Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie最新文献

{"title":"Corrigendum to \"miR-615-3p promotes proliferation and migration and inhibits apoptosis through its potential target CELF2 in gastric cancer\" [Biomed. Pharmacother. 101, May 2018, pp. 406-413].","authors":"Jizhao Wang, Lin Liu, Yuchen Sun, Yumo Xue, Jingkun Qu, Shupei Pan, Huajing Li, Hangying Qu, Jiansheng Wang, Jia Zhang","doi":"10.1016/j.biopha.2024.117622","DOIUrl":"10.1016/j.biopha.2024.117622","url":null,"abstract":"","PeriodicalId":93904,"journal":{"name":"Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie","volume":" ","pages":"117622"},"PeriodicalIF":0.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142549522","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":"Gilteritinib reverses ABCB1-mediated multidrug resistance: Preclinical in vitro and animal investigations.","authors":"Meng Zhang, Mei-Ling She, Jun Chen, Xiao-Qi Zeng, Qing-Quan Xiong, Ying-Huan Cen, Jia-An Ye, Guo-Bin Qiu, Shu-Yi Yang, Guang-Hui Ren","doi":"10.1016/j.biopha.2024.117603","DOIUrl":"10.1016/j.biopha.2024.117603","url":null,"abstract":"<p><p>Multi-drug resistance (MDR) poses a significant challenge to cancer treatment. Targeting ATP-binding cassette subfamily B member 1 (ABCB1) is a viable strategy for overcoming MDR. This study examined the preclinical in vitro and animal studies that used gilteritinib, a FLT3 inhibitor that reverses ABCB1-mediated MDR. At nontoxic levels, gilteritinib significantly increased the susceptibility of cancer cells overexpressing ABCB1 to chemotherapeutic drugs. Furthermore, it impaired the development of drug-resistant cell colonies and 3D spheroids. Studies on the reversal mechanism have shown that gilteritinib can directly bind to the drug-binding site of ABCB1, inhibiting drug efflux activity. Consequently, the substrate's drug cytotoxicity increases in MDR cells. Furthermore, gilteritinib increased ATPase activity while leaving ABCB1 expression and subcellular distribution unchanged and inhibited AKT or ERK activation. Docking analysis indicated that Gilteritinib could interact with the drug-binding site of the ABCB1 transporter. In vivo studies have shown that gilteritinib improves the antitumor efficacy of paclitaxel in nude mice without obvious toxic effects. In conclusion, our preclinical investigations show that gilteritinib has the potential to successfully overcome ABCB1-mediated MDR in a clinical environment when combined with substrate medicines.</p>","PeriodicalId":93904,"journal":{"name":"Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie","volume":"180 ","pages":"117603"},"PeriodicalIF":0.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142549524","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":"Corrigendum to \"Calcium ion delivery by microbubble-assisted sonoporation stimulates cell death in human gastrointestinal cancer cells\" [Biomed. Pharmacother. 179 (2024) 117339].","authors":"Dawid Przystupski, Dagmara Baczyńska, Joanna Rossowska, Julita Kulbacka, Marek Ussowicz","doi":"10.1016/j.biopha.2024.117442","DOIUrl":"10.1016/j.biopha.2024.117442","url":null,"abstract":"","PeriodicalId":93904,"journal":{"name":"Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie","volume":" ","pages":"117442"},"PeriodicalIF":0.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142376439","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":"Metformin-mediated protection against doxorubicin-induced cardiotoxicity.","authors":"Ming-Li Sun, Jun-Min Dong, Chen Liu, Pu Li, Chao Zhang, Jie Zhen, Wei Chen","doi":"10.1016/j.biopha.2024.117535","DOIUrl":"10.1016/j.biopha.2024.117535","url":null,"abstract":"<p><strong>Background: </strong>A phase II clinical trial of metformin (MET) for the treatment of doxorubicin (DOX)-induced cardiotoxicity (NCT02472353) failed.</p><p><strong>Objectives: </strong>The aims of this study were to confirm MET-mediated protection against DOX-induced cardiotoxicity and its mechanism using H9C2 cells, and to establish a Wistar rat model of DOX-induced cardiotoxicity. Subsequently, Wistar rats were utilized to identify clinically relevant indicators for evaluating MET-mediated protection against DOX-induced cardiotoxicity, thereby facilitating early transition towards successful clinical trials.</p><p><strong>Methods: </strong>MET-mediated protection was assessed using cell viability and cytotoxicity experiments. Additionally, intramitochondrial reactive oxygen species (ROS) levels were measured using an ROS fluorescent probe (dihydroethidium) to confirm the oxidative stress mechanism. Eighteen Wistar rats were randomly allocated to the control, DOX, and DOX+MET groups; and the body weight, adverse drug reactions (ADRs), myocardial injury, cardiac function, oxidative stress, and histopathology of heart tissues were compared between groups.</p><p><strong>Results: </strong>H9C2 cells treated with MET/Dexrazoxane demonstrated dose-dependent protection against DOX-induced cardiotoxicity. The fluorescence intensity of H9C2 cells suggested DOX-induced cardiomyocyte toxicity and MET-mediated protection against DOX-induced cardiotoxicity. In vivo experiments confirmed that a rat model of DOX-induced cardiotoxicity was successfully established, but MET-mediated protection against DOX-induced cardiotoxicity was not demonstrated. This was attributed to insufficient energy intake because of ADRs, such as vomiting.</p><p><strong>Conclusions: </strong>We confirmed the MET-mediated protection against DOX-induced cardiomyocyte toxicity and its mechanism involving the inhibition of oxidative stress in vitro experiments. It is imperative to investigate the optimal conditions for MET-mediated protection against DOX-induced cardiotoxicity in vivo or clinical trials.</p>","PeriodicalId":93904,"journal":{"name":"Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie","volume":"180 ","pages":"117535"},"PeriodicalIF":0.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142482992","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":"Corrigendum to \"Hominis Placenta modulates PTSD-like behaviors in SPSS-induced PTSD mice: Regulating energy metabolism and neuronal activity\" [Biomed. Pharmacother. 178 (2024) 117243].","authors":"Mudan Cai, Hee Ra Park, Eun Jin Yang","doi":"10.1016/j.biopha.2024.117443","DOIUrl":"10.1016/j.biopha.2024.117443","url":null,"abstract":"","PeriodicalId":93904,"journal":{"name":"Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie","volume":" ","pages":"117443"},"PeriodicalIF":0.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142334323","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":"Dual-aptamer-decorated reduction-activated dimeric-prodrug nanoparticles for broad-spectrum treatment of leukemia.","authors":"Shan Yang, Riming Wang, Mei Liu, Yanhong Lv, Hong Fu, Xiaochen Cao, Guogang Dong","doi":"10.1016/j.biopha.2024.117543","DOIUrl":"10.1016/j.biopha.2024.117543","url":null,"abstract":"<p><p>Leukemia remains a fatal disease for most affected patients, and a simple and effective therapeutic strategy is urgently needed. Targeted delivery chemo-drugs to leukemia cells shows promise, but the diverse subtypes of leukemia make single-ligand nanomedicine often ineffective. Herein, a dual-aptamer decorated, reduction-responsive dimeric prodrug-based nanoparticle (NP), termed SXP-NPs, was developed using the two leukemia-specific aptamers Sgc8c and XQ-2d, a reduction-responsive podophyllotoxin (POD) dimeric prodrug, and DSPE-PEG2000. Because the receptors of XQ-2d (CD71) and Sgc8c (PTK7) are overexpressed in different subtypes of leukemia cells, SXP-NPs can broadly and selectively recognize these leukemia cells after intravenous administration, subsequently releasing POD in response to the intracellular high-reduction environment to kill the leukemia cells. In vitro experiments showed that these simple SXP-NPs can specifically bind to various leukemia cancer cells and kill them. In vivo experiments revealed that SXP-NPs can remarkably reduce spleen weight, decrease white blood cell counts, and extend overall survival in a preclinical leukemia animal model. The in vitro and in vivo validation demonstrated that SXP-NPs offer several advantages, including high drug-loading potential, broad-spectrum recognition of leukemia cells, reduced systemic toxicity, and enhanced therapeutic effects of the drug. Taken together, this study provides a simple and effective strategy for broad-spectrum leukemia therapy and highlights the clinical potential of SXP-NPs.</p>","PeriodicalId":93904,"journal":{"name":"Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie","volume":"180 ","pages":"117543"},"PeriodicalIF":0.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142482969","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":"Targeted breast cancer therapy using novel nanovesicle formulations of Olea europaea extract.","authors":"María Del Carmen Villegas-Aguilar, María de la Luz Cádiz-Gurrea, Andres Salumets, David Arráez-Román, Antonio Segura-Carretero, Alberto Sola-Leyva, María Paz Carrasco-Jiménez","doi":"10.1016/j.biopha.2024.117583","DOIUrl":"10.1016/j.biopha.2024.117583","url":null,"abstract":"<p><p>Olive leaf is a byproduct of the olive tree that is rich in phenolic compounds with potential anticarcinogenic effects against various cancers, including breast cancer. Nevertheless, the ingestion or topical application of such plant extracts faces certain limitations. These limitations can be addressed by encapsulating the extracts in nanovesicles to enhance their release and bioavailability. This study aims to develop nanovesicles using Olea europaea leaf extract to exploit its potential anti-cancer properties. Soy lecithin was used to form liposomes for encapsulation of the olive leaf extract. In addition, ethanol and glycerol were added to form ethosomes and glycerosomes, respectively. The antiproliferative effect of both the free extract and the three formed nanovesicles was tested in MCF7 and MCF10A cell lines. To comprehend the mechanisms leading to reduced cell viability after exposure to olive leaf extract and its nanovesicles, levels of reactive oxygen species (ROS), mitochondrial membrane potential, and apoptotic stage were evaluated. The results suggest that both, the nanovesicles and the free extract, are antiproliferative agents against MCF7 tumour cells. However, when examining the impact of olive leaf extract and the formulated nanovesicles on MCF10A cells, no reduction in cell viability was observed. Our findings indicate that the anti-tumour effect of the extract and its nanovesicles may be due to increased oxidative stress, mediated by mitochondrial damage. The mechanism through which olive leaf extract exerts its antiproliferative effect on the breast cancer tumour line implies that apoptosis may be induced by the extract via the involvement of a mitochondria-dependent ROS-mediated pathway.</p>","PeriodicalId":93904,"journal":{"name":"Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie","volume":"180 ","pages":"117583"},"PeriodicalIF":0.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142483003","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":"PAD inhibition downregulates the cellular fibrotic behavior of senescent myofibroblasts derived from dilated cardiomyopathy.","authors":"Alia Sadiq, Justyna Fert-Bober","doi":"10.1016/j.biopha.2024.117579","DOIUrl":"10.1016/j.biopha.2024.117579","url":null,"abstract":"<p><strong>Background: </strong>Dilated cardiomyopathy (DCM) is characterized by enlarged, weakened heart ventricles due to chronic fibrosis. Dysfunctional senescent myofibroblasts and excessive citrullination have been implicated in fibrotic diseases. Peptidylarginine deiminases (PADs) are involved in the citrullination of ECM proteins. However, their role in regulating the cellular functions of cardiac myofibroblasts in DCM, is not well understood. This study aimed to evaluate the role of PADs in the cellular biology and fibrotic behavior of myofibroblasts in DCM.</p><p><strong>Results: </strong>Aged cardiac myofibroblasts derived from dilated cardiomyopathy (DCM, N=5) and healthy (HCF, N=3) participants (35-60 years), were cultured in TGFB-conditioned medium and treated with an irreversible pan-PAD inhibitor BB-Cl-amidine. Our findings showed that, compared with HCFs, DCM myofibroblasts showed high expression of PAD-2, PAD-3, citrullinated proteins and ECM proteins (vimentin, fibronectin, actin, and b-Tubulin). BB-Cl-amidine-mediated PAD inhibition directly affected the cell biology of DCM myofibroblasts, as shown by the reduced migration and invasion of DCM myofibroblasts. It also augmented the apoptosis by activating caspase-3 and decreased senescence by regulating p-53. PAD inhibition did not affect the citrullination of vimentin or fibronectin; however, it decreased collagen 1 A expression.</p><p><strong>Conclusions: </strong>This study revealed that elevated PAD expression facilitates cellular processes mainly senescence, migration, and invasion. PAD inhibition resulted in the downregulation of these cellular functions, thereby reducing the fibrotic behavior of DCM myofibroblasts.</p>","PeriodicalId":93904,"journal":{"name":"Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie","volume":"180 ","pages":"117579"},"PeriodicalIF":0.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142514594","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":"Fraxinellone protects against cardiac injury and decreases ventricular fibrillation susceptibility during myocardial ischemia-reperfusion.","authors":"Rui Huang, Xing Zhong, Pusong Tang, Qingning Huang, Xin Chen, Lu Ye, Dan Luo, Yaqin Yang, Yuhua Lei","doi":"10.1016/j.biopha.2024.117560","DOIUrl":"10.1016/j.biopha.2024.117560","url":null,"abstract":"<p><strong>Background: </strong>Acute myocardial ischemia/reperfusion injury (MIRI) with complicated mechanisms contributes to a high risk of ventricular arrhythmia, high lethality, and even sudden death. In vitro, Fraxinellone (FRA) exhibits an array of biologic activities and may possess cardioprotective effects. However, no relevant studies have examined FRA's protective potential against MIRI and related ventricular arrhythmias. The present study was undertaken to determine the effectiveness of FRA on MIRI and ventricular fibrillation (VF) susceptibility in rats and to elucidate the underlying mechanisms.</p><p><strong>Methods: </strong>48 healthy male Sprague-Dawley (SD) rats were randomly divided into the following four groups: Sham+vehicle(n=12), Sham+FRA(n=12), I/R+vehicle(n=12) and I/R+FRA(n=12). Histopathology, electrophysiological examination, HRV analysis in combination with molecular biology were used to investigate the therapeutic benefits of FRA on cardiac injury and VF susceptibility during myocardial IR. Finally, the potential mechanism by which FRA protects myocardium from MIRI was explored.</p><p><strong>Results: </strong>Pretreatment with FRA ameliorated myocardial fibrosis after MIRI in vivo, alleviated myocardial injury, inflammation, oxidative stress and apoptosis in vivo and in vitro, thereby protecting myocardium from MIRI injury. In addition, FRA administration could improve HRV, prolong ventricular effective refractory period (ERP) and action potential duration (APD), attenuate VF induction rate, and contribute to improving ventricular sympathetic nerve remodeling and ion channel remodeling. Mechanistically, FRA may reduce MIRI via the PI3K/AKT pathway.</p><p><strong>Conclusion: </strong>FRA may exert cardioprotective effects during MIRI by inhibiting myocardial inflammation, oxidative stress and apoptosis, and decrease VF susceptibility by improving sympathetic remodeling and ion channel remodeling, which might represent a potential therapeutic strategy for attenuation of MIRI.</p>","PeriodicalId":93904,"journal":{"name":"Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie","volume":"180 ","pages":"117560"},"PeriodicalIF":0.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142514590","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":"Liposomal formulation with thiazolic compounds against bacterial efflux pumps.","authors":"Ray Silva de Almeida, Priscilla Ramos Freitas, Ana Carolina Justino de Araujo, Saulo Relison Tintino, Jaime Ribeiro-Filho, Gustavo Marinho Miranda, Gustavo Miguel Sigueira, Sheila Alves Gonçalves, Diogo Teixeira Carvalho, Thiago Belarmino de Souza, Laís Regina Dos Santos Folquitto, Danielle Ferreira Dias, António Raposo, Ariana Saraiva, Heesup Han, Henrique Douglas Melo Coutinho","doi":"10.1016/j.biopha.2024.117600","DOIUrl":"10.1016/j.biopha.2024.117600","url":null,"abstract":"<p><p>This study aimed to evaluate the effects of liposome-encapsulated eugenol-based thiazolic derivatives against efflux pump-carrying bacteria. The Minimum Inhibitory Concentration (MIC) was determined to evaluate the antibacterial activity and antibiotic potentiation against Pseudomonas aeruginosa and Staphylococcus aureus, as well as to analyze the inhibition of efflux pumps in S. aureus strains 1199B and K2068 in the ethidium bromide assay. The direct antibacterial activity analysis showed no clinically relevant results since the compounds presented MICs ≥1024 µg/mL. Regarding the analysis of antibiotic potentiation against multidrug-resistant (MDR) strains of S. aureus, compound LF16 reduced norfloxacin MIC from 128 µg/mL to 64 µg/mL. All associated with gentamicin caused a significant antibiotic MIC reduction. None of the compounds could potentate the activity of norfloxacin against P. aeruginosa. However, all of them potentiated the activity of gentamicin against the same strain. Only the LF 26 caused a significant MIC reduction in the ethidium bromide assay, suggesting efflux inhibition in the S. aureus 1199B strain. Similar results were observed with the K2068 strain. Observing antibiotic MIC reduction S. aureus strains carrying the NorA and MepA proteins brought additional evidence of efflux pump inhibition. Our results indicate that while eugenol-based thiazoles didn't exhibit direct activity, they can potentiate the antibiotics activity against MDR strains of P. aeruginosa and S. aureus. Among them, compound LF 26 potentiated the inhibitory effects of ethidium bromide and antibiotics against S. aureus strains carrying the NorA and MepA proteins, indicating a potential role of this class of compounds as efflux pump inhibitors.</p>","PeriodicalId":93904,"journal":{"name":"Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie","volume":"180 ","pages":"117600"},"PeriodicalIF":0.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142549525","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}