Chemico-Biological Interactions最新文献

{"title":"TUG1 protects against ferroptosis of hepatic stellate cells by upregulating PDK4-mediated glycolysis","authors":"Xiangting Zhang ,&nbsp;Luying Zhao ,&nbsp;Kanglei Ying ,&nbsp;Jun Xu ,&nbsp;Yangjin Huang ,&nbsp;Ruhuang Zhu ,&nbsp;Yinrong Ding ,&nbsp;Weimin Cai ,&nbsp;Xiao Wu ,&nbsp;Dan Miao ,&nbsp;Qian Xu ,&nbsp;Yuan Zeng ,&nbsp;Fujun Yu","doi":"10.1016/j.cbi.2023.110673","DOIUrl":"10.1016/j.cbi.2023.110673","url":null,"abstract":"<div><p><span><span>The induction of ferroptosis in hepatic stellate cells (HSCs) has shown promise in reversing </span>liver fibrosis<span>. And ferroptosis has been confirmed to be associated with glycolysis. The objective of this study is to determine whether ferroptosis inhibition in HSCs, induced by elevation of recombinant pyruvate<span> dehydrogenase kinase isozyme 4 (PDK4)-mediated glycolysis, could mediate the pathogenesis of liver fibrosis. Liver fibrosis was induced using CCl</span></span></span>₄<span>, the level of which was assessed through histochemical staining. Lentivirus was used to modulate the expression of specific genes. And underlying mechanisms were explored using primary HSCs extracted from normal mice. The results confirmed that Taurine up-regulated gene 1 (TUG1) expression was upregulated in liver fibrotic tissues and HSCs, showing a positive correlation with fibrosis. In addition, TUG1 attenuated ferroptosis in HSCs by promoting PDK4-mediated glycolysis, thereby promoting the progression of liver fibrosis. Moreover, TUG1 was observed to impact HSCs activation, exacerbating liver fibrosis to some extent. In conclusion, our study revealed that TUG1 expression was elevated in mouse models of liver fibrosis and activated HSCs, which inhibited ferroptosis in HSCs through PDK4-mediated glycolysis. This finding may open up a new therapeutic strategy for liver fibrosis.</span></p></div>","PeriodicalId":274,"journal":{"name":"Chemico-Biological Interactions","volume":"383 ","pages":"Article 110673"},"PeriodicalIF":5.1,"publicationDate":"2023-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10647942","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"How do different bile acid derivatives affect rat macrophage function – Friends or foes?","authors":"Nikola M. Stojanović ,&nbsp;Pavle J. Randjelović ,&nbsp;Aleksandra Maslovarić ,&nbsp;Miloš Kostić ,&nbsp;Vidak Raičević ,&nbsp;Marija Sakač ,&nbsp;Srđan Bjedov","doi":"10.1016/j.cbi.2023.110688","DOIUrl":"10.1016/j.cbi.2023.110688","url":null,"abstract":"<div><p><span>Due to an increased need for new immunomodulatory agents, many previously known molecules have been structurally modified in order to obtain new drugs, preserving at the same time some of the benevolent characteristics of the parent molecule. This study aimed to evaluate the immunomodulatory potential of a selected library of bile acid<span> derivatives (BAD) using a broad spectrum of assays, evaluating rat peritoneal macrophages viability, cell membrane damage, lysosomal and adhesion function, and nitric oxide<span> and cytokine production as a response to lipopolysaccharide stimulation. Also, </span></span></span><em>in silico</em> studies on two bile acid-activated receptors were conducted and the results were related to the observed <em>in vitro</em><span> effects. All tested BAD exerted significant toxicity in concentrations higher than 10 μM, which was determined based on mitochondria and cell membrane damage in a panel of assays. On the other hand, at lower concentrations, the tested BAD proved to be immunomodulatory since they affected lysosomal function, cell adhesion capacities and the ability to produce inflammatory cytokines in response to a stimulus. One of the compounds proved to exhibit significant toxicity toward macrophages, but also caused a concentration-dependent decrease in nitric oxide levels and was identified as a potential farnesoid X receptor agonist.</span></p></div>","PeriodicalId":274,"journal":{"name":"Chemico-Biological Interactions","volume":"383 ","pages":"Article 110688"},"PeriodicalIF":5.1,"publicationDate":"2023-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10648880","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gypenosides suppress hepatocellular carcinoma cells by blocking cholesterol biosynthesis through inhibition of MVA pathway enzyme HMGCS1","authors":"Man-Yu Xiao,&nbsp;Fang-Fang Li,&nbsp;Peng Xie,&nbsp;Yan-Shuang Qi,&nbsp;Jin-Bo Xie,&nbsp;Wen-Jing Pei,&nbsp;Hao-Tian Luo,&nbsp;Mei Guo,&nbsp;Yu-Long Gu,&nbsp;Xiang-Lan Piao","doi":"10.1016/j.cbi.2023.110674","DOIUrl":"10.1016/j.cbi.2023.110674","url":null,"abstract":"<div><p><span><span><span>Hepatocellular carcinoma (HCC) is one of the most common malignant tumors with high morbidity and mortality. Targeting abnormal cholesterol metabolism is a potential therapeutic direction. Therefore, more natural </span>drugs targeting cholesterol in HCC need to be developed. </span>Gypenosides (Gyp), the major constituent of </span><span><em>Gynostemma pentaphyllum</em></span><span>, has been demonstrated to have pharmacological properties on anti-cancer, anti-obesity, and hepatoprotective. We investigated whether Gyp, isolated and purified by our lab, could inhibit HCC progression by inhibiting cholesterol synthesis. The present research showed that Gyp inhibited proliferation and migration, and induced apoptosis in Huh-7 and Hep3B cells. Metabolomics, transcriptomics, and target prediction all suggested that lipid metabolism<span> and cholesterol biosynthesis were the mechanisms of Gyp. Gyp could limit the production of cholesterol and target HMGCS1, the cholesterol synthesis-related protein. Downregulation of HMGCS1 could suppress the progression and abnormal cholesterol metabolism of HCC. In terms of mechanism, Gyp suppressed mevalonate<span> (MVA) pathway mediated cholesterol synthesis by inhibiting HMGCS1 transcription factor SREBP2. And the high expression of HMGCS1 in HCC human specimens was correlated with poor clinical prognosis. The data suggested that Gyp could be a promising cholesterol-lowering drug for the prevention and treatment of HCC. And targeting SREBP2-HMGCS1 axis in MVA pathway might be an effective HCC therapeutic strategy.</span></span></span></p></div>","PeriodicalId":274,"journal":{"name":"Chemico-Biological Interactions","volume":"383 ","pages":"Article 110674"},"PeriodicalIF":5.1,"publicationDate":"2023-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10282828","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Laxiflorin B covalently binds the tubulin colchicine-binding site to inhibit triple negative breast cancer proliferation and induce apoptosis","authors":"Heng Yang ,&nbsp;Tiantian Zhang ,&nbsp;Chunlan Chen ,&nbsp;Chengyao Chiang ,&nbsp;Kai Chen ,&nbsp;Yan Wu ,&nbsp;Zhengxin Liu ,&nbsp;Yajun Zhou ,&nbsp;Lizhi Zhu ,&nbsp;Duo Zheng","doi":"10.1016/j.cbi.2023.110681","DOIUrl":"10.1016/j.cbi.2023.110681","url":null,"abstract":"<div><p>Laxiflorin B is a natural <em>ent</em><span>-kaurane diterpenoid that can be isolated from the leaves of the </span><span><em>Isodon</em><em> eriocalyx</em></span> var. <em>laxiflora</em><span><span>, a perennial shrub native to parts of China. While this compound has potent cytotoxic activity against various tumor cells, the anti-tumor targets and molecular mechanisms of Laxiflorin B are unclear. Here, we show that Laxiflorin B exhibits strong antiproliferative and proapoptotic effects on triple-negative breast cancer (TNBC) cells. At the mechanistic level, we show that β-tubulin (TUBB) is a cellular target of Laxiflorin B. By covalently binding the Cys239 and C354 residues of the TUBB colchicine-binding site, Laxiflorin B disturbs microtubule integrity and structure in vitro and in vivo. Cytotoxicity analyses also showed that the α, β-unsaturated carbonyl in the D ring of Laxiflorin B is responsible for mediating its covalent binding and anti-tumor activity. To assess the therapeutic effects of Laxiflorin B, we synthesized a Laxiflorin B-ALA pro-drug and delivered it by intraperitoneal injection (10 mg/kg) into a 4T1 orthotopic tumor mouse model. Drug treatment had anti-tumor effects without inducing notable weight loss or organ dysfunction. We conclude that Laxiflorin B is a promising </span>colchicine binding site inhibitor that might be exploited in the context of TNBC treatment in the future.</span></p></div>","PeriodicalId":274,"journal":{"name":"Chemico-Biological Interactions","volume":"383 ","pages":"Article 110681"},"PeriodicalIF":5.1,"publicationDate":"2023-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10283325","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic characteristics of voriconazole – Induced liver injury in rats","authors":"Qian Du,&nbsp;Mengmeng Teng,&nbsp;Luting Yang,&nbsp;Chao Meng,&nbsp;Yulan Qiu,&nbsp;Chuhui Wang,&nbsp;Jiaojiao Chen,&nbsp;Taotao Wang,&nbsp;Siying Chen,&nbsp;Yu Luo,&nbsp;Jinyao Sun,&nbsp;Yalin Dong","doi":"10.1016/j.cbi.2023.110693","DOIUrl":"10.1016/j.cbi.2023.110693","url":null,"abstract":"<div><p>Voriconazole<span><span> (VOR) – induced liver injury is a common adverse reaction, and can lead to serious clinical outcomes. It is of great significance to describe the metabolic characteristics of VOR – induced liver injury and to elucidate the potential mechanisms. This study investigated the changes of plasma metabolic profiles in a rat model of VOR – induced liver injury by non – targeted metabolomics. Correlation analysis was performed between differentially expressed metabolites and plasma liver function indexes. The metabolites with strong correlation were determined for their predictive performance for liver injury using receiver operating characteristic (ROC) curve analysis. Potential biomarkers were then screened combined with liver pathological scores. Finally, the expression level of genes that involved in lipid metabolism were determined in rat liver to verify the mechanism of VOR – induced liver injury we proposed. VOR – induced liver injury in rats was characterized by plasma </span>alanine<span> aminotransferase (ALT) and aspartate<span><span><span> aminotransferase (AST) elevation, the lipid droplets accumulation in liver, as well as inflammation and </span>fibrosis. Significant changes of plasma metabolites were observed, with a decrease in lipid metabolites accounting for over 50% of all changed metabolites, and alterations of cholesterol and </span>bile acids<span> metabolites. The decrease of 3 phosphatidylcholine (PC) in plasma could indicate the occurrence of VOR – induced liver injury. Decreased fatty acids (FA) oxidation and bile acid excretion might be the potential mechanisms of VOR – induced liver injury. This study provided new insights into the molecular characterization of VOR – induced liver injury.</span></span></span></span></p></div>","PeriodicalId":274,"journal":{"name":"Chemico-Biological Interactions","volume":"383 ","pages":"Article 110693"},"PeriodicalIF":5.1,"publicationDate":"2023-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10648919","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Particle-induced osteolysis is mediated by endoplasmic reticulum stress-associated osteoblast apoptosis","authors":"Xin Yu ,&nbsp;Hao Ding ,&nbsp;Dongsheng Wang ,&nbsp;Zhengrong Ren ,&nbsp;Bin Chen ,&nbsp;Qi Wu ,&nbsp;Tao Yuan ,&nbsp;Yang Liu ,&nbsp;Lei Zhang ,&nbsp;Jianning Zhao ,&nbsp;Zhongyang Sun","doi":"10.1016/j.cbi.2023.110686","DOIUrl":"10.1016/j.cbi.2023.110686","url":null,"abstract":"<div><p><span>Osteoblast dysfunction plays a crucial role in periprosthetic osteolysis and aseptic loosening, and </span>endoplasmic reticulum<span> (ER) stress is recognized as an important causal factor of wear particle-induced osteolysis. However, the influence of ER stress on osteoblast activity during osteolysis and its underlying mechanisms remain elusive. This study aims to investigate whether ER stress is involved in the detrimental effects of wear particles on osteoblasts. Through our investigation, we observed elevated expression levels of ER stress and apoptosis markers in particle-stimulated bone specimens and osteoblasts. To probe further, we employed the ER stress inhibitor, 4-PBA, to treat particle-stimulated osteoblasts. The results revealed that 4-PBA effectively alleviated particle-induced osteoblast apoptosis and mitigated osteogenic reduction. Furthermore, our study revealed that wear particle-induced ER stress in osteoblasts coincided with mitochondrial damage, calcium overload, and oxidative stress<span>, all of which were effectively alleviated by 4-PBA treatment. Encouragingly, 4-PBA administration also improved bone formation and attenuated osteolysis in a mouse calvarial model. In conclusion, our results demonstrate that ER stress plays a crucial role in mediating wear particle-induced osteoblast apoptosis and impaired osteogenic function. These findings underscore the critical involvement of ER stress in wear particle-induced osteolysis and highlight ER stress as a potential therapeutic target for ameliorating wear particle-induced osteogenic reduction and bone destruction.</span></span></p></div>","PeriodicalId":274,"journal":{"name":"Chemico-Biological Interactions","volume":"383 ","pages":"Article 110686"},"PeriodicalIF":5.1,"publicationDate":"2023-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10283799","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sequences, phylogeny and evolution of mitochondrial delta-1-pyrroline-5-carboxylate dehydrogenases (ALDH4A1). Evidence for a second locus (ALDH4A2) in Drosophila","authors":"Roger S. Holmes","doi":"10.1016/j.cbi.2023.110679","DOIUrl":"10.1016/j.cbi.2023.110679","url":null,"abstract":"<div><p><span><em>ALDH4A1</em></span><span><span> genes encode mitochondrial enzymes<span><span> of delta-1-pyrroline-5-carboxylate metabolism, generating glutamate<span> from either proline or </span></span>ornithine. Analyses were undertaken of several vertebrate and invertebrate genomes using reported human and mouse ALDH4A1 amino acid sequences. ALDH4A1 sequences and structures were highly conserved, including residues involved in catalysis, </span></span>coenzyme binding and enzyme structure, previously reported for mouse and human ALDH4A1. The human </span><em>ALDH4A1</em><span> gene contained 15 coding exons and was more highly expressed in human liver and kidney cortex. Vertebrate ALDH4A1 mitochondrial leader sequences exhibited diverse sequences. Phylogeny studies supported the appearance of the </span><em>ALDH4A1</em> gene in invertebrate evolution which has been conserved and retained throughout subsequent vertebrate evolution as a single <em>ALDH4A1</em><span> gene. Exceptions included polyploidy observed for the Atlantic salmon (</span><em>Salmo salar</em>) and African toad (<span><em>Xenopus laevis</em></span>) genes. An examination of <em>ALDH4A1</em> sequences from related <em>Drosophila</em> species supported the appearance of a second <em>ALDH4A</em> gene (<em>ALDH4A2</em>) and time dependent evolutionary changes over the past 50 million years for both genes.</p></div>","PeriodicalId":274,"journal":{"name":"Chemico-Biological Interactions","volume":"383 ","pages":"Article 110679"},"PeriodicalIF":5.1,"publicationDate":"2023-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10304402","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Butyrylcholinesterase and lipid metabolism: Possible dual role in metabolic disorders","authors":"Lupe Furtado-Alle,&nbsp;Luciane V. Tureck,&nbsp;Carolina S. de Oliveira,&nbsp;João V.M. Hortega,&nbsp;Ricardo L.R. Souza","doi":"10.1016/j.cbi.2023.110680","DOIUrl":"10.1016/j.cbi.2023.110680","url":null,"abstract":"<div><p><span><span><span><span>Butyrylcholinesterase (BChE), an enzyme primarily found in the liver, plasma, and brain, has been recognized for its role in the hydrolysis of </span>choline esters. Recent studies have shed light on its involvement in </span>lipid metabolism<span>, revealing its potential as a crucial player in maintaining lipid homeostasis. However, the interactions between external factors and BChE activity in lipid metabolic pathways remain a complex subject of study. This review summarizes the current knowledge regarding BChE activity and lipid metabolism and seeks to clarify the nature of this relationship as causal or consequential. Evidence supports the role of BChE in energy homeostasis disruption, such as obesity and related </span></span>metabolic disorders<span>, where it exhibits lipolytic activity and mediates fatty acid use and storage. The unexpected functions of BChE in lipoprotein synthesis and the impact of polymorphic variants of the </span></span><em>BCHE</em> gene suggest a central role in lipid metabolism; however, further investigation is needed to confirm and describe these functions, especially considering the metabolic context. Furthermore, exploring therapeutic interventions in lipid metabolism disorders contributes to elucidating their implications on BChE activity, but attention to the metabolic status and genotypes as possible factors in this interaction is needed. In summary, further research in this field holds promise for improving our understanding of the complex interplay between BChE and lipid metabolism, and its potential clinical applications. However, the available data corroborate the dual role of BChE activity, both as a critical responsive element to metabolic challenges and as a predisposition factor to metabolic diseases.</p></div>","PeriodicalId":274,"journal":{"name":"Chemico-Biological Interactions","volume":"383 ","pages":"Article 110680"},"PeriodicalIF":5.1,"publicationDate":"2023-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10283301","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protective effects of phosphocreatine on human vascular endothelial cells against hydrogen peroxide-induced apoptosis and in the hyperlipidemic rat model","authors":"Zhongyuan Tang ,&nbsp;Zonghui Zhang ,&nbsp;Jiaqi Wang ,&nbsp;Zhengwu Sun ,&nbsp;Eskandar Qaed ,&nbsp;Xinming Chi ,&nbsp;Jun Wang ,&nbsp;Yazeed Jamalat ,&nbsp;Zhaohong Geng ,&nbsp;Zeyao Tang ,&nbsp;Qiying Yao","doi":"10.1016/j.cbi.2023.110683","DOIUrl":"10.1016/j.cbi.2023.110683","url":null,"abstract":"<div><p><span><span>Phosphocreatine (PCr) has been shown to have a cardio-protective effect during cardiopulmonary resuscitation (CPR). However, little is known about its impact on </span>atherosclerosis. In this study, we first evaluated the pharmacological effects of PCr on antioxidative defenses and mitochondrial protection against hydrogen peroxide (H</span>₂O₂<span><span>) induced human umbilical vascular endothelial cells (HUVECs) damage. Then we investigated the hypolipidemic and antioxidative effects of PCr on </span>hyperlipidemic rat model. Via </span><em>in vitro</em> studies, H₂O₂<span> significantly reduced cell viability<span> and increased apoptosis rate of HUVECs, while pretreatment<span> with PCr abolished its apoptotic effect. PCr could reduce the generation of ROS induced by H</span></span></span>₂O₂<span><span>. Moreover, PCr could increase the activity of SOD<span> and the content of NO, as well as decrease the activity of LDH and the content of </span></span>MDA. PCr could also antagonize H</span>₂O₂-induced up-regulation of Bax, cleaved-caspase3, cleaved-caspase9, and H₂O₂-induced down-regulation of Bcl-2 and p-Akt/Akt ratio. In addition, PCr reduced U937 cells’ adhesion to H₂O₂-stimulated HUVECs. Via <em>in vivo</em><span><span> study, PCr could decrease MDA, TC, TG and LDL-C levels in hyperlipidemic rats. Finally, different-concentration PCr could increase the </span>leaching of TC, HDL, and TG from fresh human atherosclerotic plaques. In conclusion, PCr could suppress H</span>₂O₂-induced apoptosis in HUVECs and reduce hyperlipidemia through inhibiting ROS generation and modulating dysfunctional mitochondrial system, which might be an effective new therapeutic strategy to further prevent atherosclerosis.</p></div>","PeriodicalId":274,"journal":{"name":"Chemico-Biological Interactions","volume":"383 ","pages":"Article 110683"},"PeriodicalIF":5.1,"publicationDate":"2023-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10283322","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Indole alkaloids from marine resources: Understandings from therapeutic point of view to treat cancers","authors":"Fahadul Islam ,&nbsp;Zerrouki Dehbia ,&nbsp;Mehrukh Zehravi ,&nbsp;Rajib Das ,&nbsp;M. Sivakumar ,&nbsp;Karthickeyan Krishnan ,&nbsp;Abdul Ajeed Mohathasim Billah ,&nbsp;Bharadhan Bose ,&nbsp;Avoy Ghosh ,&nbsp;Shyamjit Paul ,&nbsp;Firzan Nainu ,&nbsp;Irfan Ahmad ,&nbsp;Talha Bin Emran","doi":"10.1016/j.cbi.2023.110682","DOIUrl":"10.1016/j.cbi.2023.110682","url":null,"abstract":"<div><p><span>Cancer is the leading cause of mortality all over the world. Scientific investigation has demonstrated that disruptions in the process of autophagy are frequently interrelated with the emergence of cancer. Hence, scientists are seeking permanent solutions to counter the deadly disease. Indole alkaloids<span> have been extensively studied and are acknowledged to exhibit several bioactivities. The current state of disease necessitates novel pharmacophores development. In recent decades, indole alkaloids have become increasingly significant in cancer treatment and are also used as adjuvants. A substantial amount of pharmacologically active molecules come from indole alkaloids, which are widely distributed in nature. Indole alkaloids derived from marine organisms show immense potential for therapeutic applications and seem highly effective in cancer treatment. A couple of experiments have been conducted preclinically to investigate the possibility of indole alkaloids in cancer treatment. Marine-derived indole alkaloids possess the ability to exhibit anticancer properties through diverse antiproliferative mechanisms. Certain indole alkaloids, including </span></span>vincristine<span> and vinblastine<span>, were verified in clinical trials<span> or are presently undergoing clinical assessments for preventing and treating cancer. Indole alkaloids from marine resources hold a significant functionality in identifying new antitumor agents. The current literature highlights recent advancements in indole alkaloids that appear to be anticancer agents and the underlying mechanisms.</span></span></span></p></div>","PeriodicalId":274,"journal":{"name":"Chemico-Biological Interactions","volume":"383 ","pages":"Article 110682"},"PeriodicalIF":5.1,"publicationDate":"2023-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10275785","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}