Biochemical and biophysical research communications最新文献

{"title":"Hyperbaric oxygen improves combined drug-induced hyperuricemia model in rats by remodeling gut microbiota and regulating host metabolism","authors":"Ya Li ,&nbsp;Xinxin Li ,&nbsp;Huaxian Li ,&nbsp;Weiwei Yan ,&nbsp;Qing Dai ,&nbsp;Peijun Han ,&nbsp;Wenlan Wang","doi":"10.1016/j.bbrc.2026.153371","DOIUrl":"10.1016/j.bbrc.2026.153371","url":null,"abstract":"<div><div>This study aimed to investigate the ameliorative effect of hyperbaric oxygen (HBO) on a rat model of hyperuricemia induced by combined drugs and its underlying mechanism. A rat model of drug-induced hyperuricemia (HUA)was established by using a combination of yeast, potassium oxonate (PO) and hypoxanthine (Hx). During the modeling process, hyperbaric oxygen therapy was also administered. Serum uric acid (UA), creatinine (Cr)and blood urea nitrogen (BUN)levels were measured, and HE staining was used to evaluate the histopathological damage of small intestine and kidney tissues. Serum non-targeted metabolomics analysis was conducted, and 16 S rRNA gene sequencing was used to analyze the changes in intestinal flora structure, to evaluate the therapeutic effect of hyperbaric oxygen therapy. The results showed that HBO therapy could significantly reduce the UA, Cr and BUN levels and alleviate the histopathological damage of small intestine and kidney tissues in model rats. At the same time, HBO therapy could regulate the imbalance of intestinal flora, reduce potential pathogenic bacteria, and reduce the endogenous production of UA by decreasing the relative abundance of <em>Bacteroides</em> and <em>Alistipes</em>. Further serum metabolomics analysis indicated that HBO therapy could improve the differential metabolites in HUA rats, and the pathways of these differential metabolites were mainly related to glutathione metabolism, as well as <span>d</span>-glutamine and <span>d</span>-glutamate metabolism. HBO therapy could regulate key pathways such as purine metabolism and amino acid metabolism, and promote the generation of UA excretion-related metabolites. This study confirmed that HBO could improve combined drug-induced HUA by remodeling the intestinal flora structure and regulating the host metabolic pathways, providing new experimental evidence and potential targets for non-pharmacological treatment of HUA.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"804 ","pages":"Article 153371"},"PeriodicalIF":2.2,"publicationDate":"2026-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146103427","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Simetryn induces arteriovenous malformations in zebrafish embryos through activation of Erk signaling","authors":"Zhonghao Xiao ,&nbsp;Daoyu Wu ,&nbsp;Chenglong Duan ,&nbsp;Ji Zhang ,&nbsp;Weitao Hu ,&nbsp;Jingrong Tang ,&nbsp;Ziang Wang ,&nbsp;Huimin Li ,&nbsp;Xiaowen Shi ,&nbsp;Sizhou Huang ,&nbsp;Zigang Cao","doi":"10.1016/j.bbrc.2026.153339","DOIUrl":"10.1016/j.bbrc.2026.153339","url":null,"abstract":"<div><div>Arteriovenous malformations (AVMs) represent a congenital, high-flow vascular anomaly characterized by direct, aberrant connections between arteries and veins. This pathology leads to diverse clinical manifestations including skin discoloration, pain, ulceration, hemorrhage, and disfigurement. While most current animal AVM models rely on genetic engineering, chemically induced models remain scarce. In this study, we report that simetryn, a triazine herbicide, can induce AVM-like phenotypes in zebrafish embryos. Exposure to simetryn caused aberrant vascular development and erythrocyte accumulation within the caudal vascular plexus. We also observed a reduction in caudal lymphatic vessels and disrupted of cerebral vasculature. In the caudal vascular plexus, cellular proliferation was decreased while apoptosis was increased. Mechanistically, simetryn upregulated levels of phosphorylated <em>Erk (p-Erk</em>),. Notably, these AVM-like phenotypes were ameliorated by co-treatment with trametinib, a <em>MEK</em> inhibitor acting upstream of <em>Erk</em>. Our findings establish a novel, drug-induced zebrafish model of AVMs, which holds promise for facilitating high-throughput drug screening and advance the study of AVM pathogenesis.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"804 ","pages":"Article 153339"},"PeriodicalIF":2.2,"publicationDate":"2026-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146071119","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"STOML2 is not essential for spermatogenesis and male fertility in mice","authors":"Fan Yang ,&nbsp;Jiayi Su ,&nbsp;Yaru Li ,&nbsp;Jieyu Zhao ,&nbsp;Eoin C. Whelan ,&nbsp;Wenhua Xu ,&nbsp;Guanghua Li ,&nbsp;Tingting Ge ,&nbsp;Lu Yuan ,&nbsp;Haoyu Liu ,&nbsp;Changmin Niu ,&nbsp;Luping Yu ,&nbsp;Ying Zheng","doi":"10.1016/j.bbrc.2026.153369","DOIUrl":"10.1016/j.bbrc.2026.153369","url":null,"abstract":"<div><div>Stomatin-like protein 2 (STOML2) localizes to the mitochondrial inner membrane and regulates mitochondrial biogenesis and function. STOML2's role in spermatogenesis is unknown but given that proper mitochondrial function is required proper male germ cell development and function, we elected to study STOML2's role in the testis. The expression pattern of STOML2 in mouse testes was investigated by RT-PCR and Western blot. <em>Stoml2</em> RNA was highly expressed in mouse testes and STOML2 protein was localized in the cytoplasm of testicular germ cells. A <em>Stoml2</em> knockout (KO) mouse model was generated and phenotypes were assessed. <em>Stoml2</em> KO male mice displayed normal morphology and weight of testes and epididymides, as well as normal fertility. The number and morphology of sperm from <em>Stoml2</em> KO mice were not changed significantly. Histological analyses of KO testes revealed normal spermatogenesis, and the number of testicular germ cells and Sertoli cells were not significantly altered. Taken together, our results demonstrate that STOML2 is not required for spermatogenesis and male fertility in mice.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"804 ","pages":"Article 153369"},"PeriodicalIF":2.2,"publicationDate":"2026-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146071118","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"High-intensity interval training promotes cartilage repair and ameliorates ferroptosis via SIRT1 in osteoarthritis","authors":"Changsheng Lin ,&nbsp;Chunyan Liu ,&nbsp;Xiao Zhang ,&nbsp;Fang Zhou ,&nbsp;Yuqin Ma ,&nbsp;Ziqi Ye ,&nbsp;Kaizong Huang ,&nbsp;Anliang Chen ,&nbsp;Kai Cheng ,&nbsp;Xueping Li","doi":"10.1016/j.bbrc.2026.153303","DOIUrl":"10.1016/j.bbrc.2026.153303","url":null,"abstract":"<div><div>Osteoarthritis (OA) is a progressive degenerative joint disease characterized by cartilage degradation, inflammation, and pain. High-intensity interval training (HIIT) has emerged as a promising non-pharmacological intervention that may improve joint function by promoting cartilage repair and attenuating inflammation. This study investigated the effects of HIIT on cartilage ferroptosis and the underlying molecular mechanisms, focusing on SIRT1 in a rat model of knee OA.</div><div>Sprague–Dawley rats were induced with OA via intra-articular monosodium iodoacetate (MIA) and then subjected to a 6-week HIIT program. Outcomes included gait analysis, mechanical and thermal pain thresholds, histological staining, and molecular assays. HIIT significantly improved gait parameters and pain thresholds, indicating functional recovery. Histology showed enhanced cartilage matrix integrity and repair. HIIT modulated ferroptosis-related markers, including GPX4 and ACSL4, and upregulated SIRT1 with activation of NRF2 signaling and improved iron metabolism within cartilage. Pharmacologic inhibition of SIRT1 (EX527) reversed these benefits, underscoring SIRT1's pivotal role in mediating HIIT's therapeutic effects. In vitro, IL-1β-stimulated primary chondrocytes exhibited reduced SIRT1/NRF2/GPX4 and increased TFRC/ACSL4, whereas lentiviral SIRT1 overexpression restored NRF2-GPX4 signaling and decreased TFRC/ACSL4, supporting a chondrocyte-intrinsic SIRT1-NRF2-GPX4 axis in regulating ferroptosis-associated responses.</div><div>In conclusion, while direct evidence of ferroptosis markers such as lipid peroxidation and mitochondrial changes is lacking, HIIT alleviates ferroptosis-associated cartilage damage and promotes cartilage repair in OA through SIRT1-dependent mechanisms. These findings support HIIT as a potential non-pharmacological strategy for OA management and provide a mechanistic basis for exercise-based interventions aimed at preserving joint function and reducing OA-related disability.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"804 ","pages":"Article 153303"},"PeriodicalIF":2.2,"publicationDate":"2026-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146071120","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Peroxiredoxin 2 contributes to the malignant phenotype of glioblastoma cells","authors":"Kamila Szumska,&nbsp;Fatmanur Sabir,&nbsp;Monika Szeliga","doi":"10.1016/j.bbrc.2026.153370","DOIUrl":"10.1016/j.bbrc.2026.153370","url":null,"abstract":"<div><div>Glioblastoma (GBM) is the most malignant primary brain tumor. To adapt to intrinsic oxidative stress, GBM cells upregulate antioxidant systems. Out of six peroxiredoxins (PRDX) involved in protecting cells from oxidative stress, PRDX1 and PRDX4 are proteins that have been attributed with GBM-promoting properties. The role of PRDX2 in these tumors remains elusive. We have recently reported that treatment with conoidin A (CONA), considered a covalent inhibitor of PRDX2, diminished growth of GBM cells. The question arose whether PRDX2 itself affects the growth of GBM cells and whether the decrease in survival observed under CONA treatment could be due to inhibition of PRDX2 activity. To address this issue, we silenced <em>PRDX2</em> in human GBM cells, U87MG and LN229, which reduced cell viability to a degree similar to that observed in PRDX4-deficient GBM cells used here as an acknowledged reference. Additionally, <em>PRDX2</em> silencing inhibited growth of U87MG cells and increased the level of reactive oxygen species. Furthermore, such modulation reduced susceptibility to CONA, suggesting that this compound exerts its effect on cell viability at least partially through PRDX2 inhibition.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"804 ","pages":"Article 153370"},"PeriodicalIF":2.2,"publicationDate":"2026-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146077010","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondrial changes in clear cell renal cell carcinoma: mechanisms and potential targets","authors":"Jiayi Yang ,&nbsp;Xiaoyan Pan ,&nbsp;Xiaoyan Luo ,&nbsp;Xueting Zheng ,&nbsp;Jiali Wang","doi":"10.1016/j.bbrc.2026.153354","DOIUrl":"10.1016/j.bbrc.2026.153354","url":null,"abstract":"<div><div>Renal cell carcinoma (RCC), the most common type of urogenital cancer, accounts for about 80 % of malignant renal tumors. Clear cell renal cell carcinoma (ccRCC), composed of cells filled with lipid droplets in cytoplasm, is the most common subtype of RCC. Mechanisms underlying ccRCC progression and metastasis are complicated and remain far from being clarified. Mitochondria, which serve as cellular energy supplier and central signal hubs, are involved in various physiological and pathological processes. Mounting evidence has revealed that mitochondrial changes, such as mutations, abnormal mitophagy and metabolisms and excessive reactive oxide species (ROS) are closely related with the progression, prognosis, metastasis and drug resistance of RCC and ccRCC. In this review, we'll provide an overview on mitochondrial changes in RCC, especially in ccRCC, and discuss their possible roles in the tumorigenesis and prognosis as well as their potential in serving as biomarkers and therapeutic targets.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"804 ","pages":"Article 153354"},"PeriodicalIF":2.2,"publicationDate":"2026-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146077013","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expression of concern to \"A structurally novel hemopexin fold protein of rice plays role in chlorophyll degradation\" [Biochem. Biophys. Res. Commun. (2012) 420 (4) 862-868].","authors":"Tirthartha Chattopadhyay, Sudipta Bhattacharyya, Amit K Das, Mrinal K Maiti","doi":"10.1016/j.bbrc.2026.153385","DOIUrl":"10.1016/j.bbrc.2026.153385","url":null,"abstract":"","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"804 ","pages":"153385"},"PeriodicalIF":2.2,"publicationDate":"2026-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146197295","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NMR-driven insights into the evolutionary adaptation and dynamic regulation of Mycobacterium tuberculosis adenylate kinase: The critical role of glycine-mediated flexibility","authors":"Chae Yeong Lee ,&nbsp;Woo Cheol Lee ,&nbsp;Kyusung Chae ,&nbsp;Eunhee Kim ,&nbsp;Eunha Hwang ,&nbsp;Yangmee Kim","doi":"10.1016/j.bbrc.2026.153357","DOIUrl":"10.1016/j.bbrc.2026.153357","url":null,"abstract":"<div><div>Adenylate kinase (Adk) is essential for cellular energy homeostasis as it catalyzes the reversible transfer of γ-phosphate from ATP to AMP. In most long-variants, such as <em>Escherichia coli</em> Adk, large-scale domain motions, concerted movements of the AMP-binding domain (AMPbd) and ATP-lid, are essential for catalytic efficiency. However, the structural diversity observed in Adk variants, especially the short-variant Adk from <em>Mycobacterium tuberculosis</em> (MtAdk) featuring a truncated ATP-lid, raises questions regarding the adaptation of its dynamic regulation and functional mechanisms to support survival in resource-limited and hostile environments. Here, using ¹⁵N-chemical exchange saturation transfer experiments, we identified key glycine residues, G32 and G46 in AMPbd and G128 within the ATP-lid, that undergo slow conformational exchange on the millisecond timescale. Glycine substitutions with proline revealed their critical roles: G32P and G128P mutations significantly impaired catalytic turnover, whereas G46P exerted a moderate effect. Molecular dynamics simulations revealed that these substitutions restrict local flexibility; G32P and G128P lock the enzyme in an open, less active conformation, whereas G46P destabilizes the hinge region, thereby hindering proper domain closure. Our integrated approach reveals that these glycine-mediated flexibilities are essential for substrate recognition and catalysis in MtAdk. These findings highlight the fundamental mechanistic divergence between short- and long-variant Adks, emphasizing glycine-mediated conformational plasticity as key in enzyme regulation, with promising implications in targeted therapies against bacterial survival strategies.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"804 ","pages":"Article 153357"},"PeriodicalIF":2.2,"publicationDate":"2026-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146077008","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Medium-chain fatty acids activate fructose metabolism via up-regulating GLUT5-KHK axis","authors":"Jiru Hou,&nbsp;Jiaxuan Li,&nbsp;Chong Zhao,&nbsp;Shutao Yin,&nbsp;Hongbo Hu","doi":"10.1016/j.bbrc.2026.153358","DOIUrl":"10.1016/j.bbrc.2026.153358","url":null,"abstract":"<div><div>Fructose is an abundant monosaccharide in the human diet and an important source of energy in the human body. GLUT5, a member of facilitative glucose transporter family, is the only membrane transporter that specifically transports fructose in the human body, and plays an important role in dietary fructose uptake and metabolism. Previous studies have shown that medium-chain fatty acids (MCFAs) can regulate glucose metabolism via modulating glucose transporters. However, it has not been addressed if MCFAs can regulate GLUT5-mediated fructose metabolism. In the present study, we demonstrated for the first time that MCFAs but not short chain or long chain fatty acids are able to promote fructose uptake in both IEC-18 rat intestinal epithelial cells and human MDA-MB-231 breast cancer cells (a commonly used cell line for fructose metabolism-related study) measured by 1-NBD-Fructose-based assay, which are well correlated with the activation of GLUT5-KHK axis. Moreover, the activation of GLUT5-ketohexokinase (KHK) axis was also achieved in vivo by the treatment with tricapylin, a precursor of octanoic acid (OA), leading to the improvement in fructose-based energy recovery after fasting. The findings of the present study not only provide novel mechanistic support for MCFAs as regulator of carbohydrate metabolism, but also denote that MCFAs could be useable for managing fructose-associated metabolic diseases or as an enhancer for energy recovery after fasting or exercise.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"804 ","pages":"Article 153358"},"PeriodicalIF":2.2,"publicationDate":"2026-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146071117","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CD59 promotes pancreatic cancer progression via a tumor cell-intrinsic JAK2-STAT3 signaling axis","authors":"Zihan Li ,&nbsp;Xingyi Chen ,&nbsp;Yanjun Wu ,&nbsp;Yi Xu","doi":"10.1016/j.bbrc.2026.153609","DOIUrl":"10.1016/j.bbrc.2026.153609","url":null,"abstract":"<div><div>Pancreatic cancer is a highly aggressive malignancy with limited therapeutic options. Although the complement system has been implicated in tumor biology, its tumor cell–intrinsic roles in pancreatic cancer remain unclear. Here, we identify the complement regulatory protein CD59 as a critical driver of pancreatic cancer progression through a cell-intrinsic signaling mechanism. CD59 is significantly upregulated in pancreatic tumors and correlates with poor patient survival. Functional assays demonstrate that CD59 promotes tumor cell proliferation and growth in vitro and in vivo, whereas its depletion suppresses these effects. Mechanistically, CD59 interacts with JAK2 to activate the JAK2–STAT3 pathway, and transcriptomic analyses identify CACNA1D as a STAT3-dependent effector mediating CD59-driven proliferation. Notably, KRAS inhibition induces compensatory activation of the CD59–JAK2–STAT3 axis, while combined targeting of CD59 or STAT3 with KRAS more effectively inhibits tumor cell growth. These findings define a tumor cell–intrinsic oncogenic function of CD59 and highlight the CD59–JAK2–STAT3–CACNA1D pathway as a potential therapeutic target in pancreatic cancer.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"812 ","pages":"Article 153609"},"PeriodicalIF":2.2,"publicationDate":"2026-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147453424","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}