Although neurogenic pulmonary edema (NPE) often occurs after aneurysmal subarachnoid hemorrhage (SAH), the mechanism of NPE progression after SAH remains unclear. This study investigates whether pulmonary endothelial glycocalyx (PEG) impairment accompanies NPE after SAH. Accordingly, SAH was induced by endovascular perforation in male mice. The lung tissues of the mice were removed 24 h after SAH induction. The degree of pulmonary edema and lung injury, and the extent of PEG injury were assessed. Water content of lung tissue by the wet/dry method in the SAH group was significantly increased compared to that in the sham group (81.7 % vs. 78.8 %, P < 0.01), which suggested NPE following SAH. Lung injury score by hematoxylin and eosin staining in the SAH group, assessed using a semiquantitative scoring system, was also significantly worse than that in the sham group (7.1 vs. 1.2, P < 0.001). Scanning electron microscopy images clearly demonstrated that the moss-like glycocalyx lined the endothelial lumen without any interruption in sham mice, whereas those microstructures were severely devastated in SAH mice. Moreover, the fluorescence intensity of tomato lectin was significantly reduced in SAH mice compared to that in sham mice (13.3 vs. 30.7, P < 0.001), thereby indicating the loss of PEG. Our results indicate that PEG, which is essential for regulating vascular permeability, is severely impaired after experimental SAH. Maintaining the integrity of PEG is a promising therapeutic strategy for NPE after SAH.
虽然神经源性肺水肿（NPE）常发生在动脉瘤性蛛网膜下腔出血（SAH）后，但SAH后NPE进展的机制尚不清楚。本研究探讨SAH后肺内皮糖萼（PEG）损伤是否伴随NPE。因此，雄性小鼠血管内穿孔可诱发SAH。小鼠在SAH诱导后24 h切除肺组织。评估肺水肿、肺损伤程度及PEG损伤程度。经干湿法测定，SAH组肺组织含水量明显高于sham组（81.7 % vs. 78. %,P <； 0.01），提示SAH后肺组织发生NPE。使用半定量评分系统评估SAH组苏木精和伊红染色肺损伤评分，SAH组的肺损伤评分也明显低于sham组（7.1 vs. 1.2, P <； 0.001）。扫描电镜图像清楚地显示，假手术小鼠的内皮腔内排列着苔藓样的糖萼，没有任何中断，而SAH小鼠的这些微结构严重破坏。此外，与假手术小鼠相比，SAH小鼠的番茄凝集素荧光强度显著降低（13.3 vs. 30.7, P <； 0.001），表明PEG丢失。我们的研究结果表明，实验性SAH后，对调节血管通透性至关重要的PEG严重受损。维持PEG的完整性是一种很有前途的治疗SAH后NPE的策略。
{"title":"Pulmonary edema following subarachnoid hemorrhage is associated with impairment of pulmonary vascular endothelial glycocalyx","authors":"Nozomi Sasaki , Yusuke Egashira , Hideshi Okada , Chihiro Takada , Shinomi Sasaibe , Masaki Kumagai , Yoshiki Kuse , Shinsuke Nakamura , Hirofumi Matsubara , Yukiko Enomoto , Toru Iwama , Tsuyoshi Izumo , Hideaki Hara , Masamitsu Shimazawa","doi":"10.1016/j.bbrep.2025.102420","DOIUrl":"10.1016/j.bbrep.2025.102420","url":null,"abstract":"<div><div>Although neurogenic pulmonary edema (NPE) often occurs after aneurysmal subarachnoid hemorrhage (SAH), the mechanism of NPE progression after SAH remains unclear. This study investigates whether pulmonary endothelial glycocalyx (PEG) impairment accompanies NPE after SAH. Accordingly, SAH was induced by endovascular perforation in male mice. The lung tissues of the mice were removed 24 h after SAH induction. The degree of pulmonary edema and lung injury, and the extent of PEG injury were assessed. Water content of lung tissue by the wet/dry method in the SAH group was significantly increased compared to that in the sham group (81.7 % vs. 78.8 %, <em>P</em> < 0.01), which suggested NPE following SAH. Lung injury score by hematoxylin and eosin staining in the SAH group, assessed using a semiquantitative scoring system, was also significantly worse than that in the sham group (7.1 vs. 1.2, <em>P</em> < 0.001). Scanning electron microscopy images clearly demonstrated that the moss-like glycocalyx lined the endothelial lumen without any interruption in sham mice, whereas those microstructures were severely devastated in SAH mice. Moreover, the fluorescence intensity of tomato lectin was significantly reduced in SAH mice compared to that in sham mice (13.3 vs. 30.7, <em>P</em> < 0.001), thereby indicating the loss of PEG. Our results indicate that PEG, which is essential for regulating vascular permeability, is severely impaired after experimental SAH. Maintaining the integrity of PEG is a promising therapeutic strategy for NPE after SAH.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"45 ","pages":"Article 102420"},"PeriodicalIF":2.2,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145797520","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}
Pub Date : 2026-03-01Epub Date: 2025-12-14DOI: 10.1016/j.bbrep.2025.102407
Ce Shi , Lei Chen , Jinshuang Li , Tingting Shi , Chun Yang , Liguo Zhao
Osteoporosis, a prevalent metabolic bone disorder, exhibits an age-related increase in incidence, profoundly impacting patients’ quality of life. Recent studies have underscored the fundamental role of mitochondria in bone metabolism, emphasizing the intricate link mitochondrial dysfunction and the viability and functionality of bone cells. Beyond their role in energy production, mitochondria are critical in modulating cellular apoptosis, oxidative stress, and calcium ion homeostasis, all of which are essential for maintaining bone health. Emerging evidence suggests that mitochondrial dysfunction plays an integral role in the pathogenesis of osteoporosis, yet significant challenges persist in this field. This review seeks to elucidate the critical role of mitochondria in osteoporosis research, examine their intricate relationship with bone metabolism, and synthesize current research advances alongside future directions. Ultimately, it aims to offer novel insights for the prevention and treatment of osteoporosis.
{"title":"The pivotal role of mitochondria in osteoporosis: From pathogenesis to future therapies","authors":"Ce Shi , Lei Chen , Jinshuang Li , Tingting Shi , Chun Yang , Liguo Zhao","doi":"10.1016/j.bbrep.2025.102407","DOIUrl":"10.1016/j.bbrep.2025.102407","url":null,"abstract":"<div><div>Osteoporosis, a prevalent metabolic bone disorder, exhibits an age-related increase in incidence, profoundly impacting patients’ quality of life. Recent studies have underscored the fundamental role of mitochondria in bone metabolism, emphasizing the intricate link mitochondrial dysfunction and the viability and functionality of bone cells. Beyond their role in energy production, mitochondria are critical in modulating cellular apoptosis, oxidative stress, and calcium ion homeostasis, all of which are essential for maintaining bone health. Emerging evidence suggests that mitochondrial dysfunction plays an integral role in the pathogenesis of osteoporosis, yet significant challenges persist in this field. This review seeks to elucidate the critical role of mitochondria in osteoporosis research, examine their intricate relationship with bone metabolism, and synthesize current research advances alongside future directions. Ultimately, it aims to offer novel insights for the prevention and treatment of osteoporosis.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"45 ","pages":"Article 102407"},"PeriodicalIF":2.2,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145797519","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}
Pub Date : 2026-03-01Epub Date: 2026-01-06DOI: 10.1016/j.bbrep.2025.102438
Yanting Jiang , Shuyou Liu , Guolin Li , Chengcheng Tang , Yangyang Zhang , Junjie Li , Zhirong Tan , Shimeng Zhang , Zhiyou Chen , Shulong Li
tsRNAs (tRNA-derived small RNAs) are a class of noncoding small RNAs generated by nuclease-specific cleavage of mature tRNAs or their precursors. Since their functional discovery in 2009, tsRNAs have emerged as a research hotspot in molecular biology and medicine because of their unique generation mechanism, tissue-specific expression patterns, and diverse regulatory functions. Compared with traditional non-coding RNAs (such as miRNAs and lncRNAs), tsRNAs exhibit distinct biological activities in stress responses, translational regulation, and epigenetic modifications and are closely associated with the onset and progression of various human diseases. This systematic review covers the discovery history, classification characteristics, primary biological functions, and action mechanisms of tsRNAs in major diseases, including respiratory disorders, neuropsychiatric conditions, cardiovascular diseases, and tumors. It further explores the clinical translational potential of tsRNAs as disease biomarkers and therapeutic targets, identifies current challenges, and outlines future research directions. Major knowledge gaps highlighted include the lack of standardized detection methods for tsRNA subtypes, unclear specificity of their molecular targets in pathological processes, and limited validation in large clinical cohorts; key challenges involve inefficient delivery of tsRNA-based therapeutics and insufficient exploration of cross-species conservation. The review aims to provide a comprehensive reference for in-depth studies in the field of tsRNA.
{"title":"Biological functions of tsRNAs and research advances in human disease","authors":"Yanting Jiang , Shuyou Liu , Guolin Li , Chengcheng Tang , Yangyang Zhang , Junjie Li , Zhirong Tan , Shimeng Zhang , Zhiyou Chen , Shulong Li","doi":"10.1016/j.bbrep.2025.102438","DOIUrl":"10.1016/j.bbrep.2025.102438","url":null,"abstract":"<div><div>tsRNAs (tRNA-derived small RNAs) are a class of noncoding small RNAs generated by nuclease-specific cleavage of mature tRNAs or their precursors. Since their functional discovery in 2009, tsRNAs have emerged as a research hotspot in molecular biology and medicine because of their unique generation mechanism, tissue-specific expression patterns, and diverse regulatory functions. Compared with traditional non-coding RNAs (such as miRNAs and lncRNAs), tsRNAs exhibit distinct biological activities in stress responses, translational regulation, and epigenetic modifications and are closely associated with the onset and progression of various human diseases. This systematic review covers the discovery history, classification characteristics, primary biological functions, and action mechanisms of tsRNAs in major diseases, including respiratory disorders, neuropsychiatric conditions, cardiovascular diseases, and tumors. It further explores the clinical translational potential of tsRNAs as disease biomarkers and therapeutic targets, identifies current challenges, and outlines future research directions. Major knowledge gaps highlighted include the lack of standardized detection methods for tsRNA subtypes, unclear specificity of their molecular targets in pathological processes, and limited validation in large clinical cohorts; key challenges involve inefficient delivery of tsRNA-based therapeutics and insufficient exploration of cross-species conservation. The review aims to provide a comprehensive reference for in-depth studies in the field of tsRNA.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"45 ","pages":"Article 102438"},"PeriodicalIF":2.2,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145938480","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}
Chronic inflammation and a progressive loss of kidney function are hallmarks of diabetic nephropathy (DN). Th22 cells are mainly regulated by the transcription factor AHR, which is essential for their differentiation and inflammatory responses. This study aims to investigate the regulatory role of Th22 cells in the progression of DN. The GEO database was used to retrieve the GSE142025 (DN) and GSE135390 (Th22) datasets, which provided transcriptomic profiles for gene expression analysis. WGCNA was employed to identify gene co-expression modules strongly correlated with DN progression. Gene expression levels were validated by real-time PCR in 90 PBMC samples (30 per group: T2DM, DN, and healthy controls). Gene–drug interactions were subsequently predicted using the DGIdb database. In DN, 4006 differentially expressed genes (DEGs) were identified, while 831 DEGs were detected in Th22 cells. After intersecting these DEGs using a Venn diagram tool, 106 common genes were found. Following the construction of a protein-protein interaction network using the STRING database and subsequent analysis in Cytoscape, ITGAM was identified as the central hub gene. Real-time PCR analysis demonstrated significantly elevated expression levels of AHR (a major transcription factor of Th22 cells), ITGAM, and CYP1B1 (a downstream target gene of AHR) in DN patients compared to those with T2DM and healthy controls. Changes in the transcript levels of ITGAM, CYP1B1, and AHR were associated with renal biochemical parameters. Additionally, 60 drugs were predicted to regulate AHR, 12 targeted ITGAM, and 33 targeted CYP1B1. This study highlights the potential role of AHR, ITGAM, and CYP1B1 in the pathogenesis of DN. Their altered expression patterns suggest they could serve as useful biomarkers for monitoring disease progression.
{"title":"Molecular crosstalk between AHR, CYP1B1, and ITGAM in diabetic nephropathy: Integrated insights from bioinformatics and experimental validation","authors":"Seyed Amirhossein Hosseini , Parisa Ajorlou , Pegah Mousavi , Sepideh Aghamirli , Aghdas Dehghani","doi":"10.1016/j.bbrep.2025.102422","DOIUrl":"10.1016/j.bbrep.2025.102422","url":null,"abstract":"<div><div>Chronic inflammation and a progressive loss of kidney function are hallmarks of diabetic nephropathy (DN). Th22 cells are mainly regulated by the transcription factor AHR, which is essential for their differentiation and inflammatory responses. This study aims to investigate the regulatory role of Th22 cells in the progression of DN. The GEO database was used to retrieve the GSE142025 (DN) and GSE135390 (Th22) datasets, which provided transcriptomic profiles for gene expression analysis. WGCNA was employed to identify gene co-expression modules strongly correlated with DN progression. Gene expression levels were validated by real-time PCR in 90 PBMC samples (30 per group: T2DM, DN, and healthy controls). Gene–drug interactions were subsequently predicted using the DGIdb database. In DN, 4006 differentially expressed genes (DEGs) were identified, while 831 DEGs were detected in Th22 cells. After intersecting these DEGs using a Venn diagram tool, 106 common genes were found. Following the construction of a protein-protein interaction network using the STRING database and subsequent analysis in Cytoscape, ITGAM was identified as the central hub gene. Real-time PCR analysis demonstrated significantly elevated expression levels of AHR (a major transcription factor of Th22 cells), ITGAM, and CYP1B1 (a downstream target gene of AHR) in DN patients compared to those with T2DM and healthy controls. Changes in the transcript levels of ITGAM, CYP1B1, and AHR were associated with renal biochemical parameters. Additionally, 60 drugs were predicted to regulate AHR, 12 targeted ITGAM, and 33 targeted CYP1B1. This study highlights the potential role of AHR, ITGAM, and CYP1B1 in the pathogenesis of DN. Their altered expression patterns suggest they could serve as useful biomarkers for monitoring disease progression.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"45 ","pages":"Article 102422"},"PeriodicalIF":2.2,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145938988","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}
Pub Date : 2026-03-01Epub Date: 2026-01-29DOI: 10.1016/j.bbrep.2026.102470
Lara Gentemann , Fabian Röpken , Philipp Joel Mroch , Nils Noltemeyer , Sören Donath , Anna Elisabeth Seidler , Christopher Werlein , Patrick Zardo , Lavinia Neubert , Danny Jonigk , Hans-Gerd Fieguth , Alexander Heisterkamp , Katherina Sewald , Stefan Kalies
Precision-cut lung slices (PCLS) are a complex three-dimensional ex vivo model system comprised of all resident cell types of the lung, thus closely mimicking the in vivo situation in regards to structural composition and function. The herein described application of a precise airway epithelial lesion via femtosecond laser-based nanosurgery and subsequent longitudinal imaging via two-photon or confocal microscopy enables the examination of the tissue's repair responses on a single-cell level. Allowing for live observation of intercellular cross-talk, this study demonstrates an endogenous repair program is induced in human PCLS upon damage induction. As early reaction to a small epithelial lesion, physiological stress responses, including transient airway constriction and increased mucus secretion, occur, followed by epithelial restitution within 24 h. Automated cell detection and subsequent cell track analysis reveal a more linearly confined cellular movement in the course of repair. Further, non-stationary, motile cells directly interact with cell debris, thereby contributing to final resolution of the lesion. Together, these findings emphasize the suitability of PCLS, combined with localized laser-based damage induction and state-of-the-art microscopy techniques, as a model system to study complex intercellular interactions in the course of endogenous repair processes.
{"title":"Live imaging of human airway epithelial repair in precision-cut lung slices after targeted cell damage","authors":"Lara Gentemann , Fabian Röpken , Philipp Joel Mroch , Nils Noltemeyer , Sören Donath , Anna Elisabeth Seidler , Christopher Werlein , Patrick Zardo , Lavinia Neubert , Danny Jonigk , Hans-Gerd Fieguth , Alexander Heisterkamp , Katherina Sewald , Stefan Kalies","doi":"10.1016/j.bbrep.2026.102470","DOIUrl":"10.1016/j.bbrep.2026.102470","url":null,"abstract":"<div><div>Precision-cut lung slices (PCLS) are a complex three-dimensional <em>ex vivo</em> model system comprised of all resident cell types of the lung, thus closely mimicking the <em>in vivo</em> situation in regards to structural composition and function. The herein described application of a precise airway epithelial lesion via femtosecond laser-based nanosurgery and subsequent longitudinal imaging via two-photon or confocal microscopy enables the examination of the tissue's repair responses on a single-cell level. Allowing for live observation of intercellular cross-talk, this study demonstrates an endogenous repair program is induced in human PCLS upon damage induction. As early reaction to a small epithelial lesion, physiological stress responses, including transient airway constriction and increased mucus secretion, occur, followed by epithelial restitution within 24 h. Automated cell detection and subsequent cell track analysis reveal a more linearly confined cellular movement in the course of repair. Further, non-stationary, motile cells directly interact with cell debris, thereby contributing to final resolution of the lesion. Together, these findings emphasize the suitability of PCLS, combined with localized laser-based damage induction and state-of-the-art microscopy techniques, as a model system to study complex intercellular interactions in the course of endogenous repair processes.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"45 ","pages":"Article 102470"},"PeriodicalIF":2.2,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146073716","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}
Familial hypercholesterolemia (FH) is a genetic disorder characterized by markedly elevated low-density lipoprotein (LDL) cholesterol levels, which primarily progresses to premature or familial coronary heart disease (FH-CHD).
This cross-sectional study included healthy controls (N) and patients with hyperlipidemia (H), FH, CHD, and FH-CHD. We attempted to explore gene variants shared in H, FH and FH-CHD using next-generation sequencing tool. The RNA-seq transcriptome profiling from the whole peripheral blood (n = 3/group) were analyzed. The results revealed 15 intersected gene variants between the H/FH and FH-CHD groups. Aligning and mapping on the coding regions showed significant high-impact variants in 6 of the 15 genes including MAFG, AKAP1, TLR5, CHUK, EMC10, and PLRG1. The significant high-impact variations included frameshift variants in CHUK and PLRG, stop-gain variation in TLR5 at the last intron, stop-lost variation in EMC10, and splice-acceptor and donor variants in MAFG and AKAP1, respectively. Pathogenicity scoring (ACMG Criteria) interpreted that these variation effects are predicted to lose the gene functions. Based on reference databases without any validation, these gene variations are probably linked to atherogenesis and CHD development.
Conclusively, our exploratory observed that MAFG, AKAP1, TLR5, CHUK, EMC10, and PLRG1 variants had higher impacts and might be related to premature CHD development. Further classification and functional validation of these genetic variations should be considered for the feasibility of using these gene variants as contributory predictors of the FH-CHD risk in hyperlipidemia patients.
{"title":"RNA-sequencing based gene variants observed in patients with hyperlipidemia and premature coronary heart disease: A preliminary study","authors":"Wilanee Dechkhajorn , Kriengchai Prasongsukarn , Surachet Benjathummarak , Supachai Topanurak , Yaowapa Maneerat","doi":"10.1016/j.bbrep.2026.102466","DOIUrl":"10.1016/j.bbrep.2026.102466","url":null,"abstract":"<div><div>Familial hypercholesterolemia (FH) is a genetic disorder characterized by markedly elevated low-density lipoprotein (LDL) cholesterol levels, which primarily progresses to premature or familial coronary heart disease (FH-CHD).</div><div>This cross-sectional study included healthy controls (N) and patients with hyperlipidemia (H), FH, CHD, and FH-CHD. We attempted to explore gene variants shared in H, FH and FH-CHD using next-generation sequencing tool. The RNA-seq transcriptome profiling from the whole peripheral blood (n = 3/group) were analyzed. The results revealed 15 intersected gene variants between the H/FH and FH-CHD groups. Aligning and mapping on the coding regions showed significant high-impact variants in 6 of the 15 genes including <em>MAFG</em>, <em>AKAP1</em>, <em>TLR5</em>, <em>CHUK, EMC10,</em> and <em>PLRG1.</em> The significant high-impact variations included frameshift variants in <em>CHUK</em> and <em>PLRG,</em> stop-gain variation in <em>TLR5</em> at the last intron, stop-lost variation in <em>EMC10,</em> and splice-acceptor and donor variants in <em>MAFG</em> and <em>AKAP1</em>, respectively. Pathogenicity scoring (ACMG Criteria) interpreted that these variation effects are predicted to lose the gene functions. Based on reference databases without any validation, these gene variations are probably linked to atherogenesis and CHD development.</div><div>Conclusively, our exploratory observed that <em>MAFG</em>, <em>AKAP1</em>, <em>TLR5</em>, <em>CHUK, EMC10,</em> and <em>PLRG1</em> variants had higher impacts and might be related to premature CHD development. Further classification and functional validation of these genetic variations should be considered for the feasibility of using these gene variants as contributory predictors of the FH-CHD risk in hyperlipidemia patients.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"45 ","pages":"Article 102466"},"PeriodicalIF":2.2,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146073710","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}
Pub Date : 2026-03-01Epub Date: 2026-01-30DOI: 10.1016/j.bbrep.2026.102471
Lijun Zhang, Meiyan Liu, Haiyang Chen
<div><h3>Objective</h3><div>To further explore the underlying mechanism by which the traditional Mongolian medicine Anshen Buxin Liuwei Pills (ABLP) alleviates cardiac dysfunction and depressive behaviors in a model of myocardial infarction (MI) combined with depression.</div></div><div><h3>Method</h3><div>Eighteen eight-week-old C57BL/6JNifdc male mice were divided into sham group (n = 6), MI + NS group (n = 6), MI + ABLP group (n = 6). Mice in the MI + ABLP group were treated with ABLP for 4 weeks. Seventeen eight-week-old wide-type (SERT<sup>+/+</sup>) mice and reduced SERT expression (SERT<sup>+/−</sup>) mice were allocated into SERT<sup>+/+</sup> NS group (n = 5), SERT<sup>+/+</sup> ABLP group (n = 4), SERT<sup>+/−</sup> NS group (n = 4), and SERT<sup>+/−</sup> ABLP group (n = 4). Mice in the SERT<sup>+/+</sup> ABLP and SERT<sup>+/−</sup> ABLP group were treated with ABLP for 1 week. Open field test (OFT) and sucrose preference test (SPT) were conducted for assessing depressive behaviors. The echocardiographic measurements were taken for the left ventricle fractional shortening (LVFS), and left ventricle ejection fraction (LVEF). Masson's trichrome staining was carried out to assess pathological alterations in the mice myocardium. Spleen samples were collected for detecting macrophages (M), M1, M2 by flow cytometry. ELISA was performed on serum, cardiac, and cortical tissues to quantify levels of TNF-α, TNFR1, TNFR2, P65, IKB-α, 5-HT, and hs-TNI. RT-qPCR was implemented to quantify TNFR1 mRNA expression in cardiac, cortical, and hippocampal tissues. SPSS version 24.0 software was applied for statistic analysis.</div></div><div><h3>Results</h3><div>MI mice exhibited lower level of LVEF and LVFS than the sham mice, which were elevated by ABLP treatment. MI mice displayed depressive behaviors, as evidenced by a shorter total distance, slower speed, longer immobility time, shorter activity time, reduced center distance, shorter center time, decreased center entry times, shorter peripheral distance, decreased peripheral entry times, decreased sucrose water consumption and sucrose preference than the sham group (all P < 0.05); these behavioral deficits were rescued by ABLP administration. MI mice presented elevated levels of M1 cells, cardiac TNFR1, TNF-α, IKB-α and P65 proteins and TNFR1 mRNA expression, along with reduced TNFR2 proteins, relative to the sham group. ABLP significantly decreased the concentration of M1 cells, IKB-α, P65 (P < 0.05). Both the MI + NS and MI + ABLP groups had significantly higher level of cortex TNFR1, TNF-α, IKB-α, P65 proteins and TNFR1 mRNA expression, as well as lower level of cortex TNFR2 than the sham group (P < 0.05). There were no significant differences in serum hs-TNI, LVFS, LVEF, and SPT results among SERT<sup>+/+</sup> NS, SERT<sup>+/+</sup> ABLP, SERT<sup>+/−</sup> NS, and SERT<sup>+/−</sup>ABLP groups (all P > 0.05). SERT<sup>+/−</sup> NS group had longer activity time, peripheral time, shor
{"title":"Treating myocardial infarction combined with depression via regulating M1/TNF-α/TNFR1/NF-κB","authors":"Lijun Zhang, Meiyan Liu, Haiyang Chen","doi":"10.1016/j.bbrep.2026.102471","DOIUrl":"10.1016/j.bbrep.2026.102471","url":null,"abstract":"<div><h3>Objective</h3><div>To further explore the underlying mechanism by which the traditional Mongolian medicine Anshen Buxin Liuwei Pills (ABLP) alleviates cardiac dysfunction and depressive behaviors in a model of myocardial infarction (MI) combined with depression.</div></div><div><h3>Method</h3><div>Eighteen eight-week-old C57BL/6JNifdc male mice were divided into sham group (n = 6), MI + NS group (n = 6), MI + ABLP group (n = 6). Mice in the MI + ABLP group were treated with ABLP for 4 weeks. Seventeen eight-week-old wide-type (SERT<sup>+/+</sup>) mice and reduced SERT expression (SERT<sup>+/−</sup>) mice were allocated into SERT<sup>+/+</sup> NS group (n = 5), SERT<sup>+/+</sup> ABLP group (n = 4), SERT<sup>+/−</sup> NS group (n = 4), and SERT<sup>+/−</sup> ABLP group (n = 4). Mice in the SERT<sup>+/+</sup> ABLP and SERT<sup>+/−</sup> ABLP group were treated with ABLP for 1 week. Open field test (OFT) and sucrose preference test (SPT) were conducted for assessing depressive behaviors. The echocardiographic measurements were taken for the left ventricle fractional shortening (LVFS), and left ventricle ejection fraction (LVEF). Masson's trichrome staining was carried out to assess pathological alterations in the mice myocardium. Spleen samples were collected for detecting macrophages (M), M1, M2 by flow cytometry. ELISA was performed on serum, cardiac, and cortical tissues to quantify levels of TNF-α, TNFR1, TNFR2, P65, IKB-α, 5-HT, and hs-TNI. RT-qPCR was implemented to quantify TNFR1 mRNA expression in cardiac, cortical, and hippocampal tissues. SPSS version 24.0 software was applied for statistic analysis.</div></div><div><h3>Results</h3><div>MI mice exhibited lower level of LVEF and LVFS than the sham mice, which were elevated by ABLP treatment. MI mice displayed depressive behaviors, as evidenced by a shorter total distance, slower speed, longer immobility time, shorter activity time, reduced center distance, shorter center time, decreased center entry times, shorter peripheral distance, decreased peripheral entry times, decreased sucrose water consumption and sucrose preference than the sham group (all P < 0.05); these behavioral deficits were rescued by ABLP administration. MI mice presented elevated levels of M1 cells, cardiac TNFR1, TNF-α, IKB-α and P65 proteins and TNFR1 mRNA expression, along with reduced TNFR2 proteins, relative to the sham group. ABLP significantly decreased the concentration of M1 cells, IKB-α, P65 (P < 0.05). Both the MI + NS and MI + ABLP groups had significantly higher level of cortex TNFR1, TNF-α, IKB-α, P65 proteins and TNFR1 mRNA expression, as well as lower level of cortex TNFR2 than the sham group (P < 0.05). There were no significant differences in serum hs-TNI, LVFS, LVEF, and SPT results among SERT<sup>+/+</sup> NS, SERT<sup>+/+</sup> ABLP, SERT<sup>+/−</sup> NS, and SERT<sup>+/−</sup>ABLP groups (all P > 0.05). SERT<sup>+/−</sup> NS group had longer activity time, peripheral time, shor","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"45 ","pages":"Article 102471"},"PeriodicalIF":2.2,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146073823","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}
Protein aggregation and amyloid fibril formation are key events in neurodegenerative disorders such as Alzheimer's disease, and are worsened by non-enzymatic glycation, which destabilizes protein structure. Glycation by reducing sugars like glucose produces advanced glycation end products (AGEs), promoting misfolding and aggregation. β-Hydroxybutyrate (BHB), a ketone body with anti-glycation and neuroprotective properties, may counteract these effects. This study examined structural, aggregation, and fibrillar changes of human serum albumin (HSA) after prolonged glucose-induced glycation, and evaluated the modulatory role of BHB via a multi-technique approach. HSA was incubated for 120 days under four conditions: control, BHB alone, glucose alone, and glucose + BHB. Analyses included atomic force microscopy (AFM), circular dichroism (CD) spectroscopy, ANS fluorescence, Thioflavin T (ThT) fluorescence, and Congo Red assays. AGE formation was quantified to link biochemical modifications with aggregation patterns. Glucose treatment markedly increased AGE levels. AFM revealed extensive aggregation and high surface coverage in the glucose group, partially reduced by BHB. CD spectroscopy showed α-helix loss and β-sheet enrichment with glycation, while BHB preserved structure. ANS fluorescence indicated glucose-enhanced hydrophobic exposure, reduced by BHB. ThT and Congo Red assays confirmed less amyloid fibril formation in glucose + BHB samples versus glucose alone. These results suggest that glucose induces marked glycation, structural disruption, and amyloidogenic aggregation in HSA, whereas BHB provides partial protection, likely through structural stabilization and aggregation pathway modulation. BHB may offer therapeutic promise for limiting amyloid-related neurodegenerative diseases.
{"title":"β-Hydroxybutyrate attenuates glycation-induced structural destabilization and amyloidogenic aggregation in human serum albumin","authors":"Hojjat Mohammadnia , Mousa Bohlooli , Mansour Ghaffari-Moghaddam , Mostafa Khajeh , Fereshteh Taghavi","doi":"10.1016/j.bbrep.2026.102487","DOIUrl":"10.1016/j.bbrep.2026.102487","url":null,"abstract":"<div><div>Protein aggregation and amyloid fibril formation are key events in neurodegenerative disorders such as Alzheimer's disease, and are worsened by non-enzymatic glycation, which destabilizes protein structure. Glycation by reducing sugars like glucose produces advanced glycation end products (AGEs), promoting misfolding and aggregation. β-Hydroxybutyrate (BHB), a ketone body with anti-glycation and neuroprotective properties, may counteract these effects. This study examined structural, aggregation, and fibrillar changes of human serum albumin (HSA) after prolonged glucose-induced glycation, and evaluated the modulatory role of BHB via a multi-technique approach. HSA was incubated for 120 days under four conditions: control, BHB alone, glucose alone, and glucose + BHB. Analyses included atomic force microscopy (AFM), circular dichroism (CD) spectroscopy, ANS fluorescence, Thioflavin T (ThT) fluorescence, and Congo Red assays. AGE formation was quantified to link biochemical modifications with aggregation patterns. Glucose treatment markedly increased AGE levels. AFM revealed extensive aggregation and high surface coverage in the glucose group, partially reduced by BHB. CD spectroscopy showed α-helix loss and β-sheet enrichment with glycation, while BHB preserved structure. ANS fluorescence indicated glucose-enhanced hydrophobic exposure, reduced by BHB. ThT and Congo Red assays confirmed less amyloid fibril formation in glucose + BHB samples versus glucose alone. These results suggest that glucose induces marked glycation, structural disruption, and amyloidogenic aggregation in HSA, whereas BHB provides partial protection, likely through structural stabilization and aggregation pathway modulation. BHB may offer therapeutic promise for limiting amyloid-related neurodegenerative diseases.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"45 ","pages":"Article 102487"},"PeriodicalIF":2.2,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146185090","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}
Pub Date : 2026-03-01Epub Date: 2026-02-09DOI: 10.1016/j.bbrep.2026.102491
Wenjuan Cao , Chongxi Yang , Yilin Feng , Zhao Zhang , Yan Liu , Xiaodong Xu
Background
Fermentation may enhance the skincare potential of the traditional Chinese medicine Polygonatum sibiricum (PS). This study aimed to evaluate the anti-oxidant and anti-inflammatory efficacy of fermented Polygonatum sibiricum (FPS) using zebrafish models.
Methods
A UV-induced zebrafish skin oxidative stress model was established. Embryos were treated with FPS at concentrations of 0.05, 0.10, or 0.20 mg/mL. Evaluations included fin morphology, reactive oxygen species (ROS) levels, activities of antioxidant enzymes (SOD, CAT), malondialdehyde (MDA) content, skin cell apoptosis, and expression of inflammatory genes (PPAR-γ, NF-κB, iκbαa, AP-1). Additionally, a sodium lauryl sulfate (SLS)-induced inflammation model was used to assess neutrophil recruitment.
Results
FPS treatment dose-dependently ameliorated UV-induced fin shrinkage and significantly reduced ROS accumulation. At 0.20 mg/mL, FPS markedly elevated SOD and CAT activities while decreasing MDA levels (p < 0.01). It also reduced UV-triggered skin cell apoptosis and modulated key inflammatory genes. In the SLS model, FPS significantly suppressed neutrophil migration (p < 0.05). Conclusions: FPS demonstrated significant protective effects against skin damage by alleviating oxidative stress, reducing apoptosis, and suppressing inflammation in zebrafish, supporting its potential as a natural ingredient for cosmetic applications.
{"title":"Evaluation of the antioxidant and anti-inflammatory efficacy of fermented Polygonatum sibiricum using zebrafish model","authors":"Wenjuan Cao , Chongxi Yang , Yilin Feng , Zhao Zhang , Yan Liu , Xiaodong Xu","doi":"10.1016/j.bbrep.2026.102491","DOIUrl":"10.1016/j.bbrep.2026.102491","url":null,"abstract":"<div><h3>Background</h3><div>Fermentation may enhance the skincare potential of the traditional Chinese medicine <em>Polygonatum sibiricum</em> (PS). This study aimed to evaluate the anti-oxidant and anti-inflammatory efficacy of fermented <em>Polygonatum sibiricum</em> (FPS) using zebrafish models.</div></div><div><h3>Methods</h3><div>A UV-induced zebrafish skin oxidative stress model was established. Embryos were treated with FPS at concentrations of 0.05, 0.10, or 0.20 mg/mL. Evaluations included fin morphology, reactive oxygen species (ROS) levels, activities of antioxidant enzymes (SOD, CAT), malondialdehyde (MDA) content, skin cell apoptosis, and expression of inflammatory genes (PPAR-γ, NF-κB, iκbαa, AP-1). Additionally, a sodium lauryl sulfate (SLS)-induced inflammation model was used to assess neutrophil recruitment.</div></div><div><h3>Results</h3><div>FPS treatment dose-dependently ameliorated UV-induced fin shrinkage and significantly reduced ROS accumulation. At 0.20 mg/mL, FPS markedly elevated SOD and CAT activities while decreasing MDA levels (<em>p</em> < 0.01). It also reduced UV-triggered skin cell apoptosis and modulated key inflammatory genes. In the SLS model, FPS significantly suppressed neutrophil migration (<em>p</em> < 0.05). <strong>Conclusions</strong>: FPS demonstrated significant protective effects against skin damage by alleviating oxidative stress, reducing apoptosis, and suppressing inflammation in zebrafish, supporting its potential as a natural ingredient for cosmetic applications.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"45 ","pages":"Article 102491"},"PeriodicalIF":2.2,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146185093","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}
Pub Date : 2026-03-01Epub Date: 2025-12-08DOI: 10.1016/j.bbrep.2025.102401
Rena Ubukata, Hiroyuki Suzuki, Mika K. Kaneko, Yukinari Kato
Cadherin (CDH)-mediated extracellular homophilic binding is crucial for maintaining tissue homeostasis. The epithelial cell-cell adhesion molecule cadherin 1 (CDH1/E‐cadherin) forms the adherens junctions in epithelial cells, and the loss of CDH1 facilitates the migration and invasion of carcinoma cells. Although several anti-CDH1 monoclonal antibodies (mAbs) are available for western blotting and immunohistochemistry (IHC), a highly sensitive anti-CDH1 mAb suitable for flow cytometry has not been developed. We developed anti-CDH1 mAbs through a flow cytometry-based high-throughput screening. Two anti-CDH1 mAb clones, Ca1Mab-3 (IgG1, κ) and Ca1Mab-5 (IgG1, κ), reacted with human CDH1-overexpressed Chinese hamster ovary-K1 (CHO/CDH1) cells in flow cytometry. Furthermore, Ca1Mab-3 and Ca1Mab-5 recognized endogenous CDH1-expressing human luminal-type breast cancer cells, such as MCF-7, but not triple-negative breast cancer cells, like MDA-MB-231. The dissociation constant values of Ca1Mab-3 and Ca1Mab-5 for CHO/CDH1 were determined as 5.9 × 10−10 M and 1.8 × 10−9 M, respectively. Ca1Mab-3 and Ca1Mab-5 can detect endogenous CDH1 in western blotting and IHC using a cell block. Furthermore, Ca1Mab-5 is available for IHC in formalin-fixed paraffin-embedded tumor tissues. These results indicate that Ca1Mab-3 and Ca1Mab-5 are versatile for basic research and are expected to contribute to clinical applications, such as tumor diagnosis and therapy.
{"title":"Development of novel anti-CDH1/E-cadherin monoclonal antibodies for versatile applications","authors":"Rena Ubukata, Hiroyuki Suzuki, Mika K. Kaneko, Yukinari Kato","doi":"10.1016/j.bbrep.2025.102401","DOIUrl":"10.1016/j.bbrep.2025.102401","url":null,"abstract":"<div><div>Cadherin (CDH)-mediated extracellular homophilic binding is crucial for maintaining tissue homeostasis. The epithelial cell-cell adhesion molecule cadherin 1 (CDH1/E‐cadherin) forms the adherens junctions in epithelial cells, and the loss of CDH1 facilitates the migration and invasion of carcinoma cells. Although several anti-CDH1 monoclonal antibodies (mAbs) are available for western blotting and immunohistochemistry (IHC), a highly sensitive anti-CDH1 mAb suitable for flow cytometry has not been developed. We developed anti-CDH1 mAbs through a flow cytometry-based high-throughput screening. Two anti-CDH1 mAb clones, Ca<sub>1</sub>Mab-3 (IgG<sub>1</sub>, κ) and Ca<sub>1</sub>Mab-5 (IgG<sub>1</sub>, κ), reacted with human CDH1-overexpressed Chinese hamster ovary-K1 (CHO/CDH1) cells in flow cytometry. Furthermore, Ca<sub>1</sub>Mab-3 and Ca<sub>1</sub>Mab-5 recognized endogenous CDH1-expressing human luminal-type breast cancer cells, such as MCF-7, but not triple-negative breast cancer cells, like MDA-MB-231. The dissociation constant values of Ca<sub>1</sub>Mab-3 and Ca<sub>1</sub>Mab-5 for CHO/CDH1 were determined as 5.9 × 10<sup>−10</sup> M and 1.8 × 10<sup>−9</sup> M, respectively. Ca<sub>1</sub>Mab-3 and Ca<sub>1</sub>Mab-5 can detect endogenous CDH1 in western blotting and IHC using a cell block. Furthermore, Ca<sub>1</sub>Mab-5 is available for IHC in formalin-fixed paraffin-embedded tumor tissues. These results indicate that Ca<sub>1</sub>Mab-3 and Ca<sub>1</sub>Mab-5 are versatile for basic research and are expected to contribute to clinical applications, such as tumor diagnosis and therapy.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"45 ","pages":"Article 102401"},"PeriodicalIF":2.2,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145748903","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}
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