Brazilian Journal of Medical and Biological Research最新文献

{"title":"Targeting IL-17/NF-κB/VAChT/Rho-kinase signaling and oxidative stress in exacerbated chronic allergic inflammation: functional and therapeutic implications of IL-17 blockade.","authors":"L N Camargo, T M Dos Santos, B M Saraiva-Romanholo, E A Leick, C M Prado, R F Righetti, I F L C Tibério","doi":"10.1590/1414-431X2026e15063","DOIUrl":"10.1590/1414-431X2026e15063","url":null,"abstract":"<p><p>Th17 cytokines play a central role in the pathophysiology of chronic allergic pulmonary inflammation, influencing multiple signaling pathways that promote inflammation, oxidative stress, and airway remodeling. We evaluated the modulation of the NF-κB, VAChT, and Rho-kinase signaling pathways, and the effects of anti-interleukin (IL)-17 treatment on airway alterations in a murine model of chronic allergic inflammation were exacerbated by lipopolysaccharide (LPS). We studied airway hyperresponsiveness, inflammation, oxidative stress pathways, tissue remodeling, and the expression of various markers in male BALB/c mice with ovalbumin (OVA)-induced chronic allergic inflammation, with or without anti-IL-17 treatment. Twenty-four hours before the end of the experiment, the OVA-sensitized animals were treated with LPS (OVA-LPS-anti-IL-17). Mice treated with OVA-LPS-anti-IL-17 exhibited decreased elastance of the respiratory system after methacholine challenge, along with reduced infiltration of eosinophils, neutrophils, lymphocytes, and macrophages. Anti-IL-17 treatment also reduced the expression of TNF-α, TARC/eotaxin, IL-2, IL-4, IL-5, IL-6, IL-10, IL-13, IL-17, MMP-9, MMP-12, TIMP-1, TGF-β, iNOS, NF-κB, ROCK1, ROCK2, types I and III collagen, decorin, lumican, biglycan, fibronectin, and 8-iso-PGF2α in airway cells, as well as the mRNA expression of IL-17, VAChT, and arginase 1 in lung tissue, compared to the OVA and OVA-LPS groups (P<0.05), except for TNF-α and actin, which were not reduced compared to the OVA group, and Rrs, actin, and VAChT, which were not reduced compared to the OVA-LPS group. Thus, IL-17 blockade helped control bronchial hyperresponsiveness, modulate the IL-17/NF-κB/VAChT/Rho-kinase pathway, suppress chemokine expression, mitigate airway remodeling, and reduce NO-arginase expression in this asthma mouse model with LPS-induced exacerbation.</p>","PeriodicalId":9088,"journal":{"name":"Brazilian Journal of Medical and Biological Research","volume":"59 ","pages":"e15063"},"PeriodicalIF":1.9,"publicationDate":"2026-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13037830/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147590005","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Surgical induction model of femoral defect in Wistar rats for bone repair histology.","authors":"F L D de Oliveira, A C Nagato, T N França, F M Aarestrup, B J V Aarestrup","doi":"10.1590/1414-431X2025e15168","DOIUrl":"10.1590/1414-431X2025e15168","url":null,"abstract":"<p><p>The creation of bone lesions using a well-established surgical technique is essential for obtaining histological images in experimental models that aim to study the pathophysiology of bone repair. In this study, we report the steps of a surgical method to induce bone defects in Wistar rats, providing a basis for experimental studies requiring precision in these lesions, especially for future experimental tests and subsequent histological analysis. The animal model remains an important alternative for investigating the inflammatory process and bone regeneration. The model consists of creating experimental, non-critical surgical bone defects in the femurs of Wistar rats (Rattus norvegicus, 90 days old, weighing between 250-300 g) using a 2-mm spherical drill and a low-speed motor. The present report includes reproducible information on the selection of the animals and the materials needed to perform anesthesia and surgery to induce bone defects. It also provides details on post-surgical care, sample collection, and preparation of samples for histological processing. The steps presented here can significantly increase the accuracy of lesion creation and allow for more precise results in the analysis of bone architecture and repair.</p>","PeriodicalId":9088,"journal":{"name":"Brazilian Journal of Medical and Biological Research","volume":"59 ","pages":"e15168"},"PeriodicalIF":1.9,"publicationDate":"2026-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13037826/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147590053","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MMP9 regulates osteogenesis and MMP2 expression through the TGF-β1/SMAD2/3 signaling pathway in lipopolysaccharide-induced osteoblasts.","authors":"Lei Li, Yang Yang, Ximei Lu, Hui Li","doi":"10.1590/1414-431X2026e15172","DOIUrl":"10.1590/1414-431X2026e15172","url":null,"abstract":"<p><p>Matrix metalloproteinases (MMP) act as effectors and regulators in normal growth and development as well as in pathological processes. The gelatinases MMP2 and MMP9 exhibit similar structures and biological reactions. The purpose of this study was to clarify the relationship between MMP9 and MMP2 in lipopolysaccharide (LPS)-induced osteoblasts. MC3T3-E1 cells were pretreated with or without TGF-β1 inhibitor (20 nM) and SMAD2/3 inhibitor (20 nM) for 1 h, and then with pcDNA3.1-mMMP9 (0.8 μg/mL) for 48 h. Quantitative real-time PCR, western blot, and immunocytochemistry were performed to detect MMP2, TGF-β1, and/or SMAD2/3 expression. Luciferase reporter assay and electrophoretic mobility shift assay (EMSA) were performed to examine the regulatory effect of SMAD2/3 on MMP2 gene transcription. RUNX2, OSX, ALP, type I collagen, and OCN expression was detected in LPS (20 μg/mL)-stimulated MC3T3-E1 cells after MMP9 treatment. MMP9 activated the expression of TGF-β1 and phosphorylation of SMAD2/3. Phosphorylated SMAD2/3 translocalized into nuclei to bind to SMAD-binding elements in the promoter of the MMP2 gene, inhibiting MMP2 gene transcription. Additionally, MMP9 increased RUNX2, OSX, ALP, COL I, and OCN expression in LPS-induced MC3T3 cells. MMP9 may regulate osteogenesis through TGF-β1-SMAD2/3/-MMP2 signaling during the inflammation process.</p>","PeriodicalId":9088,"journal":{"name":"Brazilian Journal of Medical and Biological Research","volume":"59 ","pages":"e15172"},"PeriodicalIF":1.9,"publicationDate":"2026-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13037832/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147590015","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"1H-NMR-based metabolomics reveals that prior exercise modulates metabolic changes in the cerebral cortex and hippocampus in sleep-deprived mice.","authors":"B R D da Silva, P I G Nunes, R S de Matos, L M A Silva, E G Alves Filho, E S de Brito, P F C de Bruin, V M S de Bruin","doi":"10.1590/1414-431X2025e14816","DOIUrl":"10.1590/1414-431X2025e14816","url":null,"abstract":"<p><p>Sleep deprivation induces profound metabolic disturbances in the brain, while regular physical exercise is recognized for promoting neuroprotection and energy balance. This study investigated the effects of chronic treadmill exercise on the cortical and hippocampal metabolic profiles of sleep-deprived Swiss mice using the entire 1H-NMR spectrum. Male mice (n=48) were assigned to four groups: Control, Exercise (EX), Sleep Deprivation (SD), and Exercise before Sleep Deprivation (EX+SD). The EX group underwent 8 weeks of aerobic training, and SD was induced by 72-h total sleep deprivation. Brain metabolomic analysis revealed that the cortex and hippocampus shared a qualitatively similar metabolic composition, with taurine, creatine, and lactic acid as the most abundant metabolites. Exercise increased cortical levels of lactic acid, creatine, taurine, and other metabolites involved in glycolysis, the TCA cycle, and osmoregulation, while SD disrupted energy-related metabolites and increased glial markers such as myo-inositol. The EX+SD group exhibited a cortical metabolic profile similar to controls, indicating that prior exercise preserved neuroenergetic balance in this region. In contrast, hippocampal metabolism remained partially affected by SD, despite exercise preconditioning. These findings suggest that exercise confers region-specific metabolic resilience, especially in the cortex, by modulating pathways related to pyruvate metabolism, glutamate turnover, and astrocytic-neuronal coupling. Regular physical activity may thus act as a non-pharmacological strategy to mitigate SD-induced neurochemical imbalances.</p>","PeriodicalId":9088,"journal":{"name":"Brazilian Journal of Medical and Biological Research","volume":"59 ","pages":"e14816"},"PeriodicalIF":1.9,"publicationDate":"2026-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13037829/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147590064","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biomarker-based prediction of radial artery occlusion after cardiac catheterization.","authors":"C Alp, H Kandemir, S Ozturk","doi":"10.1590/1414-431X2025e15093","DOIUrl":"10.1590/1414-431X2025e15093","url":null,"abstract":"<p><p>Thrombotic occlusion of the radial artery is the most frequent complication of transradial angiography. This study sought to investigate biomarker-based predictors of radial artery occlusion (RAO) after coronary angiography (CAG) and/or percutaneous coronary intervention (PCI). Consecutive patients who underwent cardiac catheterization through radial artery route for diagnostic or therapeutic purposes were included in the study retrospectively. The clinical, laboratory, and angiographic data were obtained from hospital records. All patients were invited for a follow-up visit one week after discharge and radial artery pulse examination was performed. The patients with reduced or absent radial artery pulse or complaints related with the radial artery intervention site at follow-up visit were examined by a radiologist with superficial Doppler ultrasonography. The patients were categorized according to the patency of the radial artery and there were 46 patients with an occluded radial artery and 204 patients with a patent radial artery after CAG and/or PCI. Platelet count was higher in the occluded artery group than in the patent radial artery group. Creatinine level was lower and estimated glomerular filtration rate (e-GFR) was higher in the occluded radial artery group compared to the patent radial artery group. Multivariate logistic regression analysis showed that platelet count (OR: 1.010, 95%CI: 1.001-1.018, P=0.031) and creatinine (OR:0.030, 95%CI: 0.001-0.821, P=0.038), but not e-GFR (OR: 1.031, 95%CI: 0.991-1.073, P=0.128) were independently associated with RAO. Platelet count and creatinine were found to be independent predictors of RAO after transradial cardiac catheterization.</p>","PeriodicalId":9088,"journal":{"name":"Brazilian Journal of Medical and Biological Research","volume":"59 ","pages":"e15093"},"PeriodicalIF":1.9,"publicationDate":"2026-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13037827/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147590071","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Disulfidptosis modification patterns are involved in the immune microenvironment regulation of septic acute respiratory distress syndrome.","authors":"Qian Zhang, Junke Ge","doi":"10.1590/1414-431X2025e14932","DOIUrl":"10.1590/1414-431X2025e14932","url":null,"abstract":"<p><p>Disulfidptosis is a new form of programmed cell death. However, there is limited information available regarding the impact of disulfidptosis on septic acute respiratory distress syndrome (ARDS). The 16 disulfidptosis-related genes (DRGs) were collected from a previous study. Gene expression data of sepsis and septic ARDS samples were downloaded from the Gene Expression Omnibus database. The risk score model in septic ARDS was constructed based on the DRGs, followed by the investigation of immune microenvironment in septic ARDS patients. Furthermore, septic ARDS patients were divided into different subtypes based on disulfidptosis modification patterns, and their immune characteristics were investigated. Finally, the differentially expressed genes among different subtypes were identified, and a diagnostic model was constructed. The risk score model based on 6 DRGs was constructed to distinguish sepsis patients from septic ARDS patients, with good performance. The immune microenvironment in septic ARDS patients was slightly different from sepsis patients. Additionally, septic ARDS patients were divided into two subtypes based on DRGs. Finally, three diagnostic models based on 3 hub genes were constructed to classify the two subtypes in septic ARDS patients. Our findings indicated that disulfidptosis might play a role in the immune microenvironment of septic ARDS.</p>","PeriodicalId":9088,"journal":{"name":"Brazilian Journal of Medical and Biological Research","volume":"59 ","pages":"e14932"},"PeriodicalIF":1.9,"publicationDate":"2026-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12971013/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147430917","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unveiling preeclampsia: diagnostic value and potential molecular mechanisms of abnormally methylated immune-related genes.","authors":"Yuan Yuan, Qin Wang, Xiao Su, Lu Zhong","doi":"10.1590/1414-431X2025e15317","DOIUrl":"10.1590/1414-431X2025e15317","url":null,"abstract":"<p><p>Preeclampsia (PE) is a life-threatening obstetric complication, and DNA methylation and immune system disorders play a key role in its development. This study aimed to explore the potential mechanisms and values of abnormally methylated immune-related differentially expressed genes (DEGs) in PE. Gene expression profiles and methylation data of PE were downloaded from the Gene Expression Omnibus (GEO) database. Immune-related genes were downloaded from the ImmPort database. Subsequently, differential expression analysis, functional annotation, immune cell infiltration analysis, Pearson correlation analysis, construction of classification models and miRNA-mRNA interaction network, and real-time PCR validation were carried out. Ten key abnormally methylated immune-related DEGs (ESRRG, FGF10, AHNAK, STC2, PPARG, LTF, MX1, ESR1, RELB, and JAG2) were identified and may be potential diagnostic biomarkers for PE. The decision tree (DT), random forests (RF), and support vector machine (SVM) classification models constructed based on these 10 genes exhibited a certain level of diagnostic accuracy. Compared with a single DEG, these classification models may have relatively higher diagnostic reference value. Functional annotation results showed that rap1, PI3K-Akt, and calcium signaling pathways may play a regulatory role in PE. The infiltration levels of monocytes, M2 macrophages, neutrophils, Tregs, and eosinophils in the PE group were abnormal. Key abnormally methylated immune-related DEGs were significantly correlated with the infiltration levels of immune cells. Moreover, 6 miRNA-mRNA pairs (hsa-miR-181b-5p-ESR1, hsa-miR-152-3p-ESR1, hsa-miR-26b-3p-ESR1, hsa-miR-4672-ESRRG, hsa-miR-502-3p-AHNAK, and hsa-miR-3059-5p-STC2) were identified. Key abnormally methylated immune-related DEGs may be associated with the immune mechanism of PE, given their correlation with related signaling pathways and immune cell infiltration.</p>","PeriodicalId":9088,"journal":{"name":"Brazilian Journal of Medical and Biological Research","volume":"59 ","pages":"e15317"},"PeriodicalIF":1.9,"publicationDate":"2026-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12971016/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147430910","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the causal impact of mitochondrial dysfunction on epilepsy: a mendelian randomization study.","authors":"Lin-Ming Zhang, Fei Wang, Bing-Ran Zhang, Qiu-Juan Zhang, Yan-Lin Zhu, Shu-Ji Gao, Hao Wang, Ming-Wei Liu","doi":"10.1590/1414-431X2025e14524","DOIUrl":"10.1590/1414-431X2025e14524","url":null,"abstract":"<p><p>Mitochondrial dysfunction contributes critically to epileptogenesis. Therefore, identifying key mitochondrial function-associated genes in epilepsy may provide novel insights into its pathogenesis. We employed expression quantitative trait loci (eQTLs) and Mendelian randomization analyses to assess mitochondrial-epilepsy causality, with leave-one-out validation confirming the reliability and directionality of the results. The results revealed that hydroxyacylglutathione hydrolase (HAGH), oxysterol-binding protein-related protein 1A (OSBPL1A) and pantothenate kinase 2 (PANK2) were pivotal epileptogenic genes. HAGH modulates the mechanistic target of rapamycin complex 1 (mTORC1) signaling and fatty acid metabolism pathways. OSBPL1A mediates apoptotic and reactive oxygen species (ROS) pathways. PANK2 regulates phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling and Notch signaling cascades. Additionally, these genes participate in inflammatory pathways, including T cell receptor (TCR), mitogen-activated protein kinase (MAPK), and tumor necrosis factor (TNF) signaling. We demonstrated that HAGH, OSBPL1A, and PANK2 constitute core pathogenic mechanisms in epilepsy. These genes potentially govern epileptogenesis through mitochondrial regulation via neuroinflammatory, immunomodulatory, and apoptotic pathways. Our findings provide a foundation for investigating epileptogenesis, discovering therapeutic targets, and identifying prognostic biomarkers.</p>","PeriodicalId":9088,"journal":{"name":"Brazilian Journal of Medical and Biological Research","volume":"59 ","pages":"e14524"},"PeriodicalIF":1.9,"publicationDate":"2026-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12971012/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147430890","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metformin attenuates fructose-induced pulmonary fibrosis, possibly through the involvement of the TRPC6 channel.","authors":"B Serez Kaya, O Öner, D Ercetin, M A Aydın, E Akbas, M Sapmaz Metin, O Kaya","doi":"10.1590/1414-431X2026e15255","DOIUrl":"10.1590/1414-431X2026e15255","url":null,"abstract":"<p><p>Pulmonary fibrosis is a chronic, progressive, fatal lung disease characterized by abnormal lung tissue repair and intense collagen accumulation in the lungs. Despite intensive efforts, no specific treatment has been found. The aim of this study was to investigate the effects of a high-fructose diet on lung tissue, whether the use of metformin corrects the damage caused by high fructose, and the possible relationship with transient receptor potential (TRP) channels. Lung damage was induced by adding 200 g/L fructose to the drinking water of Sprague-Dawley rats (n=32) for 10 weeks. In the groups in which the effect of metformin was examined, metformin (dissolved in saline) was administered intraperitoneally at a dose of 100 mg/kg in the last two weeks of the study. Inflammation and TRP channel levels were measured by ELISA. Histopathological evaluation was also assessed by Masson's Trichrome staining. A high-fructose diet caused collagen deposition, inflammation, and intra-alveolar hemorrhage in lung tissue. Interleukin-6 and TRPC6 channel protein levels in lung tissue were higher in the high-fructose group than in the control group. These effects were prevented by metformin treatment. Metformin administration and manipulation of TRPC6 channels may be a therapeutic target for the treatment of pulmonary fibrosis.</p>","PeriodicalId":9088,"journal":{"name":"Brazilian Journal of Medical and Biological Research","volume":"59 ","pages":"e15255"},"PeriodicalIF":1.9,"publicationDate":"2026-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12971010/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147430905","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of combined trunk stretching and lumbar stabilization exercises for chronic non-specific low back pain: a randomized clinical trial.","authors":"C C C Coutinho, D D A Sampaio, N D C Pereira, A C Pássaro, V M A Oliveira, R A Casarotto","doi":"10.1590/1414-431X2025e14863","DOIUrl":"10.1590/1414-431X2025e14863","url":null,"abstract":"<p><p>This study aimed to compare the effectiveness of combining trunk stretching with lumbar segmental stabilization versus exclusively performing lumbar segmental stabilization exercises for treating chronic nonspecific low back pain (CNLBP). Thirty-four CNLBP subjects were randomized into two groups: active trunk stretching + lumbar segmental stabilization (AS+LSS, n=17) and placebo stretching + lumbar segmental stabilization (PS+LSS, n=17). One-hour sessions were performed twice a week for six weeks. Pain intensity, pain quality, functional disability, global impression of recovery, emotional state, symptoms, and adverse effects were assessed at baseline, after 6 weeks, and at 12 and 24 weeks follow-up. Both groups experienced significant reductions in pain intensity and functional disability after the intervention. Depression and anxiety showed significant improvements during the intervention but did not persist at follow-up. No statistically significant differences were observed between the groups for the studied variables. The study concluded that both protocols are beneficial for CNLBP patients, suggesting that lumbar segmental stabilization exercises alone are sufficient for reducing pain and functional disability.</p>","PeriodicalId":9088,"journal":{"name":"Brazilian Journal of Medical and Biological Research","volume":"59 ","pages":"e14863"},"PeriodicalIF":1.9,"publicationDate":"2026-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12971020/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147430859","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}