BIOMEDICINE & PHARMACOTHERAPY生物医学与药物治疗
BIOMEDICINE & PHARMACOTHERAPY(英文缩写 BIOMED PHARMACOTHER),ISSN 0753-3322,eISSN 1950-6007,中文译名:生物医学与药物治疗 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-09-27 至 2026-09-27，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2020 | 6.530 | Q1 |
| 2021 | 7.419 | Q1 |
| 2022 | 7.500 | Q1 |
| 2023 | 6.900 | Q1 |
| 2024 | 7.500 | Q1 |
BIOMEDICINE & PHARMACOTHERAPY 最新收录文献
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1. In vivo acute oral tolerability and antitumor activity of the novel small molecule YB-1 modulator AIGM-2024-4 in a DMBA- induced rat mammary tumor model.
1. 新型小分子YB-1调节剂AIGM-2024-4在DMBA诱导的大鼠乳腺肿瘤模型中的体内急性口服耐受性和抗肿瘤活性PMID:日期:2026-10-01Human Y-Box Binding Protein-1 (YB-1) is overexpressed in breast cancer and regulates multiple oncogenic pathways involved in tumor progression and therapeutic resistance. We recently reported AIGM-2024-4 as a novel structure guided small molecule modulator of full length YB-1 protein. Here, we evaluated its preliminary in vivo tolerability in healthy female rats and antitumor activity in the DMBA-induced mammary tumor model. Acute oral toxicity assessment demonstrated that AIGM-2024-4 was well tolerated at doses up to 2000 mg/kg, with no detectable treatment related adverse effects under the tested conditions. In the DMBA-induced model, repeated oral administration of AIGM-2024-4 significantly reduced tumor growth, resulting in an ∼56% reduction in tumor volume compared with the disease control group. Treatment also reduced the mitotic index, improved redox balance, enhanced antioxidant status, and improved histopathological features of mammary tumors. These antitumor effects were accompanied by altered expression of YB-1 and tumor progression associated proteins, including HER2, EGFR, ERα, and Ki-67, together with increased E-cadherin expression. Collectively, this study provides an initial integrated in vivo evaluation of AIGM-2024-4, demonstrating favorable acute oral tolerability, preliminary antitumor activity, and YB-1- associated molecular changes that support further preclinical investigation.
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2. PLGA nanoparticles for the delivery of antimicrobial peptides in a polymicrobial sepsis model.
PMID:日期:2026-10-01Antimicrobial peptides (AMPs) are evolutionarily conserved molecules that play a central role in innate immunity and represent a promising class of candidates against antimicrobial resistance. However, their clinical application is hindered by low stability in physiological conditions, susceptibility to proteolytic degradation, and dose-dependent toxicity. In this study, we evaluated the structural properties, antimicrobial activity, and therapeutic safety of two scorpion-derived AMP analogs, StigA25 and StigA31, in both free and encapsulated into poly (lactic-co-glycolic acid) (PLGA) nanoparticles. Both peptides displayed high stability in the range of temperature and pH investigated, retained activity in serum, and higher α-helical content in the presence of negatively charged lipid vesicles. Encapsulation efficiency above 95% in PLGA nanoparticles contributed to preserving the antimicrobial activity, enhanced bactericidal kinetics, and reduced hemolytic effects of tested peptides. In vitro assays indicated safety toward mammalian cells, while electron scanning microscopy revealed microbial membrane disruption. In a murine polymicrobial sepsis model, pretreatment with free and nanoformulated peptides effectively reduced bacterial load and attenuated inflammatory responses. Immunomodulation response included decreased leukocyte migration, myeloperoxidase activity, and pro-inflammatory cytokines TNF-α and IL-1β, with superior performance of the peptides in formulation. Collectively, these findings demonstrate enhanced therapeutic potential for scorpion-derived AMP analogs-loaded PLGA nanoparticles, providing a dual antimicrobial and anti-inflammatory strategy for severe infections such as sepsis, and support further development of AMP-based nanomedicines.
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3. {"_":"Biomimetic recombinant humanized type III collagen peptide-RGD loaded alginate hydrogels enhance proliferation of mesenchymal-lineage cells via Integrin αβ activation.","sub":["5","1"]}
3. 仿生重组人源化III型胶原蛋白肽-RGD负载海藻酸盐水凝胶通过整合素αβ激活促进间充质谱系细胞增殖PMID:日期:2026-10-01Alginate hydrogels (HG) are widely utilized in tissue engineering due to their biocompatibility and tunable physical properties, however, their bio-inert nature limits direct cellular interactions. Moreover, the receptor-level interactions of recombinant humanized type-III collagen-peptide (rCP) and RGD with mesenchymal-lineage cells such as mesenchymal stem cells (MSCs), human osteoblast-like cells (hFOB), and fibroblasts (FB) remain unexplored. To address these limitations, alginate hydrogels were incorporated with RGD (R-HG), rCP (rCP-HG), and both peptides (CPR-HG), and systematically evaluated for their functional, structural, and biological performance. While dual-peptide matrices are widely recognized in biomaterials research, this study specifically elucidates the distinct receptor-level responses and synergistic pathways activated by combining RGD and a specific genetic-engineered recombinant CP within an alginate backbone. Peptide incorporation enhanced HG swelling, with rCP contributing to increased hydration capacity. Drug release studies revealed sustained, media-dependent diffusion of both RGD and rCP. Notably, CPR-HG significantly elevated cell proliferation, particularly in hFOB cells. Among the cells, the incorporationof RGD and rCP significantly accelerated cellular integrin α5 and β1 expression in MSCs than hFOB and FB. SEM analysis demonstrated improved cell morphology and matrix interaction, while immunocytochemistry confirmed upregulated expression of integrin α5 and collagen-I in all cell types. Interestingly, compared to single-peptide and unmodified hydrogels, CPR-HG consistently promoted superior cellular adhesion, spreading, and integrin activation in MSCs, hFOB, and FB cells. For the first time, this study disclosed the synergistic effects of RGD and rCP in alginate hydrogels on MSCs, hFOB, and FB cells. Accordingly, a dual-incorporated CPR-HG hydrogel enhanced bioactivity and cell-specific receptor engagement, underscoring its potential as a versatile platform for advanced tissue regeneration.
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4. Monophosphoryl lipid A, the Toll-like receptor 4 agonist, mitigates acute radiation syndrome via hematopoietic stem cells regeneration.
PMID:日期:2026-10-01Hematopoietic acute radiation syndrome (H-ARS) is an unmet medical requirement. Current cytokine-based countermeasures, such as granulocyte colony-stimulating factors, provide limited benefits once the surviving hematopoietic stem and progenitor cell pools are severely depleted. Toll-like receptor (TLR) agonists have been proposed as radiomitigators; however, their efficacy across ligands and receptor subtypes has not been systematically compared under equivalent conditions. Here we screened ten TLR agonists spanning eight receptor subtypes in a lethally irradiated mouse model and found that their radiomitigative efficacy was ligand-specific rather than receptor-class-specific. Monophosphoryl lipid A (MPLA), a detoxified TLR4 agonist, and FSL-1 (TLR2/6) exerted the strongest protective effects. MPLA conferred dose-dependent survival benefits when administered after lethal total-body irradiation, and this protection was substantially abolished by myeloid differentiation primary response 88 (MyD88) inhibition and partially reduced by competitive TLR4 blockade, suggesting that the TLR4-MyD88 signaling axis contributes substantially to the radiomitigative effect. Mechanistically, MPLA did not prevent the initial radiation-induced depletion of the bone marrow (BM), but markedly accelerated the subsequent regenerative phase, restoring multilineage peripheral blood counts, splenic and BM colony-forming activity, marrow architecture, and absolute numbers of hematopoietic stem/progenitor cell populations and mesenchymal stem/stromal cells. Regeneration was accompanied by selective induction of erythropoietin and thrombopoietin in the BM without broad changes in myeloid- or lymphoid-directed cytokines. Since MPLA already has an established human safety record as a licensed vaccine adjuvant, these findings support its repurposing as a potential radiomitigator for hematopoietic acute radiation syndrome.
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5. Inhibition of the Wnt/β-Catenin pathway via an LGK974-cyclodextrin inclusion complex alleviates cardiac injury.
PMID:日期:2026-10-01Cardiac hypertrophy and fibrosis arise from molecular, physiological, and immune alterations triggered by disorders such as myocardial infarction, myocarditis, and Chagas cardiomyopathy. The Wnt/β-catenin pathway is central to this remodeling. Here,we evaluated the therapeutic potential of a supramolecular complex of the Wnt/β-catenin inhibitor LGK974 and modified cyclodextrin (CD:LGK974) to attenuate cardiac injury in experimental model of Trypanosoma cruzi (T. cruzi)-induced cardiac damage. In vivo, Balb/c mice were intraperitoneally infected with 10 ³ T. cruzi trypomastigotes and treated with CD:LGK974 via oral gavage for 21 days under different dose regimes to assess its immunomodulatory, antifibrotic, and antihypertrophic activities. The treatment significantly reduced parasitemia, cardiac hypertrophy and fibrosis in the T. cruzi infection model compared to control groups. Immunofluorescence revealed downregulation of β-catenin in treated animals. Additionally, flow cytometry demonstrated proliferation of CD4, CD8, and NK cells, along with elevated IL-10 expression in NK cells, suggesting an immunomodulatory effect. These findings indicate that CD:LGK974 attenuates cardiac injury and modulates immune response in T. cruzi-infected mice. Together, these results highlight its potential as a therapeutic strategy for reducing pathological cardiac remodeling associated with T. cruzi infection.
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6. Targeting TLR4/NF-κB/NLRP3 signaling with 6-hydroxyflavanone mitigates amyloid-β-induced Alzheimer's disease in mice.
6. 以6-羟基黄烷酮靶向TLR4/NF-κB/NLRP3信号通路可减轻淀粉样蛋白β诱导的小鼠阿尔茨海默病PMID:日期:2026-10-01Alzheimer's disease (AD) is the most common neurodegenerative disorder and is characterized by progressive cognitive decline, cholinergic dysfunction, oxidative stress, and neuroinflammation. Despite extensive research, effective disease-modifying therapies remain unavailable. 6-Hydroxyflavanone (6-OH-F), a naturally occurring flavonoid with antioxidant and anti-inflammatory properties, has not been investigated in AD. This study evaluated the neuroprotective potential of 6-OH-F against amyloid-β (Aβ)-induced AD pathology. Network pharmacology was employed to identify potential targets and pathways associated with 6-OH-F in AD. Neuro-2a cells were pretreated with 6-OH-F (12.5-50 μM) before Aβ exposure, followed by assessment of cell viability, reactive oxygen species (ROS), acetylcholinesterase (AChE), NLRP3, TNF-α, and IL-1β levels. AD was induced in mice by intracerebroventricular administration of pre-aggregated Aβ. Animals received 6-OH-F (15, 30, or 60 mg/kg, p.o.) for four weeks. Behavioral, biochemical, molecular, imaging, and histopathological analyses were subsequently performed. Network pharmacology revealed significant overlap between 6-OH-F targets and AD-associated genes, with enrichment of pathways related to neuronal function and inflammation. In vitro, 6-OH-F attenuated Aβ-induced cytotoxicity and reduced ROS, AChE, NLRP3, TNF-α, and IL-1β levels. In vivo, 6-OH-F improved cognitive performance, alleviated oxidative stress and cholinergic dysfunction, and suppressed the expression of TLR4, pNF-κB, NLRP3, ASC, caspase-1, GSDMD, pro-inflammatory cytokines, IBA1, and GFAP. Furthermore, it reduced neuronal degeneration, blood-brain barrier disruption, and cerebral hemodynamic abnormalities. 6-OH-F ameliorates Aβ-induced cognitive impairment by attenuating oxidative stress, neuroinflammation, and pyroptotic signaling, potentially through modulation of the TLR4/NF-κB/NLRP3 pathway, highlighting its therapeutic potential in Alzheimer's disease.
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8. Comparative analysis of platinum nanoparticles interactions with Mitomycin C and its activated metabolite.
PMID:日期:2026-10-01As of 2026, cancer remains one of the leading causes of death worldwide. Despite substantial medical advancements, chemotherapy remains widely used. However, conventional chemotherapeutic agents lack selectivity towards cancer cells and frequently induce severe side effects, including myelosuppression, gastrointestinal toxicity, and cardiotoxicity. Therefore, increasing attention has been directed towards the modulation of existing anticancer drugs through combination with metallic nanoparticles. Herein, we verified whether platinum nanoparticles (PtNPs) of defined sizes 5, 30, 50, and 70 nm interact with Mitomycin C (MMC) and one of its metabolites, 2,7-diaminomitosene (DAM). DLS and AFM analyses revealed differing aggregation patterns, with MMC exhibiting aggregation primarily under dry conditions. FTIR and NIR spectroscopies suggested that PtNPs interact with MMC predominantly through weak non-covalent interactions. Thermal inspection utilising ITC and DSC showed that these APIs interact in an endothermic manner; however, MMC data might be interpreted as negligible. Furthermore, Ames mutagenicity assay on Salmonella enterica serovar Typhimurium TA102 revealed dose-dependent reduction of mutagenic potential by PtNPs, with more pronounced effects observed for DAM. Cytotoxicity analyses in MCF-7 and SK-BR-3 cells showed that PtNP-MMC combinations generally reduced metabolic activity compared with MMC alone, although the effects varied with cell line, MMC concentration, and nanoparticle size and concentration. The response was more consistent in SK-BR-3 cells, whereas PtNPs generally attenuated DAM activity. As PtNPs alone affected metabolic activity at higher concentrations, the combination effects cannot be attributed solely to enhancement of MMC activity. These findings support further investigation of PtNPs as modulators of mitomycin-related compounds, although their mechanisms and therapeutic relevance require additional validation.