Chemico-biological interactions最新文献_第2页

The biological potential and health-benefits of flavonoids: A review and development opportunities. 黄酮类化合物的生物学潜力和健康益处：综述与发展机遇。

IF 5.4

Chemico-biological interactions Pub Date : 2025-09-22 DOI: 10.1016/j.cbi.2025.111755

Marco Duarte, Sílvia Santos Pedrosa, P Raaj Khusial, Ana Raquel Madureira

{"title":"The biological potential and health-benefits of flavonoids: A review and development opportunities.","authors":"Marco Duarte, Sílvia Santos Pedrosa, P Raaj Khusial, Ana Raquel Madureira","doi":"10.1016/j.cbi.2025.111755","DOIUrl":"10.1016/j.cbi.2025.111755","url":null,"abstract":"Flavonoids are a class of polyphenolic phytochemicals, representing an important group of secondary metabolites in plants. They can be divided into seven groups, depending on their chemical features, and, in nature, they can be obtained from various sources, primarily plants. Industrially, and due to the biological potential of flavonoids, there has been a notable effort to develop new methodologies that allow for the efficient and eco-friendly production of these compounds. The growing interest in natural products for various applications, such as the nutraceutical and cosmeceutical industries, lends considerable relevance to these compounds as potential functional ingredients. Further, flavonoids are heavily explored because they present relevant biological activities like antioxidant and anti-inflammatory, which could translate into health benefits at multiple levels of the human body, like cardiac function, metabolism-related diseases (e.g., diabetes, obesity), bone preservation, neuroprotection, among others. This review aims to explore the biological potential of flavonoids, clarifying their most relevant health benefits while providing an update on the current state of the art, simultaneously pointing future research directions.","PeriodicalId":93932,"journal":{"name":"Chemico-biological interactions","volume":" ","pages":"111755"},"PeriodicalIF":5.4,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145139759","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}

引用次数: 0

Sirtuin 1/3 regulates p53 deacetylation to inhibit iron poisoning-induced alveolar epithelial cell death and contributes to Rapamycin-mediated protection against limb ischemia/reperfusion-induced lung injury. Sirtuin 1/3调节p53去乙酰化，抑制铁中毒诱导的肺泡上皮细胞死亡，并参与雷帕霉素介导的肢体缺血/再灌注肺损伤保护。

IF 5.4

Chemico-biological interactions Pub Date : 2025-09-22 DOI: 10.1016/j.cbi.2025.111756

Dan Huang, Yong-Lin Liang, Lie-Liang Zhang, Bin Zhou, Bin Tang

{"title":"Sirtuin 1/3 regulates p53 deacetylation to inhibit iron poisoning-induced alveolar epithelial cell death and contributes to Rapamycin-mediated protection against limb ischemia/reperfusion-induced lung injury.","authors":"Dan Huang, Yong-Lin Liang, Lie-Liang Zhang, Bin Zhou, Bin Tang","doi":"10.1016/j.cbi.2025.111756","DOIUrl":"https://doi.org/10.1016/j.cbi.2025.111756","url":null,"abstract":"Background: Acute limb ischemia is a disorder with high morbidity and mortality globally. Unfortunately, the effectiveness of limb ischemia/reperfusion (I/R)-induced acute lung injury (ALI) therapy remains limited.Methods: I/R-induced lung injury (IRLI) rat model and LPS-stimulated cell model were established. The histological changes and collagen deposition in lungs were evaluated by H&E and Masson staining. Lung injury was assessed by pathological scoring, evaluation of arterial PaO2 and lung water content. qRT-PCR, Western blot, immunohistochemistry, immunofluorescent staining and ELISA assay were employed to detect the expression and secretion of key molecules. The oxidative stress markers were detected using commercial kits, and CCK-8, EdU incorporation, TUNEL assays and flow cytometry were employed to detect cell proliferation and apoptosis, respectively. The interaction between U2AF2 and SIRT1/3 was examined by RIP assay, and the association between SIRT1/3 and p53, as well as the acetylation of p53, were detected by co-IP.Results: Rapamycin induced SIRT1 and SIRT3 expression and deacetylase activities in the lung tissues of IRLI rats. Inhibition of SIRT1 or SIRT3 attenuated the protective effects of Rapamycin on I/R-induced lung injury, pyroptosis, oxidative stress and ferroptosis in vivo. In LPS-stimulated L2 cells, SIRT1 or SIRT3 was involved in Rapamycin-mediated protection in inflammation, pyroptosis, oxidative stress and ferroptosis. Mechanistically, Rapamycin enhanced the mRNA stability of SIRT1 or SIRT3 via recruiting U2AF2, and it also promoted p53 deacetylation by inducing SIRT1 and SIRT3.Conclusion: SIRT1/3 regulated p53 deacetylation to inhibit iron poisoning-induced alveolar epithelial cell death and contributed to Rapamycin-mediated protection against limb I/R-induced ALI.","PeriodicalId":93932,"journal":{"name":"Chemico-biological interactions","volume":" ","pages":"111756"},"PeriodicalIF":5.4,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145139727","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}

引用次数: 0

Copper exposure induces inflammation and PANoptosis through the TLR4/NF-κB signaling pathway, leading to testicular damage and impaired spermatogenesis in Wilson disease. 铜暴露会通过 TLR4/NF-κB 信号通路诱发炎症和 PAN 细胞凋亡，导致威尔逊氏病患者的睾丸损伤和精子发生障碍。

Chemico-biological interactions Pub Date : 2024-06-01 Epub Date: 2024-05-17 DOI: 10.1016/j.cbi.2024.111060

Dan Zhao, Limin Wu, Xinru Fang, Luyao Wang, Qianzhuo Liu, Pengyu Jiang, Zhihui Ji, Nian Zhang, Miaozhu Yin, Hui Han

{"title":"Copper exposure induces inflammation and PANoptosis through the TLR4/NF-κB signaling pathway, leading to testicular damage and impaired spermatogenesis in Wilson disease.","authors":"Dan Zhao, Limin Wu, Xinru Fang, Luyao Wang, Qianzhuo Liu, Pengyu Jiang, Zhihui Ji, Nian Zhang, Miaozhu Yin, Hui Han","doi":"10.1016/j.cbi.2024.111060","DOIUrl":"10.1016/j.cbi.2024.111060","url":null,"abstract":"Copper is a toxic heavy metal that causes various damage when it accumulates in the body beyond the physiological threshold. Wilson disease (WD) is an inherited disorder characterized by impaired copper metabolism. Reproductive damage in male patients with WD is gradually attracting attention. However, the underlying mechanisms of copper toxicity are unclear. In this study, we investigated the role of inflammation and PANoptosis in testicular damage and impaired spermatogenesis caused by copper deposition using the WD model toxic milk (TX) mice. Copper chelator-penicillamine and toll-like receptor 4 (TLR4) inhibitor-eritoran were used to intervene in TX mice in our animal experiment methods. Testis samples were collected from mice for further analysis. The results showed that the morphology and ultrastructure of the testis and epididymis in TX mice were damaged, and the sperm counts decreased significantly. The TLR4/nuclear factor kappa-B (NF-κB) signaling pathway was activated by copper deposition, which led to the upregulation of serum and testicular inflammatory factors in TX mice. Meanwhile, pyroptosis, apoptosis, and necroptosis were significant in the testis of TX mice. Both chelated copper or inhibited TLR4 expression markedly suppressed the TLR4/NF-κB signaling pathway, thereby reducing the expression of inflammatory factors. PANoptosis in the testis of TX mice was also reversed. Our study indicated that pathological copper exposure induces inflammation and PANoptosis through the TLR4/NF-κB signaling pathway, leading to toxic testicular damage and impaired spermatogenesis in WD.","PeriodicalId":93932,"journal":{"name":"Chemico-biological interactions","volume":" ","pages":"111060"},"PeriodicalIF":0.0,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140961149","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}

引用次数: 0

Elucidating the Molecular Mechanisms of Pterostilbene Against Cervical Cancer Through an Integrated Bioinformatics and Network Pharmacology Approach 通过综合生物信息学和网络药理学方法阐明紫檀芪抗宫颈癌的分子机制

Chemico-biological interactions Pub Date : 2024-05-01 DOI: 10.1016/j.cbi.2024.111058

Xiang Li, Dequan Yu, Qiming Wang, Yating Chen, Hanbing Jiang

引用次数: 0

Assessment of anti-hyperglycemic and anti-hyperlipidemic effects of thiazolidine-2,4-dione derivatives in HFD-STZ diabetic animal model 评估噻唑烷-2,4-二酮衍生物在 HFD-STZ 糖尿病动物模型中的降血糖和降血脂作用

Chemico-biological interactions Pub Date : 2024-02-01 DOI: 10.1016/j.cbi.2024.110902

S. Fettach, Fatima Zahra Thari, Khalid Karrouchi, Laila Benbacer, Learn-Han Lee, Abdelhakim Bouyahya, Y. Cherrah, Hassan Sefrioui, Khalid Bougrin, M. El Abbes Faouzi

引用次数: 0

Loss of VRK1 alters the nuclear phosphoproteome in the DNA damage response to doxorubicin VRK1缺失会改变DNA损伤对多柔比星反应的核磷酸蛋白组

Chemico-biological interactions Pub Date : 2024-02-01 DOI: 10.1016/j.cbi.2024.110908

Elena Navarro-Carrasco, Aurora Campos-Díaz, Eva Monte-Serrano, F. Rolfs, Richard de Goeij-de Haas, T. Pham, S. Piersma, Connie R. Jimenez, Pedro A. Lazo

引用次数: 0

Neurotoxicity of Pyrethroids in exacerbating neurodegenerative diseases: From animals' models to humans’ studies 拟除虫菊酯在加剧神经退行性疾病方面的神经毒性：从动物模型到人体研究

Chemico-biological interactions Pub Date : 2024-02-01 DOI: 10.1016/j.cbi.2024.110911

Rafael Arsuffi-Marcon, Lizandra Gomes Souza, Artur Santos-Miranda, J. Joviano-Santos

引用次数: 0