Frontiers in bioscience (Landmark edition)最新文献

{"title":"LncRNA-TUG1: Implications in the Myocardial and Endothelial Cell Oxidative Stress Injury Caused by Hemorrhagic Shock and Fluid Resuscitation.","authors":"Wei Li, Huaiyu Chen, Xueli Zhu, Mingrui Lin","doi":"10.31083/j.fbl2911376","DOIUrl":"https://doi.org/10.31083/j.fbl2911376","url":null,"abstract":"<p><strong>Background: </strong>LncRNA taurine-upregulated gene 1 (<i>TUG1</i>) can regulate vascular endothelial cell injury, a critical mechanism in treating hemorrhagic shock and fluid resuscitation (HS/R). Therefore, this study explored the influence of <i>TUG1</i> in HS/R.</p><p><strong>Methods: </strong>An <i>in vivo</i> rat model of ischemia-reperfusion (I/R) injury post-HS/R and an <i>in vitro</i> model of oxidative stress injury in rat cardiomyocyte cell line (H9C2) were constructed. <i>In vivo</i>, we silenced <i>TUG1</i> and quantified its expression along with inflammatory factors through quantitative reverse transcription polymerase chain reaction (qRT-PCR), mean arterial pressure (MAP) detection and blood gas analysis. Myocardial functional impairment was assessed via Triphenyl-2H-Tetrazolium Chloride (TTC), Hematoxylin and eosin, and Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling (TUNEL) stainings. Oxidative stress level in rat serum was measured. <i>In vitro</i>, we examined the changes of cell viability, apoptosis, oxidative stress levels, inflammatory factor secretion and nuclear factor-κB (NF-κB)/p65 expression by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), flow cytometry, Enzyme-linked immunosorbent assay (ELISA) and Western blot.</p><p><strong>Results: </strong><i>TUG1</i> level was elevated in rats of I/R model caused by HS/R. <i>TUG1</i> silencing ameliorated the decline in MAP, acid-base imbalance and myocardial tissue damage, and suppressed oxidative stress and inflammatory factor levels in model rat. <i>TUG1</i> silencing enhanced viability, impeded apoptosis, and reduced oxidative stress, inflammatory factor contents and NF-κB/p65 expression in H₂O₂ treated H9C2 cells.</p><p><strong>Conclusion: </strong><i>TUG1</i> participates in regulating oxidative stress damage and inflammation induced by HS/R.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 11","pages":"376"},"PeriodicalIF":3.3,"publicationDate":"2024-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142755971","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}

{"title":"Oncolytic Vesicular Stomatitis Virus: Optimisation Strategies for Anti-Cancer Therapies.","authors":"Margarita Zinovieva, Anastasia Ryapolova, Alexander Karabelsky, Ekaterina Minskaia","doi":"10.31083/j.fbl2911374","DOIUrl":"10.31083/j.fbl2911374","url":null,"abstract":"<p><p>Oncolytic viruses (OVs) represent a targeted anti-cancer therapy approach due to their ability not only to selectively infect and destroy malignant cells but also to induce an immune response. Vesicular stomatitis virus (VSV) offers a promising platform due to its low prevalence and pathogenicity in humans, lack of pre-existing immunity, easily manipulated genome, rapid growth to high titers in a broad range of cell lines, and inability to integrate into the host genome. However, despite its many advantages, many unresolved problems remain: problematic production based on the reverse genetics system, oncological selectivity, and the overall effectiveness of VSV monotherapy. This review will discuss various attempts at viral genome modifications aimed at improving the oncolytic properties of VSV. These strategies include inhibition of viral genes, modification of genes responsible for targeting cancer cells over healthy ones, insertion of foreign genes for boosting immune response, and changing the order of viral and inserted foreign genes. In addition, possible ways to improve VSV-based anti-tumor therapy and achieve higher efficiency will be considered by evaluating the effectiveness of various delivery methods as well as discussing treatment options by combining VSV with other groups of anticancer drugs.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 11","pages":"374"},"PeriodicalIF":3.3,"publicationDate":"2024-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142755984","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}

{"title":"Circulating Extracellular Vesicles: An Effective Biomarker for Cancer Progression.","authors":"Madhura Chatterjee, Saurabh Gupta, Sayoni Nag, Ishita Rehman, Deepak Parashar, Arindam Maitra, Kaushik Das","doi":"10.31083/j.fbl2911375","DOIUrl":"10.31083/j.fbl2911375","url":null,"abstract":"<p><p>Extracellular vesicles (EVs), the ubiquitous part of human biology, represent a small heterogenous, membrane-enclosed body that contains a diverse payload including genetic materials in the form of DNA, RNAs, small non-coding RNAs, etc. mostly mirroring their source of origin. Since, a vast majority of research has been conducted on how nucleic acids, proteins, lipids, and metabolites, associated with EVs can be effectively utilized to identify disease progression and therapeutic responses in cancer patients, EVs are increasingly being touted as valuable and reliable identifiers of cancer biomarkers in liquid biopsies. However, the lack of comprehensive clinical validation and effective standardization protocols severely limits its applications beyond the laboratories. The present review focuses on understanding the role of circulating EVs in different cancers and how they could potentially be treated as cancer biomarkers, typically due to the presence of bioactive molecules such as small non-coding RNAs, RNAs, DNA, proteins, etc., and their utilization for fine-tuning therapies. Here, we provide a brief general biology of EVs including their classification and subsequently discuss the source of circulatory EVs, the role of their associated payload as biomarkers, and how different cancers affect the level of circulatory EVs population.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 11","pages":"375"},"PeriodicalIF":3.3,"publicationDate":"2024-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142755815","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}

{"title":"NUF2 Promotes Breast Cancer Metastasis via Activating Wnt/β-Catenin Pathways.","authors":"Nijiati AiErken, Xidi Wang, Jiamei Wang, Weisen Ma, Lingfei Cui, Mingxia Zhang, Weifeng Ma, Dongwei Liu","doi":"10.31083/j.fbl2911371","DOIUrl":"https://doi.org/10.31083/j.fbl2911371","url":null,"abstract":"<p><strong>Background: </strong>Breast cancer is the most common malignancy and the leading cause of cancer death among women. NDC80 kinetochore complex component (NUF2) is demonstrated to implicate the progression of human cancer. But the role of NUF2 in breast cancer progression is unclear. Here, we aimed to study the role and regulatory mechanisms of NUF2 in breast cancer metastasis.</p><p><strong>Methods: </strong>Immunohistochemistry was used to determine UNF2 expression in clinical samples. Transwell assas were used to determine the role of NUF2 in breast cancer migration and invasion. Animal model <i>in vivo</i> was used to determine the rold of NUF2 in breast cancer metastasis.</p><p><strong>Results: </strong>NUF2 was upregulated significantly in breast cancer tissues and cells. Worse prognosis was noted in patients with high NUF2 levels compared with that in patients with low NUF2 levels. NUF2 overexpression markedly enhanced, while NUF2 knockdown inhibited, breast cancer cell invasion and migration. Mechanistically, NUF2 was observed to upregulate Wnt/β-catenin signaling pathway activity. The promoting effect of NUF2 on cell migration and invasion were blocked by inhibition of the Wnt/β-catenin pathway.</p><p><strong>Conclusions: </strong>We revealed that NUF2 promotes breast cancer progression via activating Wnt/β-catenin signaling, suggesting that NUF2 might be a new potential target for breast cancer treatment.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 11","pages":"371"},"PeriodicalIF":3.3,"publicationDate":"2024-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142755975","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}

{"title":"Joint Analysis of CCAAT/Enhancer-Binding Protein Beta and Interleukin 1 Beta in the Treatment and Prognosis of Diffuse Large B-Cell Lymphoma.","authors":"Hongmin Wang, Shuo Zhang, Mengmeng Wang, Chaozhong Wang, Jihong Xu, Ming Jiang, Xue Han, Xiaotong Yang, Liping Zhang, Baotong Chen, Aichun Liu","doi":"10.31083/j.fbl2911372","DOIUrl":"https://doi.org/10.31083/j.fbl2911372","url":null,"abstract":"<p><strong>Objective: </strong>The purpose of this study is to investigate the correlation between elevated levels of CCAAT/enhancer-binding protein beta (<i>CEBPB</i>) gene expression and unfavorable outcomes in diffuse large B-cell lymphoma (DLBCL). The goal is to elucidate potential therapeutic targets associated with this relationship.</p><p><strong>Methods: </strong>Differential expression and survival analyses were conducted using data from the Gene Expression Omnibus (GEO) database. The functions of <i>CEBPB</i> in DLBCL cells were investigated through cell culture, RNA extraction, quantitative real-time polymerase chain reaction (qRT-PCR), and Western blot. In addition, a weighted gene co-expression network analysis (WGCNA) was performed to pinpoint gene modules associated with <i>CEBPB</i>. Furthermore, experimental validation was carried out to explore the interaction between <i>CEBPB</i> and interleukin 1 beta (<i>IL1B</i>).</p><p><strong>Results: </strong>High levels of <i>CEBPB</i> expression are prominently observed in DLBCL, with its overabundance significantly linked to the diagnosis of DLBCL. Survival analysis reveals that patients exhibiting elevated <i>CEBPB</i> expression tend to experience a poorer prognosis. Further validation confirmed <i>CEBPB</i>'s role in promoting DLBCL cell proliferation and cell cycle progression. WGCNA identified <i>CEBPB</i>-related gene modules, with <i>IL1B</i> identified as a potential regulatory gene of <i>CEBPB</i>. The presence of high levels of <i>IL1B</i> has been correlated with an unfavorable prognosis in individuals diagnosed with DLBCL. Experiments demonstrate that <i>IL1B</i> promotes DLBCL cell proliferation through <i>CEBPB</i>.</p><p><strong>Conclusions: </strong>This study reveals the significant roles of <i>CEBPB</i> and <i>IL1B</i> in DLBCL, providing new theoretical foundations and potential molecular targets for the treatment and prognosis of DLBCL.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 11","pages":"372"},"PeriodicalIF":3.3,"publicationDate":"2024-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142755966","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}

{"title":"Decitabine Enhances Sorafenib Sensitivity in Renal Cell Carcinoma by Promoting BIN1 and SYNE1 Expressions.","authors":"Lijie Kang, Mengyun Jin, Yuqin Mao, Aixiao Xia","doi":"10.31083/j.fbl2910370","DOIUrl":"https://doi.org/10.31083/j.fbl2910370","url":null,"abstract":"<p><strong>Background: </strong>Renal cell carcinoma (RCC), especially clear cell RCC (ccRCC), significantly impacts health, and results in particularly poor outcomes in patients at the advanced stage. Resistance to vascular endothelial growth factor (VEGF) pathway-targeting tyrosine kinase inhibitors (TKIs) is a major barrier in effective ccRCC treatment. Herein, we aim to explore how decitabine mediates bridging integrator 1 (BIN1) and spectrin repeat containing nuclear envelope protein 1 (SYNE1) to impact resistance of ccRCC to sorafenib.</p><p><strong>Methods: </strong>Employing bioinformatics on datasets GSE64052 and CancerSea, we identified genes linked to TKI resistance, ultimately focusing on SYNE1. We assessed influences of SYNE1 overexpression and BIN1 knockdown via quantitative real-time PCR (qRT-PCR) and Western blot. Assessment of cell viability and apoptosis was accomplished using cell counting kit-8 (CCK-8) assays and flow cytometry. The investigation into the potential interactions between SYNE1 and BIN1, as well as their impacts on sorafenib sensitivity was accomplished by Co-Immunoprecipitation (Co-IP) and Glutathione-S-transferase (GST) Pull-down.</p><p><strong>Results: </strong>SYNE1 was substantially down-regulated in sorafenib-resistant ccRCC cells, and its overexpression increased sorafenib sensitivity, decreased viability and enhanced apoptosis. Interaction between BIN1 and SYNE1 was confirmed, with BIN1 level lower in resistant cells. BIN1 knockdown reduced the beneficial effects of SYNE1 overexpression on sorafenib sensitivity. Decitabine treatment elevated both SYNE1 and BIN1, while boosting apoptosis and reducing sorafenib resistance.</p><p><strong>Conclusions: </strong>SYNE1 contributes to the modulation of sorafenib resistance in ccRCC cells through interacting with BIN1. Decitabine treatment enhances expressions of these two proteins to improve TKI response, suggesting a potential strategy for counteracting resistance and bettering patient outcomes.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 10","pages":"370"},"PeriodicalIF":3.3,"publicationDate":"2024-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142549321","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}

{"title":"Diallyl Disulfide Mitigates Cadmium Hepatotoxicity by Attenuating Oxidative Stress and TLR-4/NF-κB Signaling and Upregulating PPARγ.","authors":"Reem S Alruhaimi, Emad H M Hassanein, Mohammed F Alotaibi, Mohammed A Alzoghaibi, Omnia A M Abd El-Ghafar, Mostafa K Mohammad, Sulaiman M Alnasser, Ayman M Mahmoud","doi":"10.31083/j.fbl2910369","DOIUrl":"https://doi.org/10.31083/j.fbl2910369","url":null,"abstract":"<p><strong>Background: </strong>Heavy metals can cause serious health problems that affect different organs. Cadmium (Cd) is an environmental contaminant known for its toxicological consequences on different organs. Hepatotoxicity is a serious effect of exposure to Cd with oxidative stress (OS) and inflammation playing a central role. Diallyl disulfide (DADS), an organo-sulfur compound found in garlic, is known for its cytoprotective and antioxidant effects. In this study, the effect of DADS on Cd-induced inflammation, oxidative stress and liver injury was investigated.</p><p><strong>Methods: </strong>DADS was supplemented for 14 days via oral gavage, and a single intraperitoneal dose of Cd (1.2 mg/kg body weight) was administered to rats on day 7. Blood and liver samples were collected at the end of the experiment for analyses.</p><p><strong>Results: </strong>Cd administration resulted in remarkable hepatic dysfunction, degenerative changes, necrosis, infiltration of inflammatory cells, collagen deposition and other histopathological alterations. Cd increased liver malondialdehyde (MDA) and nitric oxide (NO) (<i>p</i> < 0.001), upregulated toll-like receptor (TLR)-4, nuclear factor-kappaB (NF-κB), pro-inflammatory mediators, and caspase-3 (<i>p</i> < 0.001) whereas decreased glutathione (GSH) and antioxidant enzymes (<i>p</i> < 0.001). Cd downregulated peroxisome proliferator activated receptor gamma (PPARγ), a transcription factor involved in inflammation and OS suppression (<i>p</i> < 0.001). DADS ameliorated liver injury and tissue alterations, attenuated OS and apoptosis, suppressed TLR-4/NF-κB signaling, and enhanced antioxidants. In addition, DADS upregulated PPARγ in the liver of Cd-administered rats.</p><p><strong>Conclusions: </strong>DADS is effective against Cd-induced hepatotoxicity and its beneficial effects are linked to suppression of inflammation, OS and apoptosis and upregulation of PPARγ. DADS could be valuable to protect the liver in individuals at risk of Cd exposure, pending further studies to elucidate other underlying mechanism(s).</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 10","pages":"369"},"PeriodicalIF":3.3,"publicationDate":"2024-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142549322","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}

{"title":"Mitochondrial DNA Alterations in Glioblastoma and Current Therapeutic Targets.","authors":"Maher Kurdi, Ahmed Bamaga, Alaa Alkhotani, Thamer Alsharif, Ghada A Abdel-Hamid, Mohamed E Selim, Taghreed Alsinani, Ahmed Albeshri, Adnan Badahdah, Mazen Basheikh, Saleh Baeesa","doi":"10.31083/j.fbl2910367","DOIUrl":"https://doi.org/10.31083/j.fbl2910367","url":null,"abstract":"<p><p>Metabolic reprogramming within tumor cells involves a shift towards either glycolysis or mitochondrial respiration, depending on the stage of tumor progression. Consequently, irreversible dysfunction of the mitochondria is considered a crucial mechanism driving the progression mechanism. While numerous mutations in mitochondrial DNA (mtDNA) have been identified across various tumor types, including glioblastoma, many studies have been limited in the scope, focusing on small segments of mtDNA or utilizing sequencing methods with restricted sensitivity. As a result, several potentially significant mtDNA mutations may have been underestimated, along with their heteroplasmic states, which play a crucial role in determining the phenotypic impact of mtDNA mutation. Although both somatic and germline mtDNA mutations have been observed in different tumor types, research on the mtDNA mutations linked to glioblastoma remains scarce. The mitochondrial genome encodes thirteen protein-coding genes that are essential for the proper functioning of respiratory complex chains. Alterations in mitochondrial function manifest at various levels, including structural and functional changes, impacting mitogenic, hemodynamic, bioenergetic, and apoptotic signaling pathways. These alterations often signify a reduced efficiency of the oxidative phosphorylation system and energy production in tumor cells. As the crucial role of mitochondrial dysfunction in glioma development grows, mitochondria have emerged as promising targets for therapy aimed at overcoming chemoresistance and eliminating cancer cells. This brief review outlines the association between mtDNA alteration and glioblastoma, as well as the current advancements in therapeutic strategies targeting mtDNA alterations.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 10","pages":"367"},"PeriodicalIF":3.3,"publicationDate":"2024-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142549334","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}

{"title":"Characterization of Extracellular Vesicles by Sulfophosphovanillin Colorimetric Assay and Raman Spectroscopy.","authors":"Alexey Senkovenko, Gleb Skryabin, Evgeniia Parshina, Alexey Piryazev, Elena Tchevkina, Dmitry Bagrov","doi":"10.31083/j.fbl2910366","DOIUrl":"https://doi.org/10.31083/j.fbl2910366","url":null,"abstract":"<p><strong>Background: </strong>Detailed characterization of extracellular vesicles (EVs) is crucial for their application in medical diagnostics. However, the complexity of their chemical composition and the heterogeneity of EV populations make their characterization challenging. Here we describe two analytical procedures that can help overcome this challenge.</p><p><strong>Methods: </strong>Small EVs were isolated from conditioned cell culture media using ultracentrifugation and characterized using nanoparticle tracking analysis (NTA) and transmission electron microscopy (TEM). Raman spectroscopy was used to assess the overall composition of the isolated samples and lipids extracted from them. Sulfophosphovanillin (SPV) colorimetric assay was used to quantify the contents of lipid.</p><p><strong>Results: </strong>Six samples of EVs were characterized. The lipid contents measured using SPV assay was in reasonable agreement with the quantitative estimates based on the particle size and concentration measured using NTA. The most peaks observed in the Raman spectra could be attributed to either proteins or lipids, and their origins was confirmed by lipid extraction. The protein-to-lipid ratio was estimated based on the Raman spectra.</p><p><strong>Conclusions: </strong>The experiential procedures described in this study will help to overcome the challenge of quick and highly informative characterization of the EVs.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 10","pages":"366"},"PeriodicalIF":3.3,"publicationDate":"2024-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142549319","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}

{"title":"Estimation of Plasma Concentration of L-Carnosine and its Correlation with Core Symptoms of Autism Spectrum Disorder Children: A Pilot Clinical Trial.","authors":"Debi Ann Abraham, Udayakumar Narasimhan, Vijayakumar Thangavel Mahalingam, Manikandan Krishnan, Rajanandh Muhasaparur Ganesan, Khang Wen Goh, Ching Siang Tan, Long Chiau Ming, Chrismawan Ardianto","doi":"10.31083/j.fbl2910365","DOIUrl":"https://doi.org/10.31083/j.fbl2910365","url":null,"abstract":"<p><strong>Background: </strong>Literature indicates that L-carnosine may be deficient in autism spectrum disorder (ASD) children. The aim of the present study was to estimate the level of L-carnosine in plasma and correlate it with the Autism Treatment Evaluation Checklist (ATEC) and Childhood Autism Rating Scale 2nd Edition, Standard Version (CARS2-ST) scores. To measure L-carnosine level, a bio-analytical method was developed using reverse phase high- liquid chromatography and validated as per International Conference on Harmonization guidelines.</p><p><strong>Method: </strong>Children were supplemented with L-carnosine (10-15 mg/kg) along with standard care therapies for 2 months. Before and after supplementation, scores on the ATEC, CARS2-ST, BEARS sleep screening tool, 6-item Gastrointestinal Severity Index, and Parental Stress Scale were evaluated, and L-carnosine was measured at the end of the trial.</p><p><strong>Results: </strong>The calibration curve was linear in the range of 100-600 ng/mL (R² = 0.998). The level of L-carnosine quantified was 33.7 ± 0.2 ng/mL. There was no significant difference found in any of the outcome measures (<i>p</i> > 0.05).</p><p><strong>Conclusions: </strong>Despite the fact that L-carnosine is detectable in the blood, it was found to be ineffective in the management of ASD in children.</p><p><strong>Clinical trial registration: </strong>The study was registered in the Clinical Trial Registry-India, registration number: CTRI/2019/07/020102.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 10","pages":"365"},"PeriodicalIF":3.3,"publicationDate":"2024-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142549326","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}