Pub Date : 2024-10-28DOI: 10.1016/j.biopha.2024.117598
This review focuses on the role and underlying mechanisms of mitotic catastrophe (MC) in the regulation of drug resistance in hepatocellular carcinoma (HCC). HCC is one of the leading causes of cancer-related mortality worldwide, posing significant treatment challenges due to its high recurrence rates and drug resistance. Research suggests that MC, as a mechanism of cell death, plays a crucial role in enhancing the efficacy of HCC treatment by disrupting the replication and division mechanisms of tumor cells. The present review summarizes the molecular mechanisms of MC and its role in HCC drug resistance and explores the potential of combining MC with existing cancer therapies to improve treatment outcomes. Future research should focus on the in-depth elucidation of the molecular mechanisms of MC and its application in HCC therapy, providing new insights for the development of more effective treatments.
这篇综述重点探讨有丝分裂灾难（MC）在调节肝细胞癌（HCC）耐药性中的作用和内在机制。肝细胞癌是全球癌症相关死亡的主要原因之一，由于其高复发率和耐药性，给治疗带来了巨大挑战。研究表明，MC 作为一种细胞死亡机制，通过破坏肿瘤细胞的复制和分裂机制，在提高 HCC 治疗效果方面发挥着至关重要的作用。本综述总结了 MC 的分子机制及其在 HCC 耐药性中的作用，并探讨了将 MC 与现有癌症疗法相结合以改善治疗效果的潜力。今后的研究应侧重于深入阐明 MC 的分子机制及其在 HCC 治疗中的应用，为开发更有效的治疗方法提供新的见解。
{"title":"The regulatory role of mitotic catastrophe in hepatocellular carcinoma drug resistance mechanisms and its therapeutic potential","authors":"","doi":"10.1016/j.biopha.2024.117598","DOIUrl":"10.1016/j.biopha.2024.117598","url":null,"abstract":"<div><div>This review focuses on the role and underlying mechanisms of mitotic catastrophe (MC) in the regulation of drug resistance in hepatocellular carcinoma (HCC). HCC is one of the leading causes of cancer-related mortality worldwide, posing significant treatment challenges due to its high recurrence rates and drug resistance. Research suggests that MC, as a mechanism of cell death, plays a crucial role in enhancing the efficacy of HCC treatment by disrupting the replication and division mechanisms of tumor cells. The present review summarizes the molecular mechanisms of MC and its role in HCC drug resistance and explores the potential of combining MC with existing cancer therapies to improve treatment outcomes. Future research should focus on the in-depth elucidation of the molecular mechanisms of MC and its application in HCC therapy, providing new insights for the development of more effective treatments.</div></div>","PeriodicalId":8966,"journal":{"name":"Biomedicine & Pharmacotherapy","volume":null,"pages":null},"PeriodicalIF":6.9,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142514598","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-22DOI: 10.1016/j.biopha.2024.117585
Cancer remains one of the leading causes of death worldwide and poses a significant challenge to effective treatment due to its complexity. Angiogenesis, the formation of new blood vessels, is one of the cancer hallmarks and is a critical process in tumor growth and metastasis. The pivotal role of angiogenesis in cancer development has made antiangiogenic treatment a promising strategy for cancer therapy. To develop an effective therapy, it is essential to understand the basics of the physiological and tumor angiogenesis process. This review presents the primary factors related to physiological and tumor angiogenesis and the mechanisms of angiogenesis in tumors. We summarize potential molecular targets for cancer treatment by focusing on the vasculature, with the VEGF/VEGFR pathway being one of the most important and well-studied. Additionally, we present the advantages and limitations of currently used clinical protocols for cancer treatment targeting the VEGF/VEGFR pathway.
{"title":"Physiological and tumor-associated angiogenesis: Key factors and therapy targeting VEGF/VEGFR pathway","authors":"","doi":"10.1016/j.biopha.2024.117585","DOIUrl":"10.1016/j.biopha.2024.117585","url":null,"abstract":"<div><div>Cancer remains one of the leading causes of death worldwide and poses a significant challenge to effective treatment due to its complexity. Angiogenesis, the formation of new blood vessels, is one of the cancer hallmarks and is a critical process in tumor growth and metastasis. The pivotal role of angiogenesis in cancer development has made antiangiogenic treatment a promising strategy for cancer therapy. To develop an effective therapy, it is essential to understand the basics of the physiological and tumor angiogenesis process. This review presents the primary factors related to physiological and tumor angiogenesis and the mechanisms of angiogenesis in tumors. We summarize potential molecular targets for cancer treatment by focusing on the vasculature, with the VEGF/VEGFR pathway being one of the most important and well-studied. Additionally, we present the advantages and limitations of currently used clinical protocols for cancer treatment targeting the VEGF/VEGFR pathway.</div></div>","PeriodicalId":8966,"journal":{"name":"Biomedicine & Pharmacotherapy","volume":null,"pages":null},"PeriodicalIF":6.9,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142514595","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-22DOI: 10.1016/j.biopha.2024.117575
Sterol regulatory element binding proteins (SREBPs) are a series of cholesterol-related transcription factors. Their role in regulating brain cholesterol biosynthesis, amyloid accumulation, and tau tangles formation has been intensively studied in protein-protein interaction analysis based on genes in clinical databases. SREBPs play an important role in maintaining cholesterol homeostasis in the brain. There are three subtypes of SREBPs, SREBP-1a stimulates the expression of genes related to cholesterol and fatty acid synthesis, SREBP-1c stimulates adipogenesis, and SREBP-2 stimulates cholesterol synthase and LDL receptors. SREBP-2 is activated in response to cholesterol depletion and stimulates a compensatory upregulation of cholesterol uptake and synthesis. Previous studies have shown that inhibition of SREBP-2 reduces cholesterol and amyloid accumulation, and new research suggests that SREBPs play a multifaceted role in Alzheimer's disease. Here, we highlight the importance of SREBPs in AD, in terms of multiple pathways regulating cholesterol in the brain, and primarily demonstrate the potential of SREBP-2 inhibitors. There was a trend towards a significant increase in the expression levels of different SREBP isoforms in AD patients compared to healthy controls. Therefore, there is a close link between SREBPs and AD, and this review analyses the potential role of SREBPs in the treatment of AD. In addition, we systematically reviewed the research progress of SREBPs in AD, and this review will provide more innovative insights into the pathogenesis and treatment of AD and new strategies for drug development in AD.
甾醇调节元件结合蛋白（SREBPs）是一系列与胆固醇相关的转录因子。基于临床数据库中的基因，人们通过蛋白-蛋白相互作用分析深入研究了它们在调节大脑胆固醇生物合成、淀粉样蛋白积累和陶氏缠结形成中的作用。SREBPs 在维持大脑胆固醇平衡方面发挥着重要作用。SREBPs有三种亚型，SREBP-1a刺激胆固醇和脂肪酸合成相关基因的表达，SREBP-1c刺激脂肪生成，SREBP-2刺激胆固醇合成酶和低密度脂蛋白受体。SREBP-2 在胆固醇耗竭时被激活，并刺激胆固醇摄取和合成的代偿性上调。以前的研究表明，抑制 SREBP-2 可减少胆固醇和淀粉样蛋白的积累，而新的研究表明，SREBPs 在阿尔茨海默病中发挥着多方面的作用。在此，我们从调节大脑中胆固醇的多种途径方面强调了SREBPs在AD中的重要性，并主要展示了SREBP-2抑制剂的潜力。与健康对照组相比，AD 患者体内不同 SREBP 同工酶的表达水平有明显增加的趋势。因此，SREBPs 与 AD 之间存在密切联系，本综述分析了 SREBPs 在治疗 AD 中的潜在作用。此外，我们还系统回顾了SREBPs在AD中的研究进展，本综述将为AD的发病机制和治疗提供更多创新性见解，并为AD的药物开发提供新策略。
{"title":"The potential role of transcription factor sterol regulatory element binding proteins (SREBPs) in Alzheimer's disease","authors":"","doi":"10.1016/j.biopha.2024.117575","DOIUrl":"10.1016/j.biopha.2024.117575","url":null,"abstract":"<div><div>Sterol regulatory element binding proteins (SREBPs) are a series of cholesterol-related transcription factors. Their role in regulating brain cholesterol biosynthesis, amyloid accumulation, and tau tangles formation has been intensively studied in protein-protein interaction analysis based on genes in clinical databases. SREBPs play an important role in maintaining cholesterol homeostasis in the brain. There are three subtypes of SREBPs, SREBP-1a stimulates the expression of genes related to cholesterol and fatty acid synthesis, SREBP-1c stimulates adipogenesis, and SREBP-2 stimulates cholesterol synthase and LDL receptors. SREBP-2 is activated in response to cholesterol depletion and stimulates a compensatory upregulation of cholesterol uptake and synthesis. Previous studies have shown that inhibition of SREBP-2 reduces cholesterol and amyloid accumulation, and new research suggests that SREBPs play a multifaceted role in Alzheimer's disease. Here, we highlight the importance of SREBPs in AD, in terms of multiple pathways regulating cholesterol in the brain, and primarily demonstrate the potential of SREBP-2 inhibitors. There was a trend towards a significant increase in the expression levels of different SREBP isoforms in AD patients compared to healthy controls. Therefore, there is a close link between SREBPs and AD, and this review analyses the potential role of SREBPs in the treatment of AD. In addition, we systematically reviewed the research progress of SREBPs in AD, and this review will provide more innovative insights into the pathogenesis and treatment of AD and new strategies for drug development in AD.</div></div>","PeriodicalId":8966,"journal":{"name":"Biomedicine & Pharmacotherapy","volume":null,"pages":null},"PeriodicalIF":6.9,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142514597","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-19DOI: 10.1016/j.biopha.2024.117581
Cancer remains one of the greatest global health concerns. This is especially true for gynecological cancers, which include cervical, ovarian, and endometrial cancers, and breast cancer. Natural products used for cancer treatment offer some unique advantages. Triptolide (TPL) is a biologically active terpenoid extracted from Tripterygium wilfordii, which exhibits anti-inflammatory, immunosuppressive, antitumor, and other pharmacological activities. However, clinical applications of TPL are restricted because of poor water solubility and severe cytotoxicity; to overcome these limitations, various TPL derivatives and drug delivery systems, especially nanocarriers, have been used. Furthermore, various preclinical and clinical studies have demonstrated that TPL and its derivatives exhibit excellent antitumor effects by targeting proteins involved in multiple signaling pathways. Here, we review the progress regarding novel drug delivery systems, antitumor activities, and molecular mechanisms of action of TPL and its derivatives against gynecological and breast cancers. TPL and its derivatives inhibit tumor growth, suppress tumor metastasis, and enhance the drug sensitization of resistant cancers. In addition, TPL and its derivatives exert synergistic antitumor effects against gynecological and breast cancers when combined with existing antitumor drugs, such as carboplatin, cisplatin, and PI3K inhibitors. Moreover, we highlight the clinical potential of TPL analogs against cancer from bench to bedside and their prospects for future applications in gynecologic and breast cancers.
{"title":"Potential antitumor activity of triptolide and its derivatives: Focused on gynecological and breast cancers","authors":"","doi":"10.1016/j.biopha.2024.117581","DOIUrl":"10.1016/j.biopha.2024.117581","url":null,"abstract":"<div><div>Cancer remains one of the greatest global health concerns. This is especially true for gynecological cancers, which include cervical, ovarian, and endometrial cancers, and breast cancer. Natural products used for cancer treatment offer some unique advantages. Triptolide (TPL) is a biologically active terpenoid extracted from <em>Tripterygium wilfordii</em>, which exhibits anti-inflammatory, immunosuppressive, antitumor, and other pharmacological activities. However, clinical applications of TPL are restricted because of poor water solubility and severe cytotoxicity; to overcome these limitations, various TPL derivatives and drug delivery systems, especially nanocarriers, have been used. Furthermore, various preclinical and clinical studies have demonstrated that TPL and its derivatives exhibit excellent antitumor effects by targeting proteins involved in multiple signaling pathways. Here, we review the progress regarding novel drug delivery systems, antitumor activities, and molecular mechanisms of action of TPL and its derivatives against gynecological and breast cancers. TPL and its derivatives inhibit tumor growth, suppress tumor metastasis, and enhance the drug sensitization of resistant cancers. In addition, TPL and its derivatives exert synergistic antitumor effects against gynecological and breast cancers when combined with existing antitumor drugs, such as carboplatin, cisplatin, and PI3K inhibitors. Moreover, we highlight the clinical potential of TPL analogs against cancer from bench to bedside and their prospects for future applications in gynecologic and breast cancers.</div></div>","PeriodicalId":8966,"journal":{"name":"Biomedicine & Pharmacotherapy","volume":null,"pages":null},"PeriodicalIF":6.9,"publicationDate":"2024-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142482997","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-19DOI: 10.1016/j.biopha.2024.117584
Proteolysis Targeting Chimera (PROTAC) is an emerging and evolving technology based on targeted protein degradation (TPD). Small molecule PROTACs have shown great efficacy in degrading disease-specific proteins in preclinical and clinical studies, but also showed various limitations. In recent years, new technologies and advances in TPD have provided additional optimized strategies based on conventional PROTACs that can overcome the shortcomings of conventional PROTACs in terms of undruggable targets, bioavailability, tissue-specificity, spatiotemporal control, and degradation scope. In addition, some designs of special targeting chimeras and applications based on multidisciplinary science have shed light on novel therapeutic modalities and drug design. However, each improvement has its own advantages, disadvantages and application conditions. In this review, we summarize the exploration of PROTAC elements, depict a landscape of improvements and derived concepts of PROTACs, and expect to provide perspectives for technological innovations, combinations and applications in future targeting chimera design.
{"title":"Recent breakthroughs in innovative elements, multidimensional enhancements, derived technologies, and novel applications of PROTACs","authors":"","doi":"10.1016/j.biopha.2024.117584","DOIUrl":"10.1016/j.biopha.2024.117584","url":null,"abstract":"<div><div>Proteolysis Targeting Chimera (PROTAC) is an emerging and evolving technology based on targeted protein degradation (TPD). Small molecule PROTACs have shown great efficacy in degrading disease-specific proteins in preclinical and clinical studies, but also showed various limitations. In recent years, new technologies and advances in TPD have provided additional optimized strategies based on conventional PROTACs that can overcome the shortcomings of conventional PROTACs in terms of undruggable targets, bioavailability, tissue-specificity, spatiotemporal control, and degradation scope. In addition, some designs of special targeting chimeras and applications based on multidisciplinary science have shed light on novel therapeutic modalities and drug design. However, each improvement has its own advantages, disadvantages and application conditions. In this review, we summarize the exploration of PROTAC elements, depict a landscape of improvements and derived concepts of PROTACs, and expect to provide perspectives for technological innovations, combinations and applications in future targeting chimera design.</div></div>","PeriodicalId":8966,"journal":{"name":"Biomedicine & Pharmacotherapy","volume":null,"pages":null},"PeriodicalIF":6.9,"publicationDate":"2024-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142482998","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-17DOI: 10.1016/j.biopha.2024.117590
Myeloid-derived suppressor cells (MDSCs) represent a heterogeneous population of immature myeloid cells originating from the bone marrow, known for their potent immunosuppressive functions that contribute to tumor immune evasion and progression. This paper provides a comprehensive analysis of the multifaceted interactions between MDSCs and tumors, exploring their distinct phenotypes and immunosuppressive mechanisms. Key roles of MDSCs in tumor biology are discussed, including their involvement in the formation of the pre-metastatic niche, facilitation of angiogenesis, enhancement of vascular permeability, suppression of tumor cell apoptosis, and promotion of resistance to cancer therapies. Additionally, the review highlights recent advances in the development of MDSC-targeting therapies, with a focus on their potential to enhance anti-tumor immunity. The therapeutic potential of Traditional Chinese Medicine (TCM) in modulating MDSC quantity and function is also explored, suggesting a novel approach to cancer treatment by integrating traditional and modern therapeutic strategies.
{"title":"Targeted modulation of myeloid-derived suppressor cells in the tumor microenvironment: Implications for cancer therapy","authors":"","doi":"10.1016/j.biopha.2024.117590","DOIUrl":"10.1016/j.biopha.2024.117590","url":null,"abstract":"<div><div>Myeloid-derived suppressor cells (MDSCs) represent a heterogeneous population of immature myeloid cells originating from the bone marrow, known for their potent immunosuppressive functions that contribute to tumor immune evasion and progression. This paper provides a comprehensive analysis of the multifaceted interactions between MDSCs and tumors, exploring their distinct phenotypes and immunosuppressive mechanisms. Key roles of MDSCs in tumor biology are discussed, including their involvement in the formation of the pre-metastatic niche, facilitation of angiogenesis, enhancement of vascular permeability, suppression of tumor cell apoptosis, and promotion of resistance to cancer therapies. Additionally, the review highlights recent advances in the development of MDSC-targeting therapies, with a focus on their potential to enhance anti-tumor immunity. The therapeutic potential of Traditional Chinese Medicine (TCM) in modulating MDSC quantity and function is also explored, suggesting a novel approach to cancer treatment by integrating traditional and modern therapeutic strategies.</div></div>","PeriodicalId":8966,"journal":{"name":"Biomedicine & Pharmacotherapy","volume":null,"pages":null},"PeriodicalIF":6.9,"publicationDate":"2024-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142446308","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-17DOI: 10.1016/j.biopha.2024.117566
Acute lung injury (ALI), a multifactorial pathological condition, manifests through heightened inflammatory responses, compromised lung epithelial-endothelial barrier function, and oxidative stress, potentially culminating in respiratory failure and mortality. This study explores the intricate interplay between two crucial cellular mechanisms—extracellular vesicles (EVs) and autophagy—in the context of ALI pathogenesis and potential therapeutic interventions.EVs, bioactive membrane-bound structures secreted by cells, serve as versatile carriers of molecular cargo, facilitating intercellular communication and significantly influencing disease progression. Concurrently, autophagy, an essential intracellular degradation process, maintains cellular homeostasis and has emerged as a promising therapeutic target in ALI and acute respiratory distress syndrome.Our research unveils a fascinating "EV-Autophagy dual-drive pathway," characterized by reciprocal regulation between these two processes. EVs modulate autophagy activation and inhibition, while autophagy influences EV production, creating a dynamic feedback loop. This study posits that precise manipulation of this pathway could revolutionize ALI treatment strategies.By elucidating the mechanisms underlying this cellular crosstalk, we open new avenues for targeted therapies. The potential for engineered EVs to fine-tune autophagy in ALI treatment is explored, alongside innovative concepts such as EV-based vaccines for ALI prevention and management. This research not only deepens our understanding of ALI pathophysiology but also paves the way for novel, more effective therapeutic approaches in critical care medicine.
急性肺损伤（ALI）是一种多因素病理状态，表现为炎症反应加剧、肺上皮-内皮屏障功能受损和氧化应激，最终可能导致呼吸衰竭和死亡。EVs是细胞分泌的具有生物活性的膜结合结构，是分子货物的多功能载体，可促进细胞间的交流并显著影响疾病的进展。同时，自噬是一种重要的细胞内降解过程，它能维持细胞的稳态，并已成为 ALI 和急性呼吸窘迫综合征的一个有前景的治疗靶点。我们的研究揭示了一种迷人的 "EV-自噬双驱动途径"，其特点是这两个过程之间的相互调控。EV调节自噬的激活和抑制，而自噬影响EV的产生，从而形成一个动态反馈回路。本研究认为，对这一通路的精确操作可能会彻底改变 ALI 的治疗策略。通过阐明这种细胞串扰的内在机制，我们为靶向治疗开辟了新的途径。本研究探讨了工程EV在ALI治疗中微调自噬的潜力，以及基于EV的ALI预防和管理疫苗等创新概念。这项研究不仅加深了我们对 ALI 病理生理学的理解，还为重症监护医学中更有效的新型治疗方法铺平了道路。
{"title":"Bidirectional modulation of extracellular vesicle-autophagy axis in acute lung injury: Molecular mechanisms and therapeutic implications","authors":"","doi":"10.1016/j.biopha.2024.117566","DOIUrl":"10.1016/j.biopha.2024.117566","url":null,"abstract":"<div><div>Acute lung injury (ALI), a multifactorial pathological condition, manifests through heightened inflammatory responses, compromised lung epithelial-endothelial barrier function, and oxidative stress, potentially culminating in respiratory failure and mortality. This study explores the intricate interplay between two crucial cellular mechanisms—extracellular vesicles (EVs) and autophagy—in the context of ALI pathogenesis and potential therapeutic interventions.EVs, bioactive membrane-bound structures secreted by cells, serve as versatile carriers of molecular cargo, facilitating intercellular communication and significantly influencing disease progression. Concurrently, autophagy, an essential intracellular degradation process, maintains cellular homeostasis and has emerged as a promising therapeutic target in ALI and acute respiratory distress syndrome.Our research unveils a fascinating \"EV-Autophagy dual-drive pathway,\" characterized by reciprocal regulation between these two processes. EVs modulate autophagy activation and inhibition, while autophagy influences EV production, creating a dynamic feedback loop. This study posits that precise manipulation of this pathway could revolutionize ALI treatment strategies.By elucidating the mechanisms underlying this cellular crosstalk, we open new avenues for targeted therapies. The potential for engineered EVs to fine-tune autophagy in ALI treatment is explored, alongside innovative concepts such as EV-based vaccines for ALI prevention and management. This research not only deepens our understanding of ALI pathophysiology but also paves the way for novel, more effective therapeutic approaches in critical care medicine.</div></div>","PeriodicalId":8966,"journal":{"name":"Biomedicine & Pharmacotherapy","volume":null,"pages":null},"PeriodicalIF":6.9,"publicationDate":"2024-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142446309","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-16DOI: 10.1016/j.biopha.2024.117580
Due to changes in diet and lifestyle, the prevalence of intestinal diseases has been increasing annually. Current treatment methods exhibit several limitations, including adverse reactions and drug resistance, necessitating the development of new, safe, and effective therapies. Astragali Radix, a natural medicine utilized for over two millennia, offers unique advantages in treating intestinal ailments due to its multi-component and multi-target properties. This study aims to review the effective components of Astragali Radix that provide intestinal protection and to explore its pharmacological effects and molecular mechanisms across various intestinal diseases. This will provide a comprehensive foundation for using Astragali Radix in treating intestinal diseases and serve as a reference for future research directions. The active components of Astragali Radix with protective effects on the intestines include astragaloside (AS)-IV, AS-III, AS-II, astragalus polysaccharide (APS), cycloastagenol, calycosin, formononetin, and ononin. Astragali Radix and its active components primarily address intestinal diseases such as colorectal cancer (CRC), inflammatory bowel disease (IBD), and enterocolitis through mechanisms including anti-inflammatory actions, antioxidative stress responses, anti-proliferation and invasion activities, regulation of programmed cell death, immunoregulation, restoration of the intestinal epithelial barrier, and modulation of the intestinal microbiota and its metabolites. Consequently, Astragali Radix demonstrates significant intestinal protective activity and represents a promising natural treatment for intestinal diseases. However, the pharmacological actions and mechanisms of some active components in Astragali Radix remain unexplored. Moreover, further comprehensive toxicological and clinical studies are required to ascertain its safety and clinical effectiveness.
{"title":"Pharmacological potential of natural medicine Astragali Radix in treating intestinal diseases","authors":"","doi":"10.1016/j.biopha.2024.117580","DOIUrl":"10.1016/j.biopha.2024.117580","url":null,"abstract":"<div><div>Due to changes in diet and lifestyle, the prevalence of intestinal diseases has been increasing annually. Current treatment methods exhibit several limitations, including adverse reactions and drug resistance, necessitating the development of new, safe, and effective therapies. <em>Astragali Radix</em>, a natural medicine utilized for over two millennia, offers unique advantages in treating intestinal ailments due to its multi-component and multi-target properties. This study aims to review the effective components of <em>Astragali Radix</em> that provide intestinal protection and to explore its pharmacological effects and molecular mechanisms across various intestinal diseases. This will provide a comprehensive foundation for using <em>Astragali Radix</em> in treating intestinal diseases and serve as a reference for future research directions. The active components of <em>Astragali Radix</em> with protective effects on the intestines include astragaloside (AS)-IV, AS-III, AS-II, astragalus polysaccharide (APS), cycloastagenol, calycosin, formononetin, and ononin. <em>Astragali Radix</em> and its active components primarily address intestinal diseases such as colorectal cancer (CRC), inflammatory bowel disease (IBD), and enterocolitis through mechanisms including anti-inflammatory actions, antioxidative stress responses, anti-proliferation and invasion activities, regulation of programmed cell death, immunoregulation, restoration of the intestinal epithelial barrier, and modulation of the intestinal microbiota and its metabolites. Consequently, <em>Astragali Radix</em> demonstrates significant intestinal protective activity and represents a promising natural treatment for intestinal diseases. However, the pharmacological actions and mechanisms of some active components in <em>Astragali Radix</em> remain unexplored. Moreover, further comprehensive toxicological and clinical studies are required to ascertain its safety and clinical effectiveness.</div></div>","PeriodicalId":8966,"journal":{"name":"Biomedicine & Pharmacotherapy","volume":null,"pages":null},"PeriodicalIF":6.9,"publicationDate":"2024-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142441723","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-15DOI: 10.1016/j.biopha.2024.117555
Traumatic brain injury (TBI) exhibits high prevalence and mortality, but current treatments remain suboptimal. Traditional Chinese medicine (TCM) has long been effectively used for TBI intervention. Moreover, the recently discovered iron-dependent cell death pathway, known as ferroptosis, characterized by lipid peroxidation, as a key target in TCM-based treatments for TBI. This review provides a comprehensive overview of the latest advancements in TCM strategies targeting ferroptosis in TBI therapy, covering natural product monomers, classic formulas, and acupuncture/moxibustion. The review also addresses current challenges and outlines future research directions to further advance the development and application of TBI management strategies.
{"title":"Targeting ferroptosis in treating traumatic brain injury: Harnessing the power of traditional Chinese medicine","authors":"","doi":"10.1016/j.biopha.2024.117555","DOIUrl":"10.1016/j.biopha.2024.117555","url":null,"abstract":"<div><div>Traumatic brain injury (TBI) exhibits high prevalence and mortality, but current treatments remain suboptimal. Traditional Chinese medicine (TCM) has long been effectively used for TBI intervention. Moreover, the recently discovered iron-dependent cell death pathway, known as ferroptosis, characterized by lipid peroxidation, as a key target in TCM-based treatments for TBI. This review provides a comprehensive overview of the latest advancements in TCM strategies targeting ferroptosis in TBI therapy, covering natural product monomers, classic formulas, and acupuncture/moxibustion. The review also addresses current challenges and outlines future research directions to further advance the development and application of TBI management strategies.</div></div>","PeriodicalId":8966,"journal":{"name":"Biomedicine & Pharmacotherapy","volume":null,"pages":null},"PeriodicalIF":6.9,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142437905","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-15DOI: 10.1016/j.biopha.2024.117458
Oral cancers are a significant global health concern, with a high incidence of treatment failure primarily due to the development of drug resistance. Long non-coding RNAs (lncRNAs) have emerged as critical regulators of gene expression, playing pivotal roles in various cellular processes, including tumor progression and response to therapy. This review explores the multifaceted roles of lncRNAs in the development of drug resistance in oral cancers. We highlight the mechanisms by which lncRNAs modulate drug efflux, apoptosis, epithelial-mesenchymal transition (EMT), and other pathways associated with chemoresistance. Key lncRNAs implicated in resistance to commonly used chemotherapeutic agents in oral cancers are discussed, along with their potential as therapeutic targets. Understanding the involvement of lncRNAs in drug resistance mechanisms offers promising avenues for overcoming treatment barriers and improving patient outcomes. This review underscores the need for further research to elucidate the precise roles of lncRNAs in oral cancer resistance and their translation into clinical interventions.
{"title":"The roles of lncRNAs in the development of drug resistance of oral cancers","authors":"","doi":"10.1016/j.biopha.2024.117458","DOIUrl":"10.1016/j.biopha.2024.117458","url":null,"abstract":"<div><div>Oral cancers are a significant global health concern, with a high incidence of treatment failure primarily due to the development of drug resistance. Long non-coding RNAs (lncRNAs) have emerged as critical regulators of gene expression, playing pivotal roles in various cellular processes, including tumor progression and response to therapy. This review explores the multifaceted roles of lncRNAs in the development of drug resistance in oral cancers. We highlight the mechanisms by which lncRNAs modulate drug efflux, apoptosis, epithelial-mesenchymal transition (EMT), and other pathways associated with chemoresistance. Key lncRNAs implicated in resistance to commonly used chemotherapeutic agents in oral cancers are discussed, along with their potential as therapeutic targets. Understanding the involvement of lncRNAs in drug resistance mechanisms offers promising avenues for overcoming treatment barriers and improving patient outcomes. This review underscores the need for further research to elucidate the precise roles of lncRNAs in oral cancer resistance and their translation into clinical interventions.</div></div>","PeriodicalId":8966,"journal":{"name":"Biomedicine & Pharmacotherapy","volume":null,"pages":null},"PeriodicalIF":6.9,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142437813","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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