Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie最新文献

Corrigendum to "Ferroptosis in thyroid cancer: Potential mechanisms, effective therapeutic targets and predictive biomarker" [Biomed. Pharmacother. 177 (2024) 116971].

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie Pub Date : 2025-02-03 DOI: 10.1016/j.biopha.2025.117867

Yuying Chen, Gang Pan, Fan Wu, Yu Zhang, Yuanhui Li, Dingcun Luo

引用次数: 0

Expression of Concern: "Shexiang Baoxin Pill treats acute myocardial infarction by promoting angiogenesis via GDF15-TRPV4 signaling" [Biomed. Pharmacother. 165 (2023) 115186].

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie Pub Date : 2025-02-01 Epub Date: 2025-01-24 DOI: 10.1016/j.biopha.2024.117628

Bing-Yan Wei, Jia-Nan Hou, Chang-Ping Yan, Shi-Yuan Wen, Xiao-Sen Shang, Yong-Chang Guo, Tao Feng, Tian-Fu Liu, Zhao-Yang Chen, Xiao-Ping Chen

引用次数: 0

Expression of Concern: "Circular RNA YAP1 attenuates osteoporosis through up-regulation of YAP1 and activation of Wnt/β-catenin pathway" Biomed. Pharmacother. 129 (September) (2020) 110365.

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie Pub Date : 2025-02-01 Epub Date: 2025-01-25 DOI: 10.1016/j.biopha.2024.117623

Yongxiong Huang, Dan Xiao, Shuaihao Huang, Jianxiong Zhuang, Xiaoqing Zheng, Yunbing Chang, Dong Yin

引用次数: 0

Retraction notice to "Helenalin from Centipeda minima ameliorates acute hepatic injury by protecting mitochondria function, activating Nrf2 pathway and inhibiting NF-κB activation" [Biomed. Pharmacother. 119 (2019) 109435]. 撤回“蜈蚣的Helenalin通过保护线粒体功能、激活Nrf2通路和抑制NF-κB激活来改善急性肝损伤”[Biomed]。药理学杂志，119(2019)109435]。

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie Pub Date : 2024-12-01 Epub Date: 2024-12-09 DOI: 10.1016/j.biopha.2024.117697

Yan Li, Yongmei Zeng, Quanfang Huang, Shujuan Wen, Yuanyuan Wei, Ya Chen, Xiaolin Zhang, Facheng Bai, Zhongpeng Lu, Jinbin Wei, Xing Lin

引用次数: 0

Corrigendum to "Induction of cytotoxicity and apoptosis in FLT3 mutant expressing cells using novel pyrimido cyanoacrylates and quinoline derivatives" [Biomed. Pharmacother. 108 (2018) 893-905]. 对 "使用新型嘧啶氰基丙烯酸酯和喹啉衍生物诱导FLT3突变表达细胞的细胞毒性和凋亡 "的更正 [Biomed. Pharmacother. 108 (2018) 893-905]。

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie Pub Date : 2024-11-01 Epub Date: 2024-10-28 DOI: 10.1016/j.biopha.2024.117618

Mohammad-Ali Sobhanifar, Baratali Mashkani, Mohammad Saadatmandzadeh, Hamid Reza Sadeghnia, Seyed Hadi Mousavi

引用次数: 0

VP3.15 reduces acute cerebellum damage after germinal matrix-intraventricular hemorrhage of the preterm newborn. VP3.15可减少早产新生儿胚芽基质-脑室出血后的急性小脑损伤。

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie Pub Date : 2024-11-01 Epub Date: 2024-10-16 DOI: 10.1016/j.biopha.2024.117586

Isabel Atienza-Navarro, Angel Del Marco, Maria de Los Angeles Garcia-Perez, Alvaro Raya-Marin, Carmen Gil, Ana Martinez, Isabel Benavente-Fernandez, Simon Lubian-Lopez, Monica Garcia-Alloza

{"title":"VP3.15 reduces acute cerebellum damage after germinal matrix-intraventricular hemorrhage of the preterm newborn.","authors":"Isabel Atienza-Navarro, Angel Del Marco, Maria de Los Angeles Garcia-Perez, Alvaro Raya-Marin, Carmen Gil, Ana Martinez, Isabel Benavente-Fernandez, Simon Lubian-Lopez, Monica Garcia-Alloza","doi":"10.1016/j.biopha.2024.117586","DOIUrl":"10.1016/j.biopha.2024.117586","url":null,"abstract":"Germinal matrix-intraventricular hemorrhage (GM-IVH) is one of the most common complications of the preterm newborn. The pathology of the GM-IVH is not completely understood and even regions distant from the lesion area are severely affected. It has been suggested that cerebellar diaschisis may underlie the neurodevelopmental problems that many of these kids show, including cerebral palsy, attention deficit disorders or hyperactivity. Additionally, GM-IVH has no successful treatment. VP3.15 is a dual action phosphodiesterase 7 (PDE7) and glycogen synthase kinase-3β (GSK-3β) inhibitor that limits neuroinflammation and neuronal loss. Therefore, it might also provide a relevant tool to reduce complications associated with GM-IVH. We have used a murine model of GM-IVH to analyze the short and long-term effects of VP3.15 in brain pathology and behavioral complications. In our hands, the induction of unilateral GM-IVH to P7 CD1 mice results in a short-term (P14) compromise of the cerebellar neuronal population and Purkinje cells arborization, an increase of microglia burden in the nuclei and an overall increase of punctuate cerebellar hemorrhages. Whereas brain alterations are no longer observed in the long term (P110), these animals present overt hyperactivity when analyzed in the adulthood, supporting the long-term behavioral impairment. Also, hyperactivity significantly correlates with ipsi and contralateral cerebellar sizes, neuronal densities and myelin basic protein levels. Importantly, treatment with VP3.15 significantly reduces neuronal loss, Purkinje cells simplification, the presence of cerebellar hemorrhages, as well as hyperactivity. Altogether, our data support the neuroprotective effects of VP3.15 in GM-IVH of the PT.","PeriodicalId":93904,"journal":{"name":"Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie","volume":"180 ","pages":"117586"},"PeriodicalIF":0.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142482908","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

Astragaloside IV alleviates heatstroke brain injury and neuroinflammation in male mice by regulating microglial polarization via the PI3K/Akt signaling pathway. 黄芪皂苷IV通过PI3K/Akt信号通路调节小胶质细胞极化，减轻雄性小鼠的中暑脑损伤和神经炎症。

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie Pub Date : 2024-11-01 Epub Date: 2024-10-14 DOI: 10.1016/j.biopha.2024.117545

Zeze Wang, Zhen Luo, Yulong Tan, Genlin He, Ping Li, Xiaoqian Liu, Tingting Shen, Yishan Liu, Xuesen Yang, Xue Luo

{"title":"Astragaloside IV alleviates heatstroke brain injury and neuroinflammation in male mice by regulating microglial polarization via the PI3K/Akt signaling pathway.","authors":"Zeze Wang, Zhen Luo, Yulong Tan, Genlin He, Ping Li, Xiaoqian Liu, Tingting Shen, Yishan Liu, Xuesen Yang, Xue Luo","doi":"10.1016/j.biopha.2024.117545","DOIUrl":"10.1016/j.biopha.2024.117545","url":null,"abstract":"Heatstroke is a condition caused by overheating of the body that leads to severe central nervous system dysfunction. Although there have been numerous studies on the pathological process of heatstroke, effective treatment methods are lacking. Astragaloside IV can protect the brain from inflammation and brain damage in various inflammation-related diseases, but it has not yet been used clinically for the treatment of heatstroke. Therefore, the aim of this study was to explore the neuroprotective effect of Astragaloside IV on heatstroke-induced central nervous system damage and its mechanism. Brain injury model under heatstroke was established using artificial climate simulation cabin. By scoring neurological deficits, performing histological and immunofluorescence staining of microglia, and detecting cytokine levels, we determined that Astragaloside IV alleviated brain injury and neuroinflammation. To further explore the potential molecular mechanism, RNA sequencing was performed to investigate the differences in the brain. The results revealed that the PI3K/AKT pathway is involved. In vitro experiments further confirmed that Astragaloside IV can abrogate the phenotypic changes in microglia induced by heatstroke. Moreover, Astragaloside IV promotes the polarization of M2 microglia by activating the PI3K/AKT pathway. In summary, these results indicate that Astragaloside IV alleviates neuroinflammation and brain injury induced by heatstroke through the PI3K/AKT pathway. Astragaloside IV is a commonly used therapeutic agent in the clinic, but its use in the treatment of heatstroke-induced brain injury has not been explored. This study reveals that Astragaloside IV may be a new therapeutic agent for the treatment of heatstroke-induced brain injury.","PeriodicalId":93904,"journal":{"name":"Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie","volume":"180 ","pages":"117545"},"PeriodicalIF":0.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142482963","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

Empagliflozin attenuating renal interstitial fibrosis in diabetic kidney disease by inhibiting lymphangiogenesis and lymphatic endothelial-to-mesenchymal transition via the VEGF-C/VEGFR3 pathway. 恩格列净通过VEGF-C/VEGFR3途径抑制淋巴管生成和淋巴管内皮细胞向间质转化，从而减轻糖尿病肾病的肾间质纤维化。

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie Pub Date : 2024-11-01 Epub Date: 2024-10-16 DOI: 10.1016/j.biopha.2024.117589

Jiaan Huang, Yan Liu, Mengting Shi, Xiaoyun Zhang, Yan Zhong, Shuai Guo, Yun Ma, Limin Pan, Fan Yang, Yuehua Wang

{"title":"Empagliflozin attenuating renal interstitial fibrosis in diabetic kidney disease by inhibiting lymphangiogenesis and lymphatic endothelial-to-mesenchymal transition via the VEGF-C/VEGFR3 pathway.","authors":"Jiaan Huang, Yan Liu, Mengting Shi, Xiaoyun Zhang, Yan Zhong, Shuai Guo, Yun Ma, Limin Pan, Fan Yang, Yuehua Wang","doi":"10.1016/j.biopha.2024.117589","DOIUrl":"10.1016/j.biopha.2024.117589","url":null,"abstract":"Renal interstitial fibrosis (RIF) is a significant pathological change in diabetic kidney disease (DKD) that can be induced by endothelial-to-mesenchymal transition (EndMT). Lymphangiogenesis, mediated by the vascular endothelial growth factor-C (VEGF-C)/vascular endothelial growth factor receptor-3 (VEGFR-3) pathway, plays a crucial role in the development of RIF in DKD. Although numerous studies have demonstrated the efficacy of empagliflozin in treating renal injury, its effects on lymphangiogenesis in DKD-related RIF and the underlying mechanisms remain unclear. In the present study, significant lymphangiogenesis was assessed in the renal interstitium of patients with DKD. We subsequently explored the relationship between DKD-related RIF and lymphangiogenesis in mouse models, high-glucose (HG)-stimulated renal HK-2 cell lines, and human lymphatic endothelial cells (hLECs). Additionally, we evaluated the effects of empagliflozin on these processes. The results revealed that HG induces lymphangiogenesis, which exacerbates RIF by promoting inflammatory responses. Furthermore, hLECs directly contributed to the progression of DKD-related RIF through EndMT. Further analysis revealed that tubular epithelial cells (TECs) act as effector cells for VEGF-C, with the epithelial-to-mesenchymal transition (EMT) of TECs occurring concurrently with the EndMT of lymphatic vessels. Empagliflozin inhibited RIF in DKD by suppressing the VEGF-C/VEGFR3 pathway and reducing lymphangiogenesis. In conclusion, this study elucidates the interplay between lymphangiogenesis, EndMT, and RIF in DKD and provides new insights into the mechanism by which empagliflozin treats DKD.","PeriodicalId":93904,"journal":{"name":"Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie","volume":"180 ","pages":"117589"},"PeriodicalIF":0.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142482970","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

A novel synthetic compound, deferiprone-resveratrol hybrid (DFP-RVT), promotes hepatoprotective effects and ameliorates iron-induced oxidative stress in iron-overloaded β-thalassemic mice. 一种新型合成化合物--去铁酮-白藜芦醇混合物（DFP-RVT）可促进肝脏保护作用，并改善铁过载型β地中海贫血小鼠因铁引起的氧化应激。

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie Pub Date : 2024-11-01 Epub Date: 2024-10-17 DOI: 10.1016/j.biopha.2024.117570

Jin Li, Hataichanok Chuljerm, Kornvipa Settakorn, Honghong Xu, Yongmin Ma, Woranontee Korsieporn, Narisara Paradee, Somdet Srichairatanakool, Pimpisid Koonyosying

{"title":"A novel synthetic compound, deferiprone-resveratrol hybrid (DFP-RVT), promotes hepatoprotective effects and ameliorates iron-induced oxidative stress in iron-overloaded β-thalassemic mice.","authors":"Jin Li, Hataichanok Chuljerm, Kornvipa Settakorn, Honghong Xu, Yongmin Ma, Woranontee Korsieporn, Narisara Paradee, Somdet Srichairatanakool, Pimpisid Koonyosying","doi":"10.1016/j.biopha.2024.117570","DOIUrl":"10.1016/j.biopha.2024.117570","url":null,"abstract":"A high amount of iron in β-thalassemia patients can lead to oxidative stress and organ dysfunction, especially liver, the main iron accumulated organ. Iron catabolism causes the generation of reactive oxygen species (ROS), triggering liver inflammation, fibrosis, and cirrhosis. Deferiprone-resveratrol hybrid (DFP-RVT) is chemically synthesized by combining deferiprone (DFP) and resveratrol (RVT) which shows an iron-chelating property along with antioxidant activity. This study explored the hepatoprotective effect of DFP-RVT in iron overloaded β-knockout (BKO) thalassemic mice. The results revealed that DFP-RVT treatment improved liver function in iron-overloaded BKO mice by reducing liver enzymes and increasing hepcidin levels compared to iron overload control mice. Both DFP alone and DFP-RVT treatment groups demonstrated iron chelation effects by decreasing liver iron content (LIC), iron profiles, and iron deposition in the liver. Moreover, DFP-RVT powerfully showed antioxidant properties by decreasing liver and plasma thiobarbituric acid reactive substances (TBARs) and increasing reduced glutathione (GSH) and superoxide dismutase (SOD). Interestingly, transforming growth factor β1 (TGFβ1), which can contribute to chronic liver disease through liver injury, inflammation, fibrosis, and cirrhosis, is highly expressed in iron-overloaded mice. However, both DFP and DFP-RVT treatment significantly reduced TGFβ1 levels compared to the iron-overloaded group. Therefore, DFP-RVT could be a potent hepatoprotective compound through the mobilization of iron, reduction of ROS, improvement of liver enzymes, and alleviation of liver damage, potentially relieving liver dysfunction in iron-overloaded BKO mice.","PeriodicalId":93904,"journal":{"name":"Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie","volume":"180 ","pages":"117570"},"PeriodicalIF":0.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142482985","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

L-NRB alleviates amyotrophic lateral sclerosis by regulating P11-Htr4 signaling pathway. L-NRB通过调节P11-Htr4信号通路缓解肌萎缩性脊髓侧索硬化症。

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie Pub Date : 2024-11-01 Epub Date: 2024-10-19 DOI: 10.1016/j.biopha.2024.117588

Yunfeng Pan, Xiao Sun, Yu Tian, Miao Yu, Yun Luo, Xiaobo Sun

{"title":"L-NRB alleviates amyotrophic lateral sclerosis by regulating P11-Htr4 signaling pathway.","authors":"Yunfeng Pan, Xiao Sun, Yu Tian, Miao Yu, Yun Luo, Xiaobo Sun","doi":"10.1016/j.biopha.2024.117588","DOIUrl":"10.1016/j.biopha.2024.117588","url":null,"abstract":"Introduction: L-NRB is a compound formed as a ring cleavage product of butylphthalide and borneol in a molar ratio 1:2. This study aimed to explore the therapeutic effect of L-NRB on amyotrophic lateral sclerosis (ALS) and its possible mechanism.Methods: SOD1-G93A mice were used as an ALS model. Behavioral tests, histopathological staining, Nissl staining, immunohistochemistry, enzyme-linked immunosorbent assays, and Western blotting were used to analyze the therapeutic effect. The underlying mechanism of L-NRB in treating ALS was investigated using transcriptomic analyses.Results: It was found that L-NRB alleviated motor dysfunction, pathological changes in the gastrocnemius muscle, and motor neuron injuries. The results indicated that L-NRB had a neuroprotective function associated with the inhibition of neuroinflammation. The anti-apoptotic effect of L-NRB was found to be related to the regulation of the P11-Htr4 signaling pathway.Conclusion: In summary, the results demonstrated the therapeutic effect of L-NRB on ALS and suggest a promising new therapeutic candidate for ALS.","PeriodicalId":93904,"journal":{"name":"Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie","volume":"180 ","pages":"117588"},"PeriodicalIF":0.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142482990","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