Pharmacological Reports最新文献

{"title":"Loop diuretics inhibit kynurenic acid production and kynurenine aminotransferases activity in rat kidneys","authors":"Izabela Zakrocka, Katarzyna M. Targowska-Duda, Tomasz Kocki, Waldemar Turski, Ewa M. Urbańska, Wojciech Załuska","doi":"10.1007/s43440-024-00648-8","DOIUrl":"https://doi.org/10.1007/s43440-024-00648-8","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Background</h3><p>Loop diuretics became a cornerstone in the therapy of hypervolemia in patients with chronic kidney disease or heart failure. Apart from the influence on water and electrolyte balance, these drugs were shown to inhibit tissue fibrosis and renin-angiotensin-system activity. The kynurenine (KYN) pathway products are suggested to be uremic toxins. Kynurenic acid (KYNA) is synthesized by kynurenine aminotransferases (KATs) in the brain and periphery. The cardiovascular and renal effects of KYNA are well documented. However, high KYNA levels have been correlated with the rate of kidney damage and its complications. Our study aimed to assess the effect of loop diuretics, ethacrynic acid, furosemide, and torasemide on KYNA synthesis and KATs activity in rat kidneys in vitro.</p><h3 data-test=\"abstract-sub-heading\">Methods</h3><p>Quantitative analyses of KYNA were performed using fluorimetric HPLC detection. Additionally, molecular docking studies determined the possible interactions of investigated compounds with an active site of KAT I and KAT II.</p><h3 data-test=\"abstract-sub-heading\">Results</h3><p>All studied drugs inhibited KYNA production in rat kidneys in vitro at 0.5–1.0 mmol/l concentrations. Only ethacrynic acid at 1.0 mmol/l concentration significantly lowered KAT I and KAT II activity in kidney homogenates, whereas other drugs were ineffective. Molecular docking results indicated the common binding site for each of the studied loop diuretics and KYNA. They suggested possible residues involved in their binding to the active site of both KAT I and KAT II model.</p><h3 data-test=\"abstract-sub-heading\">Conclusions</h3><p>Our study reveals that loop diuretics may decrease KYNA synthesis in rat kidneys in vitro. The presented results warrant further research in the context of KYN pathway activity regulation by loop diuretics.</p><h3 data-test=\"abstract-sub-heading\">Graphical abstract</h3>\u0000","PeriodicalId":19947,"journal":{"name":"Pharmacological Reports","volume":"65 1","pages":""},"PeriodicalIF":4.4,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142179973","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}

{"title":"Disrupted glutamate homeostasis as a target for glioma therapy","authors":"Mikołaj Biegański, Monika Szeliga","doi":"10.1007/s43440-024-00644-y","DOIUrl":"https://doi.org/10.1007/s43440-024-00644-y","url":null,"abstract":"<p>Glutamate is the major excitatory neurotransmitter in the central nervous system (CNS). Gliomas, malignant brain tumors with a dismal prognosis, alter glutamate homeostasis in the brain, which is advantageous for their growth, survival, and invasion. Alterations in glutamate homeostasis result from its excessive production and release to the extracellular space. High glutamate concentration in the tumor microenvironment destroys healthy tissue surrounding the tumor, thus providing space for glioma cells to expand. Moreover, it confers neuron hyperexcitability, leading to epilepsy, a common symptom in glioma patients. This mini-review briefly describes the biochemistry of glutamate production and transport in gliomas as well as the activation of glutamate receptors. It also summarizes the current pre-clinical and clinical studies identifying pharmacotherapeutics targeting glutamate transporters and receptors emerging as potential therapeutic strategies for glioma.</p>","PeriodicalId":19947,"journal":{"name":"Pharmacological Reports","volume":"8 1","pages":""},"PeriodicalIF":4.4,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142179975","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}

{"title":"Association analysis of ADRB3:rs4994 with urodynamic outcome, six months after a single intra-detrusor injection of botulinum toxin, in women with overactive bladder","authors":"Sylwester Ciećwież, Klaudyna Lewandowska, Aleksandra Szylińska, Agnieszka Boroń, Dariusz Kotlęga, Jacek Kociszewski, Agnieszka Brodowska, Jeremy S.C. Clark, Andrzej Ciechanowicz","doi":"10.1007/s43440-024-00647-9","DOIUrl":"https://doi.org/10.1007/s43440-024-00647-9","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Background</h3><p>Intra-detrusor injection of botulinum neurotoxin type A (BoNT/A) is recommended as a possible treatment for patients with overactive bladder (OAB) in whom first-line therapies have failed. The c.190T &gt; C (rs4994) polymorphism in the gene encoding the beta-3 adrenergic receptor (<i>ADRB3</i>) has been suggested to be associated with predisposition to OAB or with response to OAB treatment via a cholinergic muscarinic receptor antagonist. This prospective study aimed to use a urodynamic parameter-based assessment of response, six months after a single intra-detrusor injection of BoNT/A in female OAB patients, to elucidate possible association with the <i>ADRB3</i> polymorphism.</p><h3 data-test=\"abstract-sub-heading\">Methods</h3><p>The study group consisted of 138 consecutive, Polish, adult, female OAB patients. Urodynamic parameters were recorded before injection of BoNT/A and at six months after administration. <i>ADRB3</i>:rs4994 variants were identified by the sequencing of genomic DNA extracted from buccal swabs.</p><h3 data-test=\"abstract-sub-heading\">Results</h3><p>Apart from baseline, and relative, increase in Maximum Cystometric Capacity (MCC) six months after BoNT/A injection, no significant differences were found in urodynamic parameters between reference TT homozygotes and women with at least one C allele.</p><h3 data-test=\"abstract-sub-heading\">Conclusions</h3><p>Our results do not exclude that <i>ADRB3</i>:rs4994 variants are associated with a positive urodynamic test-based response to intra-detrusor injection of BoNT/A in females with OAB.</p>","PeriodicalId":19947,"journal":{"name":"Pharmacological Reports","volume":"83 1","pages":""},"PeriodicalIF":4.4,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142179974","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}

{"title":"A hydrogen sulphide-releasing non-steroidal anti-inflammatory, ATB-346, significantly attenuates human myometrial contractions.","authors":"Ana Mijušković, Susan Wray, Sarah Arrowsmith","doi":"10.1007/s43440-024-00643-z","DOIUrl":"https://doi.org/10.1007/s43440-024-00643-z","url":null,"abstract":"<p><strong>Background: </strong>Spontaneous preterm birth is the leading cause of perinatal morbidity and mortality. Tocolytics are drugs used to inhibit uterine contractions in cases of imminent preterm birth, however, few are effective in stopping labour once initiated and all have side effects. Combination approaches involving drugs that target multiple signalling pathways that regulate contractions may increase efficacy, reduce dosage and improve tolerability. Both non-steroidal anti-inflammatory drugs (NSAIDs) and hydrogen sulphide (H₂S)-releasing compounds can reduce myometrial contractions. In a novel approach we evaluated the tocolytic properties of ATB-346-a H₂S-releasing derivative of the NSAID naproxen, shown clinically to reduce pain and inflammation in arthritis.</p><p><strong>Methods: </strong>Using organ baths, paired strips of human myometrium were exposed to increasing concentrations of ATB-346, or equimolar concentrations (10µM and 30µM) of the parent drug, naproxen, or the H₂S-releasing moiety, 4-hydroxy-thiobenzamide (TBZ), alone. The ability of ATB-346 versus the individual components of ATB-346 to decrease ex vivo spontaneous contractions was investigated, and the potency was compared to a known H₂S donor, Na₂S.</p><p><strong>Results: </strong>Acute application of Na₂S produced a concentration-dependent decrease in force amplitude and force integral (area under the curve) of contraction. ATB-346 produced a more profound decrease in contraction compared to equimolar concentrations of naproxen or TZB alone and was more potent than the equivalent concentration of Na₂S.</p><p><strong>Conclusions: </strong>ATB-346 exhibits potent tocolytic properties in human myometrium. These exciting results call for further exploration of ATB-346, with a view to repurposing this or similar drugs as novel therapies for delaying preterm labour.</p>","PeriodicalId":19947,"journal":{"name":"Pharmacological Reports","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142133443","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}

{"title":"Nanoformulation of dasatinib cannot overcome therapy resistance of pancreatic cancer cells with low LYN kinase expression.","authors":"Marilyn Kaul, Ahmed Y Sanin, Wenjie Shi, Christoph Janiak, Ulf D Kahlert","doi":"10.1007/s43440-024-00600-w","DOIUrl":"10.1007/s43440-024-00600-w","url":null,"abstract":"<p><strong>Background: </strong>Pancreatic ductal adenocarcinoma (PDAC) is one of the most difficult to treat tumors. The Src (sarcoma) inhibitor dasatinib (DASA) has shown promising efficacy in preclinical studies of PDAC. However, clinical confirmation could not be achieved. Overall, our aim was to deliver arguments for the possible reinitiating clinical testing of this compound in a biomarker-stratifying therapy trial for PDAC patients. We tested if the nanofunctionalization of DASA can increase the drug efficacy and whether certain Src members can function as clinical predictive biomarkers.</p><p><strong>Methods: </strong>Methods include manufacturing of poly(vinyl alcohol) stabilized gold nanoparticles and their drug loading, dynamic light scattering, transmission electron microscopy, thermogravimetric analysis, Zeta potential measurement, sterile human cell culture, cell growth quantification, accessing and evaluating transcriptome and clinical data from molecular tumor dataset TCGA, as well as various statistical analyses.</p><p><strong>Results: </strong>We generated homo-dispersed nanofunctionalized DASA as an AuNP@PVA-DASA conjugate. The composite did not enhance the anti-growth effect of DASA on PDAC cell lines. The cell model with high LYN expression showed the strongest response to the therapy. We confirm deregulated Src kinetome activity as a prevalent feature of PDAC by revealing mRNA levels associated with higher malignancy grade of tumors. BLK (B lymphocyte kinase) expression predicts shorter overall survival of diabetic PDAC patients.</p><p><strong>Conclusions: </strong>Nanofunctionalization of DASA needs further improvement to overcome the therapy resistance of PDAC. LYN mRNA is augmented in tumors with higher malignancy and can serve as a predictive biomarker for the therapy resistance of PDAC cells against DASA. Studying the biological roles of BLK might help to identify underlying molecular mechanisms associated with PDAC in diabetic patients.</p>","PeriodicalId":19947,"journal":{"name":"Pharmacological Reports","volume":" ","pages":"793-806"},"PeriodicalIF":3.6,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11294441/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140911955","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}

{"title":"The role of glucagon-like peptide-1/GLP-1R and autophagy in diabetic cardiovascular disease.","authors":"Zi Guo","doi":"10.1007/s43440-024-00609-1","DOIUrl":"10.1007/s43440-024-00609-1","url":null,"abstract":"<p><p>Diabetes leads to a significantly accelerated incidence of various related macrovascular complications, including peripheral vascular disease and cardiovascular disease (the most common cause of mortality in diabetes), as well as microvascular complications such as kidney disease and retinopathy. Endothelial dysfunction is the main pathogenic event of diabetes-related vascular disease at the earliest stage of vascular injury. Understanding the molecular processes involved in the development of diabetes and its debilitating vascular complications might bring up more effective and specific clinical therapies. Long-acting glucagon-like peptide (GLP)-1 analogs are currently available in treating diabetes with widely established safety and extensively evaluated efficacy. In recent years, autophagy, as a critical lysosome-dependent self-degradative process to maintain homeostasis, has been shown to be involved in the vascular endothelium damage in diabetes. In this review, the GLP-1/GLP-1R system implicated in diabetic endothelial dysfunction and related autophagy mechanism underlying the pathogenesis of diabetic vascular complications are briefly presented. This review also highlights a possible crosstalk between autophagy and the GLP-1/GLP-1R axis in the treatment of diabetic angiopathy.</p>","PeriodicalId":19947,"journal":{"name":"Pharmacological Reports","volume":" ","pages":"754-779"},"PeriodicalIF":3.6,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141420366","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}

{"title":"Luteolin for neurodegenerative diseases: a review.","authors":"Dunuvilla Kavindi Jayawickreme, Cletus Ekwosi, Apurva Anand, Marta Andres-Mach, Piotr Wlaź, Katarzyna Socała","doi":"10.1007/s43440-024-00610-8","DOIUrl":"10.1007/s43440-024-00610-8","url":null,"abstract":"<p><p>Neurodegenerative diseases such as Parkinson's disease, Alzheimer's disease, Huntington's disease, and multiple sclerosis affect millions of people around the world. In addition to age, which is a key factor contributing to the development of all neurodegenerative diseases, genetic and environmental components are also important risk factors. Current methods of treating neurodegenerative diseases are mostly symptomatic and do not eliminate the cause of the disease. Many studies focus on searching for natural substances with neuroprotective properties that could be used as an adjuvant therapy in the inhibition of the neurodegeneration process. These compounds include flavonoids, such as luteolin, showing significant anti-inflammatory, antioxidant, and neuroprotective activity. Increasing evidence suggests that luteolin may confer protection against neurodegeneration. In this review, we summarize the scientific reports from preclinical in vitro and in vivo studies regarding the beneficial effects of luteolin in neurodegenerative diseases. Luteolin was studied most extensively in various models of Alzheimer's disease but there are also several reports showing its neuroprotective effects in models of Parkinson's disease. Though very limited, studies on possible protective effects of luteolin against Huntington's disease and multiple sclerosis are also discussed here. Overall, although preclinical studies show the potential benefits of luteolin in neurodegenerative disorders, clinical evidence on its therapeutic efficacy is still deficient.</p>","PeriodicalId":19947,"journal":{"name":"Pharmacological Reports","volume":" ","pages":"644-664"},"PeriodicalIF":3.6,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11294387/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141432478","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}

{"title":"Effects of carvedilol on human prostate tissue contractility and stromal cell growth pointing to potential clinical implications.","authors":"Sheng Hu, A Elif Müderrisoglu, Anna Ciotkowska, Oluwafemi Kale, Patrick Keller, Melanie Schott, Alexander Tamalunas, Raphaela Waidelich, Christian G Stief, Martin Hennenberg","doi":"10.1007/s43440-024-00605-5","DOIUrl":"10.1007/s43440-024-00605-5","url":null,"abstract":"<p><strong>Background: </strong>Apart from antagonizing ß-adrenoceptors, carvedilol antagonizes vascular α₁-adrenoceptors and activates G protein-independent signaling. Even though it is a commonly used antihypertensive and α₁-adrenoceptors are essential for the treatment of voiding symptoms in benign prostatic hyperplasia, its actions in the human prostate are still unknown. Here, we examined carvedilol effects on contractions of human prostate tissues, and on stromal cell growth.</p><p><strong>Methods: </strong>Contractions of prostate tissues from radical prostatectomy were induced by electric field stimulation (EFS) or α₁-agonists. Growth-related functions were examined in cultured stromal cells.</p><p><strong>Results: </strong>Concentration-response curves for phenylephrine, methoxamine and noradrenaline were right shifted by carvedilol (0.1-10 µM), around half a magnitude with 100 nM, half to one magnitude with 1 µM, and two magnitudes with 10 µM. Right shifts were reflected by increased EC₅₀ values for agonists, with unchanged E_max values. EFS-induced contractions were reduced by 21-54% with 0.01-1 µM carvedilol, and by 94% by 10 µM. Colony numbers of stromal cells were increased by 500 nM, but reduced by 1-10 µM carvedilol, while all concentrations reduced colony size. Decreases in viability were time-dependent with 0.1-0.3 µM, but complete with 10 µM. Proliferation was slightly increased by 0.1-0.5 µM, but reduced with 1-10 µM.</p><p><strong>Conclusions: </strong>Carvedilol antagonizes α₁-adrenoceptors in the human prostate, starting with concentrations in ranges of known plasma levels. In vitro, effect sizes resemble those of α₁-blockers used for the treatment of voiding symptoms, which requires concentrations beyond plasma levels. Bidirectional and dynamic effects on the growth of stromal cells may be attributed to \"biased agonism\".</p>","PeriodicalId":19947,"journal":{"name":"Pharmacological Reports","volume":" ","pages":"807-822"},"PeriodicalIF":3.6,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11294394/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141301312","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}

{"title":"β-Carboline derivatives are potent against Acute Myeloid Leukemia in vitro and in vivo.","authors":"Maura Lima Pereira Bueno, Mary Ann Foglio, Paula Baréa, Aline Rufino de Oliveira, Maria Helena Sarragiotto, Sara T Olalla Saad, Fernanda Marconi Roversi","doi":"10.1007/s43440-024-00614-4","DOIUrl":"10.1007/s43440-024-00614-4","url":null,"abstract":"<p><strong>Background: </strong>β-carboline alkaloids exert a distinguished ability to impair cell growth and induce cell death in a variety of cancers and the evaluation of such new therapeutic candidates may denote new possibilities for leukemia treatment. In this present study, we screened 12 β-carboline derivatives containing different substituents at 1- and 3-positions of β-carboline nucleus for their antineoplastic activities in a panel of leukemia cell lines.</p><p><strong>Methods: </strong>The cytotoxic effects of the β-carboline derivatives were evaluated in different leukemia cell lines as well as reactive oxygen species (ROS) generation, autophagy, and important signaling pathways.</p><p><strong>Results: </strong>Treatment with the β-carboline derivatives resulted in a potent antineoplastic activity leading to a reduced cell viability that was associated with increased cell death in a concentration-dependent manner. Interestingly, the treatment of primary mononuclear cells isolated from the peripheral blood of healthy donors with the β-carboline derivatives showed a minor change in cell survival. The antineoplastic activity occurs by blocking ROS production causing consequent interruption of the PI3K/AKT and MAPK/ERK signaling and modulating autophagy processes. Notably, in vivo, AML burden was diminished in peripheral blood and bone marrow of a xenograft mouse model.</p><p><strong>Conclusions: </strong>Our results indicated that β-carboline derivatives have an on-target malignant cell-killing activity and may be promising candidates for treating leukemia cells by disrupting crucial events that promote leukemia expansion and chemotherapy resistance.</p>","PeriodicalId":19947,"journal":{"name":"Pharmacological Reports","volume":" ","pages":"838-850"},"PeriodicalIF":3.6,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141432480","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}

{"title":"In vitro biological evaluation of a novel folic acid-targeted receptor quantum dot-β-cyclodextrin carrier for C-2028 unsymmetrical bisacridine in the treatment of human lung and prostate cancers.","authors":"Joanna Pilch, Agnieszka Potęga, Patrycja Kowalik, Agata Kowalczyk, Piotr Bujak, Artur Kasprzak, Ewa Paluszkiewicz, Anna Maria Nowicka","doi":"10.1007/s43440-024-00606-4","DOIUrl":"10.1007/s43440-024-00606-4","url":null,"abstract":"<p><strong>Background: </strong>Traditional small-molecule chemotherapeutics usually do not distinguish tumors from healthy tissues. However, nanotechnology creates nanocarriers that selectively deliver drugs to their site of action. This work is the next step in the development of the quantum dot-β-cyclodextrin-folic acid (QD-β-CD-FA) platform for targeted and selected delivery of C-2028 unsymmetrical bisacridine in cancer therapy.</p><p><strong>Methods: </strong>Herein, we report an initial biological evaluation (using flow cytometry and light microscopy) as well as cell migration analysis of QD-β-CD(C-2028)-FA nanoconjugate and its components in the selected human lung and prostate cancer cells, as well as against their respective normal cells.</p><p><strong>Results: </strong>C-2028 compound induced apoptosis, which was much stronger in cancer cells compared to normal cells. Conjugation of C-2028 with QD_green increased cellular senescence, while the introduction of FA to the conjugate significantly decreased this process. C-2028 nanoencapsulation also reduced cell migration. Importantly, QD_green and QD_green-β-CD-FA themselves did not induce any toxic responses in studied cells.</p><p><strong>Conclusions: </strong>In conclusion, the results demonstrate the high potential of a novel folic acid-targeted receptor quantum dot-β-cyclodextrin carrier (QD_green-β-CD-FA) for drug delivery in cancer treatment. Nanoplatforms increased the amount of delivered compounds and demonstrated high suitability.</p>","PeriodicalId":19947,"journal":{"name":"Pharmacological Reports","volume":" ","pages":"823-837"},"PeriodicalIF":3.6,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11294431/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141420365","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}