitro and in vivo inflammation models. These findings establish JCII-8,10,11 as potent anti-inflammatory agents, hindering inflammatory mediators and impeding NF-κB/p65 nuclear translocation via JNK and ERK MAPK phosphorylation in BV2 cells. The study positions them as potential therapeutics for inflammation-related conditions. Additionally, JCII-11 exhibited greater activity compared to other tested JCII compounds.","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142399243","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Pyronaridine Inhibited MUC5AC Mucin Gene Expression by Regulation of Nuclear Factor Kappa B Signaling Pathway in Human Pulmonary Mucoepidermoid Cells. 吡咯烷酮通过调控核因子卡巴B信号通路抑制人肺黏液表皮样细胞中MUC5AC黏蛋白基因的表达

IF 3 3区医学

Biomolecules & Therapeutics Pub Date : 2024-09-01 Epub Date: 2024-08-02 DOI: 10.4062/biomolther.2024.072

Rajib Hossain, Hyun Jae Lee, Choong Jae Lee

引用次数: 0

The Combination of Gefitinib and Acetaminophen Exacerbates Hepatotoxicity via ROS-Mediated Apoptosis. 吉非替尼与对乙酰氨基酚联用会通过ROS介导的细胞凋亡加剧肝毒性

IF 3 3区医学

Biomolecules & Therapeutics Pub Date : 2024-09-01 Epub Date: 2024-06-14 DOI: 10.4062/biomolther.2023.209

Jiangxin Xu, Xiangliang Huang, Yourong Zhou, Zhifei Xu, Xinjun Cai, Bo Yang, Qiaojun He, Peihua Luo, Hao Yan, Jie Jin

{"title":"The Combination of Gefitinib and Acetaminophen Exacerbates Hepatotoxicity via ROS-Mediated Apoptosis.","authors":"Jiangxin Xu, Xiangliang Huang, Yourong Zhou, Zhifei Xu, Xinjun Cai, Bo Yang, Qiaojun He, Peihua Luo, Hao Yan, Jie Jin","doi":"10.4062/biomolther.2023.209","DOIUrl":"10.4062/biomolther.2023.209","url":null,"abstract":"Gefitinib is the well-tolerated first-line treatment of non-small cell lung cancer. As it need for analgesics during oncology treatment, particularly in the context ofthe coronavirus disease, where patients are more susceptible to contract high fever and sore throat. This has increased the likelihood of taking both gefitinib and antipyretic analgesic acetaminophen (APAP). Given that gefitinib and APAP overdose can predispose patients to liver injury or even acute liver failure, there is a risk of severe hepatotoxicity when these two drugs are used concomitantly. However, little is known regarding their safety at therapeutic doses. This study simulated the administration of gefitinib and APAP at clinically relevant doses in an animal model and confirmed that gefitinib in combination with APAP exhibited additional hepatotoxicity. We found that gefitinib plus APAP significantly exacerbated cell death, whereas each drug by itself had little or minor effect on hepatocyte survival. Mechanistically, combination of gefitinib and APAP induces hepatocyte death via the apoptotic pathway obviously. Reactive oxygen species (ROS) generation and DNA damage accumulation are involved in hepatocyte apoptosis. Gefitinib plus APAP also promotes the expression of Kelch-like ECH-associated protein 1 (Keap1) and downregulated the antioxidant factor, Nuclear factor erythroid 2-related factor 2 (Nrf2), by inhibiting p62 expression. Taken together, this study revealed the potential ROS-mediated apoptosis-dependent hepatotoxicity effect of the combination of gefitinib and APAP, in which the p62/Keap1/Nrf2 signaling pathway participates and plays an important regulatory role.","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":" ","pages":"647-657"},"PeriodicalIF":3.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11392667/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141316649","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

β-Lapachone Exerts Hypnotic Effects via Adenosine A₁ Receptor in Mice. β-拉帕醌通过腺苷 A1 受体对小鼠产生催眠作用

IF 3 3区医学

Biomolecules & Therapeutics Pub Date : 2024-09-01 Epub Date: 2024-08-21 DOI: 10.4062/biomolther.2024.106

Do Hyun Lee, Hye Jin Jee, Yi-Sook Jung

{"title":"β-Lapachone Exerts Hypnotic Effects via Adenosine A1 Receptor in Mice.","authors":"Do Hyun Lee, Hye Jin Jee, Yi-Sook Jung","doi":"10.4062/biomolther.2024.106","DOIUrl":"10.4062/biomolther.2024.106","url":null,"abstract":"Sleep is one of the most essential physiological phenomena for maintaining health. Sleep disturbances, such as insomnia, are often accompanied by psychiatric or physical conditions such as impaired attention, anxiety, and stress. Medication used to treat insomnia have concerns about potential side effects with long-term use, so interest in the use of alternative medicine is increasing. In this study, we investigated the hypnotic effects of β-lapachone (β-Lap), a natural naphthoquinone compound, using pentobarbital-induced sleep test, immunohistochemistry, real-time PCR, and western blot in mice. Our results indicated that β-Lap exerts a significant hypnotic effect by showing a decrease in sleep onset latency and an increase in total sleep time in pentobarbital-induced sleep model. The results of c-Fos immunostaining showed that β-Lap decreased neuronal activity in the basal forebrain and lateral hypothalamus, which are wakefulness-promoting brain regions, while increasing in the ventrolateral preoptic nucleus, a sleep-promoting region; all these effects were significantly abolished by 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), an adenosine A1 receptor (A1R) antagonist. Western blot analysis showed that β-Lap increased extracellular signalregulated kinase phosphorylation and nuclear factor-kappa B translocation from the cytoplasm to the nucleus; these effects were inhibited by DPCPX. Additionally, β-Lap increased the mRNA levels of A1R. Taken together, these results suggest that β-Lap exerts hypnotic effects, potentially through A1R.","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":" ","pages":"531-539"},"PeriodicalIF":3.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11392670/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142008227","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Glycogen Phosphorylase Inhibitor Promotes Hair Growth via Protecting from Oxidative-Stress and Regulating Glycogen Breakdown in Human Hair follicles. 糖原磷酸化酶抑制剂通过保护人体毛囊免受氧化应激和调节糖原分解促进毛发生长

IF 3 3区医学

Biomolecules & Therapeutics Pub Date : 2024-09-01 Epub Date: 2024-08-06 DOI: 10.4062/biomolther.2024.098

Bomi Park, Daeun Kim, Hairu Zhao, SoonRe Kim, Byung Cheol Park, Sanghwa Lee, Yurim Lee, Hee Dong Park, Dongchul Lim, Sunyoung Ryu, Jae Sung Hwang

{"title":"Glycogen Phosphorylase Inhibitor Promotes Hair Growth via Protecting from Oxidative-Stress and Regulating Glycogen Breakdown in Human Hair follicles.","authors":"Bomi Park, Daeun Kim, Hairu Zhao, SoonRe Kim, Byung Cheol Park, Sanghwa Lee, Yurim Lee, Hee Dong Park, Dongchul Lim, Sunyoung Ryu, Jae Sung Hwang","doi":"10.4062/biomolther.2024.098","DOIUrl":"10.4062/biomolther.2024.098","url":null,"abstract":"Hair growth cycles are mainly regulated by human dermal papilla cells (hDPCs) and human outer root sheath cells (hORSCs). Protecting hDPCs from excessive oxidative stress and hORSCs from glycogen phosphorylase (PYGL) is crucial to maintaining the hair growth phase, anagen. In this study, we developed a new PYGL inhibitor, Hydroxytrimethylpyridinyl Methylindolecarboxamide (HTPI) and assessed its potential to prevent hair loss. HTPI reduced oxidative damage, preventing cell death and restored decreased level of anagen marker ALP and its related genes induced by hydrogen peroxide in hDPCs. Moreover, HTPI inhibited glycogen degradation and induced cell survival under glucose starvation in hORSCs. In ex-vivo culture, HTPI significantly enhanced hair growth compared to the control with minoxidil showing comparable results. Overall, these findings suggest that HTPI has significant potential as a therapeutic agent for the prevention and treatment of hair loss.","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":" ","pages":"640-646"},"PeriodicalIF":3.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11392663/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141892804","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Gilteritinib Reduces FLT3 Expression in Acute Myeloid Leukemia Cells. 吉利替尼能减少急性髓性白血病细胞中的 FLT3 表达

IF 3 3区医学

Biomolecules & Therapeutics Pub Date : 2024-09-01 Epub Date: 2024-08-02 DOI: 10.4062/biomolther.2023.215

Thị Lam Thái, Sun-Young Han

{"title":"Gilteritinib Reduces FLT3 Expression in Acute Myeloid Leukemia Cells.","authors":"Thị Lam Thái, Sun-Young Han","doi":"10.4062/biomolther.2023.215","DOIUrl":"10.4062/biomolther.2023.215","url":null,"abstract":"Acute myeloid leukemia (AML) is a genetically diverse and challenging malignancy, with mutations in the FLT3 gene being particularly common and deleterious. Gilteritinib, a potent FLT3 inhibitor, has been approved by the U.S. Food and Drug Administration (FDA) for the treatment of relapsed/refractory AML with FLT3 mutations. Although gilteritinib was developed based on its inhibitory activity against FLT3 kinase, it is important to understand the precise mechanisms of its antileukemic activity in managing drug resistance and discovering biomarkers. This study was designed to elucidate the effect of gilteritinib on the FLT3 expression level. The results showed that gilteritinib induced a dose-dependent decrease in both FLT3 phosphorylation and expression. This reduction was particularly pronounced after 48 h of treatment. The decrease in FLT3 expression was found to be independent of changes in FLT3 mRNA transcription, suggesting post-transcriptional regulatory mechanisms. Further studies were performed in various AML cell lines and cells with both FLT3 wild-type and FLT3 mutant exhibited FLT3 reduction by gilteritinib treatment. In addition, other FLT3 inhibitors were evaluated for their ability to reduce FLT3 expression. Other FLT3 inhibitors, midostaurin, crenolanib, and quizartinib, also reduced FLT3 expression, consistent with the effect of gilteritinib. These findings hold great promise for optimizing gilteritinib treatment in AML patients. However, it is important to recognize that further research is warranted to gain a full understanding of these mechanisms and their clinical implications in the context of FLT3 reduction.","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":" ","pages":"577-581"},"PeriodicalIF":3.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11392668/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141874070","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Domperidone, a Dopamine Receptor D2 Antagonist, Induces Apoptosis by Inhibiting the ERK/STAT3-Mediated Pathway in Human Colon Cancer HCT116 Cells. 多巴胺受体 D2 拮抗剂多潘立酮通过抑制 ERK/STAT3 介导的途径诱导人结肠癌 HCT116 细胞凋亡

IF 3 3区医学

Biomolecules & Therapeutics Pub Date : 2024-09-01 Epub Date: 2024-06-25 DOI: 10.4062/biomolther.2024.048

So Jin Sim, Jeong-Hoon Jang, Joon-Seok Choi, Kyung-Soo Chun

{"title":"Domperidone, a Dopamine Receptor D2 Antagonist, Induces Apoptosis by Inhibiting the ERK/STAT3-Mediated Pathway in Human Colon Cancer HCT116 Cells.","authors":"So Jin Sim, Jeong-Hoon Jang, Joon-Seok Choi, Kyung-Soo Chun","doi":"10.4062/biomolther.2024.048","DOIUrl":"10.4062/biomolther.2024.048","url":null,"abstract":"Colorectal cancer (CRC) continues to demonstrate high incidence and mortality rates, emphasizing that implementing strategic measures for prevention and treatment is crucial. Recently, the dopamine receptor D2 (DRD2), a G protein-coupled receptor, has been reported to play multiple roles in growth of tumor cells. This study investigated the anticancer potential of domperidone, a dopamine receptor D2 antagonist, in HCT116 human CRC cells. Domperidone demonstrated concentration- and time-dependent reductions in cell viability, thereby inducing apoptosis. The molecular mechanism revealed that domperidone modulated the mitochondrial pathway, decreasing mitochondrial Bcl-2 levels, elevating cytosolic cytochrome C expression, and triggering caspase- 3, -7, and -9 cleavage. Domperidone decreased in formation of β-arrestin2/MEK complex, which contributing to inhibition of ERK activation. Additionally, treatment with domperidone diminished JAK2 and STAT3 activation. Treatment of U0126, the MEK inhibitor, resulted in reduced phosphorylation of MEK, ERK, and STAT3 without alteration of JAK2 activation, indicating that domperidone targeted both MEK-ERK-STAT3 and JAK2-STAT3 signaling pathways, respectively. Immunoblot analysis revealed that domperidone also downregulated DRD2 expression. Domperidone-induced reactive oxygen species (ROS) generation and N-acetylcysteine treatment mitigated ROS levels and restored cell viability. An in vivo xenograft study verified the significant antitumor effects of domperidone. These results emphasize the multifaceted anticancer effects of domperidone, highlighting its potential as a promising therapeutic agent for human CRC.","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":" ","pages":"568-576"},"PeriodicalIF":3.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11392662/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141445357","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Decellularized Matrices for the Treatment of Tissue Defects: from Matrix Origin to Immunological Mechanisms. 用于治疗组织缺损的脱细胞基质：从基质起源到免疫机制。

IF 3 3区医学

Biomolecules & Therapeutics Pub Date : 2024-09-01 Epub Date: 2024-08-02 DOI: 10.4062/biomolther.2024.050

Xinyue Wang, Jiqiang Guo, Qing Yu, Luyao Zhao, Xiang Gao, Li Wang, Meiling Wen, Junrong Yan, Meiwen An, Yang Liu

{"title":"Decellularized Matrices for the Treatment of Tissue Defects: from Matrix Origin to Immunological Mechanisms.","authors":"Xinyue Wang, Jiqiang Guo, Qing Yu, Luyao Zhao, Xiang Gao, Li Wang, Meiling Wen, Junrong Yan, Meiwen An, Yang Liu","doi":"10.4062/biomolther.2024.050","DOIUrl":"10.4062/biomolther.2024.050","url":null,"abstract":"Decellularized matrix transplantation has emerged as a promising therapeutic approach for repairing tissue defects, with numerous studies assessing its safety and efficacy in both animal models and clinical settings. The host immune response elicited by decellularized matrix grafts of natural biological origin plays a crucial role in determining the success of tissue repair, influenced by matrix heterogeneity and the inflammatory microenvironment of the wound. However, the specific immunologic mechanisms underlying the interaction between decellularized matrix grafts and the host immune system remain elusive. This article reviews the sources of decellularized matrices, available decellularization techniques, and residual immunogenic components. It focuses on the host immune response following decellularized matrix transplantation, with emphasis on the key mechanisms of Toll-like receptor, T-cell receptor, and TGF-β/SMAD signaling in the stages of post-transplantation immunorecognition, immunomodulation, and tissue repair, respectively. Furthermore, it highlights the innovative roles of TLR10 and miR-29a-3p in improving transplantation outcomes. An in-depth understanding of the molecular mechanisms underlying the host immune response after decellularized matrix transplantation provides new directions for the repair of tissue defects.","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":" ","pages":"509-522"},"PeriodicalIF":3.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11392660/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141874111","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Interleukin-1β Signaling Contributes to Cell Cycle Arrest and Apoptotic Cell Death by Leptin via Modulation of AKT and p38MAPK in Hepatocytes. 白细胞介素-1β信号通过调节肝细胞中的 AKT 和 p38MAPK 促使细胞周期停滞和瘦素导致细胞凋亡

IF 3 3区医学

Biomolecules & Therapeutics Pub Date : 2024-09-01 Epub Date: 2024-08-02 DOI: 10.4062/biomolther.2023.232

Ananda Baral, Pil-Hoon Park

{"title":"Interleukin-1β Signaling Contributes to Cell Cycle Arrest and Apoptotic Cell Death by Leptin via Modulation of AKT and p38MAPK in Hepatocytes.","authors":"Ananda Baral, Pil-Hoon Park","doi":"10.4062/biomolther.2023.232","DOIUrl":"10.4062/biomolther.2023.232","url":null,"abstract":"Leptin, an adipose tissue-derived hormone, has exhibited the potent hepatotoxic effects. However, the underlying molecular mechanisms are not fully understood. In this study, we have elucidated the mechanisms by which leptin exerts cytotoxic effects in hepatocytes, particularly focusing on the role of interleukin-1β (IL-1β) signaling. Leptin significantly induced maturation and secretion of IL-1β in cultured rat hepatocytes. Interestingly, inhibition of IL-1β signaling by pretreatment with an IL-1 receptor antagonist (IL-1Ra) or gene silencing of type I IL-1 receptor (IL-1R1) markedly abrogated leptin-induced cell cycle arrest. The critical role of IL-1β signaling in leptin-induced cell cycle arrest is mediated via upregulation of p16, which acts as an inhibitor of cyclin-dependent kinase. In addition, leptin-induced apoptotic cell death was relieved by inhibition of IL-1β signaling, as determined by annexin V/7-AAD binding assay. Mechanistically, IL-1β signaling contributes to apoptotic cell death and cell cycle arrest by suppressing AKT and activation of p38 mitogen-activated protein kinase (p38MAPK) signaling pathways. Involvement of IL-1β signaling in cytotoxic effect of leptin was further confirmed in vivo using hepatocyte specific IL-1R1 knock out (IL-1R1 KO) mice. Essentially similar results were obtained in vivo, where leptin administration caused the upregulation of apoptotic markers, dephosphorylation of AKT, and p38MAPK activation were observed in wild type mice liver without significant effects in the livers of IL-1R1 KO mice. Taken together, these results demonstrate that IL-1β signaling critically contributes to leptin-induced cell cycle arrest and apoptosis, at least in part, by modulating p38MAPK and AKT signaling pathways.","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":" ","pages":"611-626"},"PeriodicalIF":3.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11392659/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141874071","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Investigating the Immune-Stimulating Potential of β-Glucan from Aureobasidium pullulans in Cancer Immunotherapy. 研究 Aureobasidium pullulans β-葡聚糖在癌症免疫疗法中的免疫刺激潜力

IF 3 3区医学

Biomolecules & Therapeutics Pub Date : 2024-09-01 Epub Date: 2024-08-02 DOI: 10.4062/biomolther.2024.047

Jae-Hyeon Jeong, Dae-Joon Kim, Seong-Jin Hong, Jae-Hee Ahn, Dong-Ju Lee, Ah-Ra Jang, Sungyun Kim, Hyun-Jong Cho, Jae-Young Lee, Jong-Hwan Park, Young-Min Kim, Hyun-Jeong Ko

{"title":"Investigating the Immune-Stimulating Potential of β-Glucan from Aureobasidium pullulans in Cancer Immunotherapy.","authors":"Jae-Hyeon Jeong, Dae-Joon Kim, Seong-Jin Hong, Jae-Hee Ahn, Dong-Ju Lee, Ah-Ra Jang, Sungyun Kim, Hyun-Jong Cho, Jae-Young Lee, Jong-Hwan Park, Young-Min Kim, Hyun-Jeong Ko","doi":"10.4062/biomolther.2024.047","DOIUrl":"10.4062/biomolther.2024.047","url":null,"abstract":"β-glucan, a polysaccharide found in various sources, exhibits unique physicochemical properties, yet its high polymerization limits clinical applications because of its solubility. Addressing this limitation, we introduce PPTEE-glycan, a highly purified soluble β-1,3/1,6-glucan derived from Aureobasidium pullulans. The refined PPTEE-glycan demonstrated robust immune stimulation in vitro, activated dendritic cells, and enhanced co-stimulatory markers, cytokines, and cross-presentation. Formulated as a PPTEE + microemulsion (ME), it elevated immune responses in vivo, promoting antigen-specific antibodies and CD8+ T cell proliferation. Intratumoral administration of PPTEE + ME in tumor-bearing mice induced notable tumor regression, which was linked to the activation of immunosuppressive cells. This study highlights the potential of high-purity Aureobasidium pullulans-derived β-glucan, particularly PPTEE, as promising immune adjuvants, offering novel avenues for advancing cancer immunotherapy.","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":" ","pages":"556-567"},"PeriodicalIF":3.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11392664/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141874072","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0