{"title":"The natural statin α,β-dehydromonacolin K exerts anti-secretory effect in human intestinal epithelial cells via a nonsense-mediated mRNA decay-dependent mechanism.","authors":"Saravut Satitsri, Rungtiwa Khumjiang, Chittreeya Tansakul, Wararat Chiangjong, Nuttapon Apichaiyarat, Taya Kitiyakara, Yanisa Purintrapibal, Vatcharin Rukachaisirikul, Chatchai Muanprasat","doi":"10.1080/13880209.2025.2544930","DOIUrl":"https://doi.org/10.1080/13880209.2025.2544930","url":null,"abstract":"<p><strong>Context: </strong>cAMP-induced intestinal chloride secretion plays a pivotal role in the pathogenesis of secretory diarrheas.</p><p><strong>Objective: </strong>In this study, we investigated the antisecretory effects of α,β-dehydromonacolin K, a derivative of lovastatin from <i>Aspergillus sclerotiorum</i>, on cAMP-induced chloride secretion in human T84 cells and fluid secretion in human colonoids.</p><p><strong>Materials and methods: </strong>Short-circuit current analyses and swelling assays were used to investigate the effects of α,β-dehydromonacolin K on chloride transport and fluid secretion, respectively. Proteomic analyses were performed to determine the potential anti-diarrheal mechanisms of α,β-dehydromonacolin K.</p><p><strong>Results: </strong>In T84 cells, α,β-dehydromonacolin K inhibited cAMP-induced chloride secretion with an IC<sub>50</sub> of ∼ 6.32 μM. Apical chloride current analyses demonstrated that α,β-dehydromonacolin K inhibited CFTR chloride channels stimulated by cAMP agonists with an IC<sub>50</sub> of ∼ 1 μM. Basolateral potassium current analyses indicated that α,β-dehydromonacolin K had no effect on basolateral potassium channel activities. In a three-dimensional (3D) model of human colonoids, α,β-dehydromonacolin K (20 µM) suppressed both cAMP-induced and calcium-induced fluid secretion by ∼ 70%. Proteomic analyses of human colonoids revealed that α,β-dehydromonacolin K interacted with 33 proteins, including those associated with non-sense-mediated mRNA decay (NMD). Notably, the inhibitory effects of α,β-dehydromonacolin K on cAMP-induced chloride and fluid secretion were significantly diminished in the presence of SMG1i, an inhibitor of serine/threonine-protein kinase SMG1 involved in NMD, suggesting that α,β-dehydromonacolin K inhibits cAMP-induced chloride-driven fluid secretion in human intestinal epithelial cells by mechanisms involving SMG1-dependent NMD pathways.</p><p><strong>Discussion and conclusions: </strong>α, β-Dehydromonacolin K represents a promising class of natural compounds that exert antisecretory effects in human intestinal epithelia <i>via</i> a novel mechanism of action involving SMG1 in NMD pathways.</p>","PeriodicalId":19942,"journal":{"name":"Pharmaceutical Biology","volume":"63 1","pages":"645-662"},"PeriodicalIF":4.8,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12377102/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144964806","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}
Pharmaceutical BiologyPub Date : 2025-12-01Epub Date: 2025-08-01DOI: 10.1080/13880209.2025.2534573
Esraa M Abdelhady, Mohammed N A Khalil, Mohamed A Rabeh, Saad A Alshehri, Omar Sabry, Mona M Hashem
{"title":"Unveiling the cytotoxicity of Red Sea <i>Moorena producens via</i> LC-QTOF-MS/MS chemical profiling, network pharmacology, and molecular docking.","authors":"Esraa M Abdelhady, Mohammed N A Khalil, Mohamed A Rabeh, Saad A Alshehri, Omar Sabry, Mona M Hashem","doi":"10.1080/13880209.2025.2534573","DOIUrl":"10.1080/13880209.2025.2534573","url":null,"abstract":"<p><strong>Context: </strong>Breast and liver cancers remain significant global health challenges, necessitating the discovery of novel anticancer agents. Marine cyanobacteria, such as <i>Moorena producens</i> belonging to the family: Oscillatoriaceae, are rich sources of bioactive compounds with potential anticancer properties.</p><p><strong>Objective: </strong>This study aims to identify and characterize bioactive compounds from <i>M. producens</i> and evaluate their anticancer activity against breast and liver cancer cell lines.</p><p><strong>Materials and methods: </strong><i>M. producens</i> was collected and authenticated using 16S rRNA sequencing. The ethanolic extract was analyzed using LC-QTOF-MS/MS to identify the potential bioactive metabolites. Network pharmacology analysis was employed to predict the potential targets of these compounds. The crude extract was fractionated, and the fractions were screened for the anticancer activity against MCF-7 and HepG2 cell lines.</p><p><strong>Results: </strong>LC-QTOF-MS/MS analysis identified 25 metabolites, including apocarotenoids, spirovetivane alkaloids, and toxins. Network pharmacology analysis suggested that malyngamide D, isomalyngamide I, mueggelone, 11,12-didehydrospironostoic acid, and 12-hydroxy-2-oxo-11-epi-hinesol were potential bioactive compounds targeting proto-oncogene tyrosine-protein kinase (Src), mitogen-activated protein kinase 3(MAPK3), and MAPK1 kinases. Molecular docking studies further supported these findings, with 11,12-didehydrospironostoic acid exhibiting strong binding affinities to Src and MAPK1 kinases. Among the nine fractions obtained, Fraction 1 showed the most potent anticancer activity against both MCF-7 and HepG2 cell lines, with IC<sub>50</sub> values, 59.63 ± 7.1 and 149.23 ± 0.9 µg/mL, respectively.</p><p><strong>Discussion and conclusion: </strong>The results of this study highlight the potential of <i>M. producens</i> as a source of novel anticancer compounds. Further investigation of the bioactive compounds in Fractions 1 and 2 may lead to the discovery of promising anticancer agents.</p>","PeriodicalId":19942,"journal":{"name":"Pharmaceutical Biology","volume":"63 1","pages":"549-566"},"PeriodicalIF":4.8,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12320260/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144760678","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}
Pharmaceutical BiologyPub Date : 2025-12-01Epub Date: 2025-09-11DOI: 10.1080/13880209.2025.2555815
Algirdas Valys, Živilė Strazdaitė-Žielienė, Algirdas Mikalkėnas, Jurga Būdienė, Enrika Celitan, Saulius Serva, Elena Servienė
{"title":"Essential oils expose diverse targets on non-enveloped ScV-L-A totivirus.","authors":"Algirdas Valys, Živilė Strazdaitė-Žielienė, Algirdas Mikalkėnas, Jurga Būdienė, Enrika Celitan, Saulius Serva, Elena Servienė","doi":"10.1080/13880209.2025.2555815","DOIUrl":"10.1080/13880209.2025.2555815","url":null,"abstract":"<p><strong>Context: </strong>The spread of novel viruses substantiates the need for alternative antiviral agents. Plant-based extracts, such as essential oils (EOs), are highly relevant due to their generally human-friendly nature and broad spectrum of bioactive properties. Most EO antiviral activity is targeting enveloped viruses. <i>Orthototiviridae</i> family yeast virus ScV-L-A offers a novel, safe, non-enveloped virus model system for antiviral substance evaluation.</p><p><strong>Objective: </strong>This study aimed to investigate the antiviral efficacy of EOs and their constituents against non-enveloped ScV-L-A totivirus.</p><p><strong>Materials and methods: </strong>The composition of EOs was determined using GC-MS. Native ScV-L-A viral particles were prepared from yeast cells <i>via</i> cesium chloride gradient ultracentrifugation. The antiviral effect of EOs and their principal components was evaluated by following the synthesis of radio-labeled viral transcripts. TEM was employed to investigate the impact of target substances on ScV-L-A capsid integrity.</p><p><strong>Results: </strong>Tested EOs inhibited viral RNA polymerase activity in both liquid and vapor phases. Citral-rich EOs exhibited the strongest antiviral action, with lemon myrtle EO possessing the lowest half-maximal inhibitory concentration and highest timewise efficacy. Coriander and mandarin EOs showed the lowest polymerase-inhibiting capacity. EOs were more efficient compared to the action of single compounds. All EOs except for that of mandarin, dominated by limonene, were more effective in the liquid rather than the vapor phase. Tea tree and mandarin EOs were found to damage ScV-L-A capsid structure.</p><p><strong>Discussion and conclusion: </strong>This study highlighted the efficacy of EOs in targeting non-enveloped viruses and revealed their potential for sustainable control of viral infection.</p>","PeriodicalId":19942,"journal":{"name":"Pharmaceutical Biology","volume":"63 1","pages":"663-682"},"PeriodicalIF":4.8,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12427481/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145033979","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":"Naringenin inhibits ferroptosis to reduce radiation-induced lung injury: insights from network Pharmacology and molecular docking.","authors":"Junlin Jiang, Xianhui Deng, Chengkai Xu, Yaxian Wu, Jianfeng Huang","doi":"10.1080/13880209.2025.2465312","DOIUrl":"10.1080/13880209.2025.2465312","url":null,"abstract":"<p><strong>Context: </strong>Naringenin is a natural flavanone with potent pharmacological properties. It has demonstrated therapeutic potential in treating various diseases and organ injuries, including radiation-induced lung injury (RILI). Ferroptosis is a newly type of cell death, and naringenin has been shown to attenuates ferroptosis.</p><p><strong>Objective: </strong>To evaluate the inhibitory effect and molecular mechanism of naringenin on ferroptosis during RILI process.</p><p><strong>Materials & methods: </strong>Firstly, BEAS-2B and HUVECs cells were pre-incubated with naringenin for 1 h prior to 8 Gy of X-ray irradiation to evaluate oxidative stress, inflammation, and the mRNA levels of ferroptosis-related genes. Next, target genes of naringenin, RILI, and ferroptosis were identified using the TCMSP, SwissTargetPrediction, and GeneCards databases. The target network was constructed with Cytoscape and STRING. Finally, the core target genes were identified through <i>in vitro</i> experiments by qRT-PCR, western blot and immunofluorescence staining.</p><p><strong>Results: </strong>Naringenin effectively reduced radiation-induced increasement of oxidative stress, inflammation, and ferroptosis markers in both cell lines. Network pharmacology identified 14 target genes, with prostaglandin endoperoxide synthase (PTGS2) and Valosin-containing protein (VCP) mRNA levels being prominent, which were crucial for ferroptosis regulation. Molecular docking revealed strong binding interactions between naringenin and the two target proteins. Subsequently, experimental validation confirmed that naringenin reduced the elevated levels of PTGS2 and VCP induced by radiation.</p><p><strong>Discussion & conclusion: </strong>Naringenin alleviates radiation-induced lung damage by inhibiting ferroptosis, with PTGS2 and VCP emerging as potential therapeutic targets.</p>","PeriodicalId":19942,"journal":{"name":"Pharmaceutical Biology","volume":"63 1","pages":"1-10"},"PeriodicalIF":3.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11841155/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143449905","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}
Pharmaceutical BiologyPub Date : 2025-12-01Epub Date: 2025-02-25DOI: 10.1080/13880209.2025.2469607
Zhebin Xiang, Bo Ma, Xiujun Pei, Wenjie Wang, Weilun Gong
{"title":"Mechanism of action of genistein on breast cancer and differential effects of different age stages.","authors":"Zhebin Xiang, Bo Ma, Xiujun Pei, Wenjie Wang, Weilun Gong","doi":"10.1080/13880209.2025.2469607","DOIUrl":"10.1080/13880209.2025.2469607","url":null,"abstract":"<p><strong>Context: </strong>Genistein, a soy-derived isoflavone, exhibits structural similarities with 17β-estradiol and demonstrates antioxidant, anti-inflammatory, and estrogenic properties. Despite its low bioavailability limiting its clinical application, it shows potential for breast cancer prevention and treatment.</p><p><strong>Objective: </strong>This review aims to summarize the pharmacological effects and molecular mechanisms of genistein in breast cancer, focusing on its therapeutic potential, strategies to overcome bioavailability limitations, and its role in personalized medicine. Differential impacts among population subgroups are also discussed.</p><p><strong>Methods: </strong>A systematic review was conducted using PubMed, ScienceDirect, and Google Scholar databases. Studies were selected based on their focus on genistein's mechanisms of action, strategies to enhance its bioavailability, and interactions with other therapies.</p><p><strong>Results: </strong>Genistein exerted anticancer effects by modulating estrogen receptor β (ERβ), inhibiting angiogenesis, arresting the cell cycle, and inducing apoptosis. Its antioxidant properties help mitigate tumor-associated oxidative stress. Bioavailability enhancement strategies, such as nanoparticle and lipid-based formulations, show promise. Age-dependent effects were evident, with distinct responses observed in prepubertal, menopausal, and postmenopausal populations, underscoring its potential for personalized therapies. Furthermore, genistein influences epigenetic modifications, including DNA methylation and miRNA expression, bolstering its anticancer efficacy.</p><p><strong>Conclusion: </strong>Genistein is a promising candidate for breast cancer therapy, particularly for personalized treatment. Strategies to enhance bioavailability and further clinical research are essential to optimize its therapeutic potential and evaluate its efficacy in combination therapies.</p>","PeriodicalId":19942,"journal":{"name":"Pharmaceutical Biology","volume":"63 1","pages":"141-155"},"PeriodicalIF":3.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11864014/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143493093","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":"Harmine derivative H-2-168 induces the death of <i>Echinococcus granulosus</i> by regulating mitochondrial fusion and fission.","authors":"Yuehong Gong, Meiling Zhao, Meichi Pan, Yicong Zhao, Junpeng Liu, Hao Wen, Jianhua Wang","doi":"10.1080/13880209.2025.2485898","DOIUrl":"10.1080/13880209.2025.2485898","url":null,"abstract":"<p><strong>Context: </strong>H-2-168 has pharmacological effects similar to those of harmine, with less toxicity. The health of cells and organisms depends on a delicate balance between mitochondrial fusion and fission.</p><p><strong>Objective: </strong>This study investigated the roles of H-2-168 and mitochondrial fusion and fission in <i>Echinococcus granulosus</i>.</p><p><strong>Materials and methods: </strong>Notably, <i>E. granulosus</i> were isolated from fresh sheep livers, and then treated with H-2-168 (25 μg/mL), mitochondrial division inhibitor 1 (Mdivi-1, 25 μg/mL) or the combination of H-2-168:Mdivi-1 (25 μg/mL:12.5 μg/mL). After 24 h of culture, the indices related to <i>E. granulosus</i> were measured. Additionally, Drp1 was knocked down to explore its effects on <i>E. granulosus</i> growth.</p><p><strong>Results: </strong>The EC<sub>50</sub> values of H-2-168, Mdivi-1 and H-2-168:Mdivi-1 against <i>E. granulosus</i> were 44.171, 117.882 and 32.924 μg/mL, respectively. Compared with H-2-168 or Mdivi-1, the combination of H-2-168 and Mdivi-1 showed better inhibitory effects on <i>E. granulosus</i> viability, as well as increased levels of ROS and LDH, decreased ATP levels, inhibited mitochondrial activity and reduced mitochondrial membrane potential (<i>p</i> < 0.05), with the upregulation of Caspase-3, Cyt-c, Drp1, Fis1 and downregulation of Bcl-2, Mfn2 and OPA1. Additionally, <i>Drp1</i> knockdown was successfully performed in <i>E. granulosus</i>, which significantly inhibited <i>E. granulosus</i> viability (<i>p</i> < 0.05) and further downregulated Mfn2 expression induced by H-2-168.</p><p><strong>Discussion and conclusion: </strong><i>Drp1</i> is closely associated with mitochondrial fusion and fission, and H-2-168 may promote <i>E. granulosus</i> death through disrupting the balance between mitochondrial fusion and fission.</p>","PeriodicalId":19942,"journal":{"name":"Pharmaceutical Biology","volume":"63 1","pages":"188-200"},"PeriodicalIF":3.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11980216/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143795892","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}
Pharmaceutical BiologyPub Date : 2025-12-01Epub Date: 2025-07-24DOI: 10.1080/13880209.2025.2537123
Lu Chen, Yuting Xia, Liangliang Min, Yuqin Zhang, Da Huang, Yulu Zhang, Aihua You, Zhihua Li
{"title":"Sophoridine inhibits proliferation and migration by targeting PIM1 in breast cancer.","authors":"Lu Chen, Yuting Xia, Liangliang Min, Yuqin Zhang, Da Huang, Yulu Zhang, Aihua You, Zhihua Li","doi":"10.1080/13880209.2025.2537123","DOIUrl":"10.1080/13880209.2025.2537123","url":null,"abstract":"<p><strong>Context: </strong>Sophoridine, an alkaloid quinolizidine derived from <i>Sophora flavescens</i> Aiton (Fabaceae), has strong anti-tumor activity in a variety of malignancies. Nevertheless, the effects and underlying mechanism of sophoridine on breast cancer are not fully understood.</p><p><strong>Objective: </strong>To identify the key targets and potential pharmacological mechanisms of sophoridine against breast cancer.</p><p><strong>Materials and methods: </strong>MCF-10A, MCF-7 and MDA-MB-231 cells were treated with sophoridine for 24 or 48 h. MTT, colony formation assay, flow cytometry, wound healing, and Transwell assay were employed to illustrate the anti-tumor effects of sophoridine on breast cancer. Network pharmacology and molecular docking were used to determine the targets for sophoridine in breast cancer, and confirmed by molecular dynamics simulation and CETSA-western blot assay. Additionally, the functional rescue and signaling pathway regulated by sophoridine was analyzed.</p><p><strong>Results: </strong>Sophoridine suppressed the proliferation, migration, and invasion of breast cancer cells. The IC<sub>50</sub> value of sophoridine for 48 h in MCF-10A, MCF-7 and MDA-MB-231 was 363 μM, 87.96 μM and 81.07 μM, respectively. PIM1 was the key target for sophoridine in breast cancer. Furthermore, PIM1 overexpression significantly reversed the suppressive impacts of sophoridine on growth and migration in breast cancer cells. Mechanistically, sophoridine inhibited the phosphorylation of ASK1 and activated JNK/p38 MAPK signaling pathway by downregulating PIM1 expression, and thus exhibited anti-tumor effects.</p><p><strong>Discussion and conclusion: </strong>Taken together, sophoridine relies on targeting PIM1 to inhibit cell proliferation and migration in breast cancer, which might be related to the activation of ASK1/MAPK axis, suggesting the therapeutic potential of sophoridine for breast cancer.</p>","PeriodicalId":19942,"journal":{"name":"Pharmaceutical Biology","volume":"63 1","pages":"503-523"},"PeriodicalIF":4.8,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12302398/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144708387","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":"Qing-Xin-Jie-Yu Granule attenuates myocardial infarction-induced inflammatory response by regulating the MK2/TTP pathway.","authors":"Jianghan Qi, Xiaoyao Gao, Ying Han, Meiling Yang, Chenyi Wei, Ling Zhang, Jianfeng Chu","doi":"10.1080/13880209.2025.2467377","DOIUrl":"10.1080/13880209.2025.2467377","url":null,"abstract":"<p><strong>Context: </strong>Qing-Xin-Jie-Yu Granule (QXJYG) has shown promise in the treatment of myocardial infarction. However, the mechanism of action of QXJYG underlying its anti-inflammation remain unknown.</p><p><strong>Objective: </strong>The study aimed to evaluate the effectiveness and mechanism of QXJYG in a mouse model of myocardial infarction and hypoxia-induced H9C2 cells.</p><p><strong>Materials and methods: </strong>Myocardial infarction was induced in mice <i>via</i> left anterior descending coronary artery ligation, and hypoxia-induced H9C2 cells was served as the <i>in vitro</i> model. The cardiac function was evaluated by echocardiography, while myocardial tissue pathology was examined using HE and Masson's trichrome staining. Changes in serum markers of cardiac injury were measured using ELISA kits. The levels of inflammatory cytokines in both the serum and cardiac tissue were quantified using the Bio-Plex Pro Mouse Chemokine assay, and hypoxia-induced inflammatory factors in H9C2 cells were assessed by RT-qPCR. Additionally, western blot analysis was conducted to evaluate the expression of proteins related to the MK2/TTP signaling pathway both <i>in vivo</i> and <i>in vitro</i> experiments.</p><p><strong>Results: </strong>QXJYG significantly enhanced cardiac function in mice with myocardial infarction, as evidenced by improved myocardial tissue structure, reduced collagen fiber deposition, and lowered serum levels of creatine kinase isoenzyme MB (CK-MB), cardiac Troponin T (cTnT), and brain Natriuretic Peptide (BNP). QXJYG may reduce the expression of inflammatory factors in both the heart and serum of myocardial infarction-induced mice and attenuate hypoxia-induced levels of inflammatory factors in cardiomyocytes by decreasing the ratio of p-MK2/MK2 and increasing the protein expression of TTP.</p><p><strong>Discussion and conclusions: </strong>QXJYG improved cardiac function and reduced injury, fibrosis, and inflammation after myocardial infarction, likely through modulation of the MK2/TTP signaling pathway.</p>","PeriodicalId":19942,"journal":{"name":"Pharmaceutical Biology","volume":"63 1","pages":"128-140"},"PeriodicalIF":3.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11849043/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143468813","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}
Pharmaceutical BiologyPub Date : 2025-12-01Epub Date: 2025-07-15DOI: 10.1080/13880209.2025.2530995
Jason Valmy, Stephanie Greenfield, Satoru Shindo, Toshihisa Kawai, Jorge Cervantes, Bo-Young Hong
{"title":"Anti-inflammatory effect of chamomile from randomized clinical trials: a systematic review and meta-analyses.","authors":"Jason Valmy, Stephanie Greenfield, Satoru Shindo, Toshihisa Kawai, Jorge Cervantes, Bo-Young Hong","doi":"10.1080/13880209.2025.2530995","DOIUrl":"10.1080/13880209.2025.2530995","url":null,"abstract":"<p><strong>Context: </strong>Chamomile is a widely recognized medicinal herb, and it has been used for its various medicinal properties. Chamomile's widespread recognition and application in medicine highlights its significance in herbal therapeutic practices globally.</p><p><strong>Objective: </strong>To explore chamomile as a low-risk antimicrobial and anti-inflammatory agent, utilizing clinical characteristics derived from the existing body of evidence from randomized clinical trials within the current literature.</p><p><strong>Methods: </strong>We conducted a systematic review of randomized clinical trials using the search terms 'chamomile anti-inflammatory antimicrobial randomized clinical trials' and 'chamomile anti-inflammatory antimicrobial'. We sourced data from databases including PubMed, Google Scholar, Cochrane Library, and ClinicalTrials.gov. We then performed a meta-analysis using R to assess the efficacy of chamomile as an anti-inflammatory and an antimicrobial agent, and its impact on mucosal recovery in clinical settings.</p><p><strong>Results: </strong>A total of 11 randomized clinical trials were identified. The mean difference, confidence intervals, and standard error from the extracted means and standard deviations for relevant outcomes were calculated. Statistical tests from the meta-analysis demonstrated that chamomile exhibited statistically significant reductions in mucositis severity and pain level, indicating the anti-inflammatory effects of chamomile.</p><p><strong>Conclusion: </strong>This study highlights chamomile's potential as a natural alternative for managing inflammation and microbial infections, offering a promising alternative to standard treatments. Our study suggests chamomile has the potential to act as a natural anti-inflammatory agent. A future study with a larger sample size may provide clinical evidence of this effect.</p><p><p><b>Systematic review registration number (PROSPERO):</b> CRD42024566615.</p>","PeriodicalId":19942,"journal":{"name":"Pharmaceutical Biology","volume":"63 1","pages":"490-502"},"PeriodicalIF":3.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12269088/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144643156","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":"Anti-aging potential of <i>Monascus purpureus</i> pigments in skin care.","authors":"Rittipun Rungruang, Tasanee Panichakul, Napassorn Peasura, Sasithorn Kongruang","doi":"10.1080/13880209.2025.2557983","DOIUrl":"10.1080/13880209.2025.2557983","url":null,"abstract":"<p><strong>Context: </strong>Natural pigments derived from microbial sources are garnering increasing attention owing to their multifunctional roles in cosmetic and biomedical applications.</p><p><strong>Objective: </strong>We investigated the antioxidant and biological activities of biocolor extracts of <i>Monascus purpureus</i> cultivated in potato dextrose broth supplemented with 1% Tubtim chumphae (<i>Oryza sativa</i> L., Poaceae) broken rice (MPTR).</p><p><strong>Materials and methods: </strong><i>M. purpureus</i> TISTR 3615 pigment yield and quality under fermentation conditions with and without 1% Tubtim chumphae broken rice were examined. Liquid chromatography was performed to determine and quantify the key components of the extracts. The biological activities of the extracts were investigated using antioxidant and enzyme inhibition assays. Cell viability assay was performed to determine the safety of the extracts on human dermal fibroblasts. Furthermore, cellular collagen and elastin production promoted by the extracts was also investigated.</p><p><strong>Results: </strong>Notably, MPTR extract demonstrated superior pigment production compared with conventional potato dextrose broth cultured fungi. MPTR extract exhibited potent antioxidant properties and was non-cytotoxic to human skin fibroblasts at concentrations up to 0.5 mg/mL. MPTR extract effectively inhibited collagenase and elastase enzymes, and induced cellular collagen type I and elastin production. Moreover, MPTR extract promoted wound healing, significantly reducing the wound area by up to 90% within 48 h.</p><p><strong>Discussion and conclusion: </strong>MPTR extract from <i>M. purpureus</i> TISTR 3615 fermented with broken rice exhibited antioxidant properties as well as collagenase and elastase inhibitory activities, and promoted cellular collagen type I and elastin production. MPTR extract is a promising skin anti-aging agent for cosmetic and cosmeceutical applications.</p>","PeriodicalId":19942,"journal":{"name":"Pharmaceutical Biology","volume":"63 1","pages":"683-697"},"PeriodicalIF":4.8,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12447460/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145081268","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}