Chemico-biological interactions最新文献

PP2A attenuates α-amanitin-induced liver injury by promoting autophagy and inhibiting apoptosis in mouse models. 在小鼠模型中，PP2A通过促进自噬和抑制细胞凋亡来减轻α-amanitin诱导的肝损伤。

Chemico-biological interactions Pub Date : 2025-05-14 DOI: 10.1016/j.cbi.2025.111558

Hui Xu, Jian Sun, Yu Zhao, Yaxiong Zhou, Kuan Wang, Xiang Liu, Jieyan Yang, Peng Wu, Shengkui Wang, John P Kastelic, Weijie Qu, Limei Zhang, Xiaolong Gu

{"title":"PP2A attenuates α-amanitin-induced liver injury by promoting autophagy and inhibiting apoptosis in mouse models.","authors":"Hui Xu, Jian Sun, Yu Zhao, Yaxiong Zhou, Kuan Wang, Xiang Liu, Jieyan Yang, Peng Wu, Shengkui Wang, John P Kastelic, Weijie Qu, Limei Zhang, Xiaolong Gu","doi":"10.1016/j.cbi.2025.111558","DOIUrl":"https://doi.org/10.1016/j.cbi.2025.111558","url":null,"abstract":"Poisoning caused by the mushroom toxin α-amanitin accounts for ∼90% of food poisoning deaths resulting from mushrooms in China. However, Drosophila melanogaster uses PP2A to mitigate effects of α-amanitin. Our objectives were to test the hypothesis that modulation of PP2A protects mammals against deleterious effects of α-amanitin. In in vitro experiments, α-amanitin significantly suppressed both gene and protein expression of PP2A. Inhibiting PP2A promoted apoptosis induced by α-amanitin while suppressing autophagy. In vivo α-amanitin increased liver coefficient and AST/ALT indexes, plus caused pathological changes, ultrastructural alterations, TUNEL-positive cells, and Cleaved-caspase-3 expression. Inhibiting PP2A activity worsened these end points, but increasing PP2A activity lessened them. Furthermore, α-amanitin reduced feed intake and body weight while increasing health scores and causing concentration-dependent mortality in mice. In contrast, enhancing PP2A significantly mitigated α-amanitin-induced effects on health with 100% survival. In conclusion, targeting PP2A is a novel therapeutic approach to mitigate α-amanitin toxicity.","PeriodicalId":93932,"journal":{"name":"Chemico-biological interactions","volume":" ","pages":"111558"},"PeriodicalIF":0.0,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144087041","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

Zn²⁺ regulates mitochondrial DNA efflux to inhibit AIM2-mediated ZBP1-PANoptosome pathway and alleviate septic myocardial injury. Zn2+调节线粒体DNA外排，抑制aim2介导的ZBP1-PANoptosome通路，减轻脓毒性心肌损伤。

Chemico-biological interactions Pub Date : 2025-05-08 DOI: 10.1016/j.cbi.2025.111525

Jun Guo, Shanshan Meng, Jin Zhang, Ni Wang, Fengmei Guo

{"title":"Zn2+ regulates mitochondrial DNA efflux to inhibit AIM2-mediated ZBP1-PANoptosome pathway and alleviate septic myocardial injury.","authors":"Jun Guo, Shanshan Meng, Jin Zhang, Ni Wang, Fengmei Guo","doi":"10.1016/j.cbi.2025.111525","DOIUrl":"https://doi.org/10.1016/j.cbi.2025.111525","url":null,"abstract":"This study was performed to investigate the mechanism by which zinc ion regulated mtDNA efflux to inhibit the AIM2-mediated ZBP1-PANoptosome pathway and alleviate sepsis-induced myocardial injury. Here we discovered that zinc ions suppressed mitochondrial DNA release, thereby protecting the heart from LPS-induced damage in mice. In addition, LPS induced mPTP opening and mediated mtDNA efflux in cardiomyocytes, which drove AIM2 activation and ZBP1-PANoptosome multiprotein complex formation, leading to pan-apoptotic cardiomyocyte death. Zn2+ prevented mPTP opening to inhibit mtDNA efflux-driven AIM2 and ZBP1-PANoptosome multiprotein complex formation and alleviate PANoptosis. Knockdown of AIM2 alleviated LPS-induced PANoptosis in cardiomyocytes. LPS-induced PANoptosis in cardiomyocytes by regulating the ZBP1/RIPK3 pathway. However, activation of the ZBP1/RIPK3 pathway partially reversed the inhibitory effect of Zn2+ on PANoptosis in cardiomyocytes. Taken together, Zn2+ regulated mitochondrial DNA efflux to inhibit the AIM2-mediated ZBP1-PANoptosome pathway to alleviate septic myocardial injury.","PeriodicalId":93932,"journal":{"name":"Chemico-biological interactions","volume":" ","pages":"111525"},"PeriodicalIF":0.0,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144055557","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