Journal of Bioenergetics and Biomembranes最新文献

{"title":"Effects of 3',4'-dihydroxyflavonol treatment on Neu N and BDNF and ICAM levels in the striatum of rats subjected to transient bilateral carotid occlusion-induced ischemia-reperfusion.","authors":"Murat Hoşgör, Ebru Kubra Uzdil, Tugce Aladag, Seda Simsek, Nejat Unlukal, Rasim Mogulkoc, Abdulkerim Kasim Baltaci","doi":"10.1007/s10863-026-10109-x","DOIUrl":"10.1007/s10863-026-10109-x","url":null,"abstract":"<p><p>Cerebral infarction is a leading cause of severe long-term disability and functional and cognitive impairment. With the advancement of acute stroke treatment, more patients are now experiencing stroke with varying degrees of impairment. The present study was conducted to determine the effects of 1-week 3,4-dihydroxyflavonol (DiOHF) administration during transient experimental cerebral ischemia-reperfusion (I/R) in rats on NeuN, Tuba1a, Tubb3, and calbindin were evaluated as markers of neuronal phenotype and cytoskeletal organization, while ICAM and BDNF were assessed in relation to inflammatory and neurotrophic processes. Changes in these markers indicate alterations in neuronal marker expression, cytoskeletal integrity, and neurotrophic and inflammatory status. In this study, a total of 28 male Wistar albino rats, aged 10-12 weeks and weighing 300-400 g, were used. 1-Control Group (n = 6): The animals in this group received no anaesthesia or surgical procedures. 2-Sham Group (n = 6): After general anaesthesia was induced in the animals in this group, the carotid artery regions were opened and closed. 3- Ischemia-Reperfusion Group (n = 8): Under general anaesthesia, the carotid arteries of the rats were isolated and ligated for 30 min, followed by ischemia. 4- Ischemia-Reperfusion + DiOHF Group (n = 8): Under general anaesthesia, the carotid arteries of the rats were ligated for 30 min, followed by ischemia. Reperfusion was then allowed. Tuba1A, Tubb3, ICAM and Calbindin were analyzed by real-time PCR, BDNF by a commercial ELISA kit, and NeuN by immunohistochemistry. I/R decreased the levels of Neu N, Tuba1a, Tubb3, calbindin and BDNF in the striatum tissues and increased ICAM levels. DiOHF supplementation halted the decrease in expression level in Tuba1a, Tubb3, Calbindin, BDNF; the Increase in Icam level.Also DiOHF supplementation prevented the decrease in the level of anti-NeuN antibody and led to an increase. The study results revealed that one week of transient I/R in rats suppressed NeuN, TUBA1A, TUBB3, calbindin and BDNF levels, which are important in neuronal phenotype and cytoskeletal organization inflammatory and neurotrophic processes. However, a week DiOHF treatment significantly corrected the distortions caused by I/R.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":"58 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2026-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13216093/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148030629","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"METTL3-catalyzed m6A modification of NSUN4 mediates m5C modification of SLC2A3 mRNA to regulate PDGF-BB-induced proliferation, hyaluronan production and glycolysis in human orbital fibroblasts.","authors":"Shu-Yan Liu, Hong Wang, Bao-Zhong Liu, Lei Jia, Ting Wang, Lin-Fei Zhou, Xiao-Li Xu, Bao-Hua Hou, Bo Yang, Li-Sha Sun, Hui Pang","doi":"10.1007/s10863-026-10110-4","DOIUrl":"10.1007/s10863-026-10110-4","url":null,"abstract":"<p><p>Thyroid eye disease (TED) is the most common extra-thyroidal complication of Graves' disease, but its molecular pathogenesis is not fully understood. This study explored the mechanism associated with methyltransferase like 3 (METTL3), NOP2/Sun RNA methyltransferase 4 (NSUN4), and solute carrier family 2 member 3 (SLC2A3) in an in vitro TED model. Human normal orbital fibroblasts were stimulated with platelet-derived growth factor BB (PDGF-BB) to establish in vitro TED model. Differentially expressed genes were screened using online databases. Western blotting was performed for protein detection, and qPCR was used for mRNA quantification. CCK-8 assay and EdU assay were conducted to examine metabolic viability and proliferation, respectively. Hyaluronan (HA) production and glycolysis metabolism were assessed via commercial kits. Methylated RNA immunoprecipitation (MeRIP), RIP, dual-luciferase reporter assay, and RNA-protein pull-down assay were utilized for interaction analysis. Bioinformatics screening obtained 1139 differential genes and 45 glycolytic genes, yielding 2 overlapping genes that were considered as glycolysis-related genes in TED. SLC2A3 was highly expressed in TED and PDGF-BB-stimulated orbital fibroblasts, and silencing SLC2A3 suppressed PDGF-BB-induced cell proliferation, HA production and glycolysis. NSUN4 mediated the m5C methylation modification to increase SLC2A3 expression in an YBX1-dependent manner. NSUN4 inhibition restrained PDGF-BB-induced effects via downregulating SLC2A3. METTL3 mediated m6A methylation modification to reduce NSUN4 expression, with YTHDF2 as a reader protein. The influences of PDGF-BB on human orbital fibroblasts were significantly alleviated by METTL3 overexpression to down-regulate NSUN4. NSUN4 downregulation caused by METTL3-induced m6A modification of NSUN4 mRNA regulated m5C modification of SLC2A3 mRNA, thereby ameliorating PDGF-BB-induced proliferation, HA generation and glycolysis of human orbital fibroblasts in TED. The evidence uncovered the specific molecular mechanism underlying TED pathogenesis.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":"58 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2026-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148054689","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dynamic changes in mitochondrial function in brain cortex synaptosomes during aging.","authors":"Paulina Lombardi, Analía G Karadayian, Juan Ignacio Guerra, Silvia Lores-Arnaiz","doi":"10.1007/s10863-026-10087-0","DOIUrl":"10.1007/s10863-026-10087-0","url":null,"abstract":"<p><p>Alterations in mitochondrial function and in reactive oxygen species generation have been associated with physiological aging. In this study, mice aged 3, 10, 20, and 24 months were utilized to investigate the changes in mitochondrial function and reactive oxygen species (ROS) at synapses. Mitochondrial membrane potential was 21% decreased in 20 months-old animals, while it increased (24%) at advanced age (24 months), compared with young mice. Coupling efficiency and ATP synthesis decreased in synaptosomes from 24-months old mice. Regarding mitochondrial respiratory complex activity, reductions in complex II-III and IV activity were observed (42% and 47%, respectively) at 10 months of age. A significant increase in complex I-III activity (48%) was found at 20 months, with no changes in complexes II-III or complex IV enzymatic activities. Likewise, complex II-III activity showed an increase (100%) at 24 months, while complex I-III significantly decreased (37%). An age-related increase in superoxide generation was observed, consistent with impaired respiratory chain function. Interestingly, H₂O₂ production rates were 43% decreased in 20-months old mice, compared to young animals. This study presents evidence that the aging process leads to changes in mitochondrial function in brain cortex synaptosomes, which become significantly impaired at the age of 20 months. Even though at more advanced ages, compensatory mechanisms might appear to counteract the impact of mitochondrial dysfunction and oxidative damage, mitochondrial bioenergetics seems to be severely compromised.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2026-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147863947","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ATF5 reduces LPS-induced cardiac injury by modulating pyroptosis via mitophagy.","authors":"Le He, Yuqi Zhao, Haixia Wang, Ling Ou, Kun Luo","doi":"10.1007/s10863-026-10102-4","DOIUrl":"10.1007/s10863-026-10102-4","url":null,"abstract":"<p><p>Myocarditis, often triggered by infections such as sepsis, involves complex mechanisms including mitochondrial dysfunction, oxidative stress and inflammation. The role of activating transcription factor 5 (ATF5) in myocarditis remains unclear. This study aimed to investigate the role of ATF5 in LPS-induced cardiac injury and its potential mechanism involving mitophagy and pyroptosis. An LPS-induced septic cardiomyopathy model was established in H9c2 cardiomyocytes and rats. ATF5 was overexpressed via plasmid transfection in vitro and in vivo. Cell viability, apoptosis, inflammatory cytokine levels, oxidative stress markers, mitophagy-related proteins (LC3-II, Parkin, PINK1, p62), and pyroptosis-related proteins (NLRP3, Caspase-1, GSDMD) were assessed using CCK-8, flow cytometry, ELISA, Western blot, and biochemical assays. Autophagy inhibitor chloroquine (CQ) and GSDMD-targeted siRNA were applied to explore mechanistic interactions. The results showed that ATF5 overexpression alleviated LPS-induced cardiomyocyte injury by enhancing cell viability, reducing apoptosis, and suppressing inflammatory cytokine release (IL-1β, IL-6 and IL-18) and myocardial injury markers (CK-MB and cTn-I). ATF5 promoted mitophagy, reduced oxidative stress (ROS, LDH, GSH-Px and SOD), and inhibited pyroptosis. Mechanistically, CQ abolished the ATF5-mediated protection against cardiomyocyte injury, which was then restored by si-GSDMD. In vivo, ATF5 overexpression improved cardiac function, attenuated fibrosis and decreased serum injury markers in LPS-treated rats. In conclusion, ATF5 enhanced mitophagy, effectively cleared damaged mitochondria, reduced ROS generation, and subsequently inhibited the pyroptosis pathway, ultimately alleviating myocardial injury.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":"58 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148054710","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondrial super complexes in the colorless chlorophycean alga Polytomella parva.","authors":"Marcos Ostolga-Chavarría, Anaiza Rico-Luna, Sergio Fuentes-Hernández, Héctor V Miranda-Astudillo, Alfredo Cabrera-Orefice, Diego González-Halphen","doi":"10.1007/s10863-026-10103-3","DOIUrl":"10.1007/s10863-026-10103-3","url":null,"abstract":"<p><p>Chlorophycean algae of the genera Chlamydomonas and Polytomella share a common photosynthetic ancestor. However, members of the Polytomella lineage have adopted a heterotrophic lifestyle, having lost the photosynthetic apparatus and relying instead on acetate or ethanol as carbon sources, with energy production centered on oxidative phosphorylation (OXPHOS). In this study, we investigated the composition of the mitochondrial supercomplexes of the colorless alga Polytomella parva. Mitochondrial membranes were solubilized using mild detergents such as glycol-diosgenin and digitonin, followed by separation of OXPHOS complexes supramolecular assemblies via Blue Native electrophoresis and Fast Protein Liquid Chromatography (FPLC). Additionally, complexome profiling of solubilized algal mitochondria resolved by Blue Native Gel Electrophoresis was carried out (data are available via ProteomeXchange with identifier PXD075371). The resulting data indicate that the OXPHOS supercomplexes of Polytomella closely resemble those observed in situ in the mitochondria of its green relative Chlamydomonas reinhardtii, as revealed by electron cryo-tomography and subtomogram averaging.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":"58 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13219087/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148054701","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"3',4'-Dihydroxyflavonol has a positive effect on the cerebellum oxidant/antioxidant system and BDNF and transmitter levels in focal brain ischemia-reperfusion.","authors":"Nisanur Coskun, Gozde Acar, Saltuk Bugra Baltaci, Ebru Kubra Uzdil, Tugce Aladag, Rasim Mogulkoc, Abdulkerim Kasım Baltaci","doi":"10.1007/s10863-026-10083-4","DOIUrl":"10.1007/s10863-026-10083-4","url":null,"abstract":"<p><p>Cerebral ischemia-reperfusion (I/R) occurs when blood flow is restored after a temporary interruption and may lead to brain dysfunction through oxidative stress and neurotransmitter imbalance. This study aimed to determine the effect of cerebral I/R and 1-week 3',4'-Dihydroxyflavonol (DiOHF) treatment on the antioxidant/antioxidant system and glutamate, GABA, and BDNF levels in cerebellum tissue in male rats. This study was performed on 28 Wistar-albino type male rats, which were formed as follows: 1-Control Group: No anesthesia or surgical procedure was applied to the animals in this group. 2-Sham Group: After general anesthesia was induced in the animals in this group, the carotid artery regions were opened and closed. After the application, solvent application was performed for 1 week (1 ml DiOHF vehicle). 3-Ischemia-Reperfusion Group: After general anesthesia, the carotid arteries were isolated in rats and ligated for 30 min, ischemia was induced, and then reperfusion was performed. 4-Ischemia-Reperfusion + DiOHF Group: After general anesthesia, the carotid arteries were ligated for 30 min and ischemia was performed in rats, then reperfusion was performed, and then DiOHF supplementation was performed for 1 week. After one week of treatment, the animals were sacrificed under general anaesthesia, and cerebellum tissues were taken. Malondialdehyde (MDA), glutathione peroxidase (GPx), catalase (CAT), superoxide dismutase (SOD), thioredoxin (TRx-2), glutamate, GABA, and brain-derived neurotrophic factor (BDNF) levels were evaluated in the relevant tissue. I/R increased MDA, glutamate, and GABA levels, while GPx, catalase, SOD, thioredoxin and BDNF levels were decreased. However, 1 week of 3',4'-Dihydroxyflavonol treatment corrected the changes that occurred with I/R. The study results show that 1 week of 3',4'-Dihydroxyflavonol treatment after I/R has a positive effect on cerebellum changes that occur in global brain I/R.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":"58 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13219156/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148054660","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A study on the mechanism of IGFBP-3 affecting autophagy to partially protect against inflammatory damage in inflammatory bowel disease.","authors":"Jiahui Liu, Jietong Ye, Shufang Ye, Lingling Chen, Yabi Zhu, Liming Wang, Kunqiang Yu, Xu Ma","doi":"10.1007/s10863-026-10084-3","DOIUrl":"10.1007/s10863-026-10084-3","url":null,"abstract":"<p><p>Given the vital role of IGF-1 binding protein-3 (IGFBP-3) in inflammatory bowel disease (IBD), this study analyzed the mechanisms of IGFBP-3 affecting autophagy and inflammatory damage in IBD. IBD was induced in mice using 2,4,6-trinitrobenzenesulfonic acid. Mice were then treated with IGFBP-3 overexpression lentivirus, a Wnt/β-catenin pathway activator (HLY78), and an autophagy inhibitor (chloroquine). Body weight changes and disease activity index (DAI) scores within 7 days, as well as colon length and colon macroscopic visible damage scores, were recorded. Colon tissue morphology was observed using HE staining, with histological damage scored. ELISA was performed to determine tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and IL-10 levels, and RT-qPCR and Western blot to measure IGFBP-3, Wnt, β-catenin, Axin2, LC3B II/I, and p62 levels in colon tissues. IBD mice exhibited decreased body weight and increased DAI scores within 7 days, along with a shortened colon length, increased macroscopic visible damage and histological damage scores, up-regulated TNF-α and IL-6 levels, and down-regulated IL-10 and IGFBP-3 levels in colon tissues. IGFBP-3 overexpression blocked the Wnt/β-catenin pathway and contributed to partial protection against inflammatory damage in colon tissues as well as promotion of autophagy in IBD mice. Inhibition of autophagy partially averted the protective effect of IGFBP-3 overexpression on inflammatory damage in IBD mice. IGFBP-3 disrupts the Wnt/β-catenin pathway and promotes autophagy, thereby partially protecting against inflammatory damage in IBD mice.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147772402","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SPC25 promotes gastric cancer cells G1/S cell cycle transition and tumorigenesis by enhancing SLC1A5-mediated glutamine metabolism.","authors":"Xinqi Yao, Jie Wu, Yu Song, Hao Shen","doi":"10.1007/s10863-026-10108-y","DOIUrl":"10.1007/s10863-026-10108-y","url":null,"abstract":"<p><p>Although spindle pole body component 25 (SPC25) has been implicated in various cancers, its precise role in GC remains unexplored. This study aimed to investigate the role and mechanism of SPC25 in GC progression. SPC25 expression was analyzed using TCGA database and 40 paired GC clinical specimens. RT-qPCR, Western blot and immunohistochemistry (IHC) staining were performed to detect the expression of SPC25 in GC samples. Flow cytometry was conducted to assess the cell cycle, and commercial kits were used to measure the levels of glutamine, glutamic acid, α-Ketoglutaric acid (α-KG) and NADPH/NADP+. MeRIP-PCR was employed to explore the regulatory role of SPC25 on the m6A levels of SLC1A5. RNA immunoprecipitation (RIP) assay to test the binding between IGF2BP2 and SPC25 transcripts. Xenograft mouse model was constructed to assess the effect of SPC25 on tumor growth in vivo. SPC25 was significantly overexpressed in GC tissues and cell lines. Silencing SPC25 repressed G1/S cell cycle transition and downregulated the expressions of several key mitotic regulators. Moreover, the interference of SPC25 repressed glutamine metabolism in GC cells, as demonstrated by reduced glutamine consumption and decreased production of α-KG, glutamate and NADPH/NADP+. SPC25 overexpression exerted the opposite effects. Mechanistically, SPC25 promoted glutamine metabolism and cell cycle progression in GC by stabilizing SLC1A5 expression through IGF2BP2-mediated m6A modification. Animal study revealed that SPC25 knockdown suppressed tumor growth in vivo. SPC25, stabilizing SLC1A5 expression through IGF2BP2 mediated m6A modification, regulated glutamine metabolism, promoted gastric cancer cells G1/S cell cycle transition and drove tumor progression.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":"58 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147772412","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The expression of glial cell-derived neurotrophic factor in the hippocampal tissue of rats with vascular dementia and its correlation with molecular pathways involved in learning and memory impairment.","authors":"Jinzhi Zhang, Yan Lin","doi":"10.1007/s10863-026-10097-y","DOIUrl":"10.1007/s10863-026-10097-y","url":null,"abstract":"<p><p>It aimed to investigate the expression of glial cell-derived neurotrophic factor (GDNF) in the hippocampal tissue of rats with vascular dementia (VD) and its correlation with learning and memory functions (LMFs). Additionally, it sought to analyze the impact of factors such as acetylcholine synthesis/metabolism imbalance and oxidative stress on the alteration of GDNF expression and their role in pathogenesis of VD, particularly regarding learning and memory deficits. Wistar rats were randomly rolled into control group (Ctrl, no treatment), sham group (Sham, exposure of bilateral common carotid arteries without occlusion), and VD group (permanent ligation of bilateral common carotid arteries). Morris water maze test assessed the LMFs of rats. Superoxide dismutase (SOD), malondialdehyde (MDA), acetylcholinesterase (AchE), and choline acetyltransferase (ChAT) level changes were monitored. Immunohistochemical staining detected CD34 and GDNF expression levels, while western blot analysis examined vascular endothelial growth factor (VEGF)A and VEGF receptor 2 (VEGFR2) protein expression levels. Rats in VD group had longer escape latencies and greater total swimming distances, along with reduced swimming speeds and fewer platform crossings versus Ctrl and Sham (P < 0.05). VD group had relatively lower hippocampal SOD, AchE, and ChAT activity levels (P < 0.05). VD group had increased CD34 expression level and decreased GDNF expression level versus Ctrl and Sham (P < 0.05). VD group exhibited higher relative expression levels of VEGFA and VEGFR2 proteins in hippocampal tissue than Ctrl and Sham (P < 0.05). VD rats exhibited observable impairments in LMFs, which may be associated with an imbalance in acetylcholine synthesis/metabolism, oxidative stress, and reduced expression level of GDNF in hippocampal tissue.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2026-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147716907","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oridonin ameliorates the ferroptosis of chondrocyte to play a chondroprotective role in osteoarthritis.","authors":"Xinchun Wu, Tingting Hua, Weihui Liu, Hong Xiao, Yunqing Ban","doi":"10.1007/s10863-026-10081-6","DOIUrl":"10.1007/s10863-026-10081-6","url":null,"abstract":"<p><p>Chondrocyte dysfunction is a pivotal event in the progression of osteoarthritis (OA). In recent years, ferroptosis has been identified as a key mechanism contributing to chondrocyte functional loss. Given the therapeutic potential of natural compounds derived from Traditional Chinese Medicine for OA, this study aims to investigate whether Oridonin (Ori) exerts a protective effect on osteoarthritic chondrocytes by inhibiting the ferroptosis pathway. Results indicated that Ori inhibited the ferroptosis-related features of chondrocyte via dosage-dependent manner. Mechanistically, acyl-CoA synthetase 4 (ACSL4) was found to be the target of Ori. More findings demonstrated that Ori was capable of suppressing ACSL4, thereby inhibiting ferroptosis in chondrocytes. In conclusion, Ori protected chondrocytes through ACSL4-mediated ferroptosis, which provided a theoretical foundation and a potential therapeutic target for OA.</p>","PeriodicalId":15080,"journal":{"name":"Journal of Bioenergetics and Biomembranes","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2026-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147716875","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}