Journal of Clinical Biochemistry and Nutrition最新文献_第4页

Ginsenoside Rg2 upregulates expression of Lilrb4 and inhibits the NF-κB signaling pathway to alleviate hemorrhagic shock/reperfusion-induced intestinal injury. 人参皂苷Rg2通过上调Lilrb4的表达，抑制NF-κB信号通路，减轻失血性休克/再灌注引起的肠道损伤。

IF 1.9 4区医学

Journal of Clinical Biochemistry and Nutrition Pub Date : 2026-03-01 Epub Date: 2025-11-28 DOI: 10.3164/jcbn.25-122

Nan Wang, Di Jia, Xin Ge

{"title":"Ginsenoside Rg2 upregulates expression of Lilrb4 and inhibits the NF-κB signaling pathway to alleviate hemorrhagic shock/reperfusion-induced intestinal injury.","authors":"Nan Wang, Di Jia, Xin Ge","doi":"10.3164/jcbn.25-122","DOIUrl":"10.3164/jcbn.25-122","url":null,"abstract":"Hemorrhagic shock/reperfusion (HS/R) injury is associated with high global mortality, and intestinal injury plays a pivotal role in driving systemic complications. This study examined the therapeutic potential of Ginsenoside Rg2 (G-Rg2) in mitigating HS/R intestinal injury and elucidated its relationship involving leukocyte immunoglobulin-like receptor B4 (Lilrb4). Using an established rat HS/R model and hypoxia/reoxygenation (H/R) IEC-6 cells, we evaluated the effects of G-Rg2 on intestinal barrier integrity, inflammatory responses, oxidative stress, and apoptosis. The results indicated that G-Rg2 treatment significantly alleviates intestinal mucosal damage, inhibits epithelial apoptosis, and restores tight junction proteins (Occludin, ZO-1). In vitro experiments revealed that G-Rg2 enhances cell viability, suppresses reactive oxygen species (ROS) overproduction, and reduces pro-inflammatory cytokines (TNF-α, IL-6, and IL-1β). Mechanistically, G-Rg2 upregulated Lilrb4 expression, and supressed NF-κB pathway activation. Collectively, these findings suggested that G-Rg2 alleviates HS/R-induced intestinal injury by the upregulation of Lilrb4 and the inhibition of the NF-κB pathway.","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"78 2","pages":"109-120"},"PeriodicalIF":1.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12989232/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147467886","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}

引用次数: 0

Icariside II suppresses NF-κB/STAT3 signaling to prevent the progression of chronic atrophic gastritis toward gastric cancer. Icariside II抑制NF-κB/STAT3信号通路阻止慢性萎缩性胃炎向胃癌发展。

IF 1.9 4区医学

Journal of Clinical Biochemistry and Nutrition Pub Date : 2026-03-01 Epub Date: 2026-01-16 DOI: 10.3164/jcbn.25-203

Mingzhe Li, Hai Shang, Qianqian Liu

{"title":"Icariside II suppresses NF-κB/STAT3 signaling to prevent the progression of chronic atrophic gastritis toward gastric cancer.","authors":"Mingzhe Li, Hai Shang, Qianqian Liu","doi":"10.3164/jcbn.25-203","DOIUrl":"10.3164/jcbn.25-203","url":null,"abstract":"Chronic atrophic gastritis is a precancerous condition in the gastric carcinogenesis cascade, in which persistent inflammation plays a central role. This study aimed to evaluate the protective effects of Icariside II, a bioactive flavonoid derived from Epimedium, against inflammation-associated gastric mucosal injury. A composite mouse model was established by oral inoculation with Helicobacter pylori, administration of N-methyl-N-nitrosourea in drinking water, and a high-salt diet. Mice were randomly assigned to a model control group, an Icariside II treatment group receiving 20 milligrams per kilogram per day by gavage, or an eradication therapy group. Icariside II alleviated gastric glandular atrophy and hyperplasia and significantly reduced interleukin-6, interleukin-1β, and tumor necrosis factor α levels in both serum and gastric tissue homogenates. In human gastric cancer cells exposed to an inflammatory stimulus with tumor necrosis factor α, Icariside II reduced cell proliferation and migration, promoted apoptosis, and decreased the release of pro-inflammatory cytokines. Mechanistic analyses showed that Icariside II suppressed inflammation-related signaling activity by reducing phosphorylation and nuclear translocation of key transcriptional regulators, leading to decreased expression of genes involved in inflammation, cell survival, and invasion. These findings indicate that Icariside II may represent a potential natural compound for preventing or delaying the progression of chronic atrophic gastritis.","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"78 2","pages":"158-167"},"PeriodicalIF":1.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12989227/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147467958","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}

引用次数: 0

METTL3-mediated m6A modification of CXCR4 drives M2 macrophage polarization and suppresses anti-tumor immunity in esophageal cancer. mettl3介导的m6A修饰CXCR4驱动M2巨噬细胞极化，抑制食管癌抗肿瘤免疫。

IF 1.9 4区医学

Journal of Clinical Biochemistry and Nutrition Pub Date : 2026-03-01 Epub Date: 2025-12-17 DOI: 10.3164/jcbn.25-180

Yuxin Sun, Sifu Huang

{"title":"METTL3-mediated m6A modification of CXCR4 drives M2 macrophage polarization and suppresses anti-tumor immunity in esophageal cancer.","authors":"Yuxin Sun, Sifu Huang","doi":"10.3164/jcbn.25-180","DOIUrl":"10.3164/jcbn.25-180","url":null,"abstract":"Dense tumor-associated macrophage infiltration correlates with poor prognosis in esophageal cancer (EC), yet the underlying molecular mechanisms remain undefined. An EC cell-macrophage co-culture system was established. M2 polarization was evaluated by flow cytometry and ELISA. qPCR and Western blot were employed to detect mRNA and protein levels. MeRIP-PCR assessed CXCR4 m6A methylation. Colony formation, wound-healing, and apoptosis assays measured EC cell proliferation, migration, and apoptosis. Compared with macrophages co-cultured with normal esophageal epithelial cells, those co-cultured with EC cells exhibited increased IL-10 and TGF-β secretion, accompanied by up-regulation of CD206, CD163, CXCR4, and METTL3. METTL3 up-regulated CXCR4 by mediating CXCR4 m6A methylation. METTL3-overexpressing macrophages elevated CD206/CD163 levels and IL-10/TGF-β secretion, whereas CXCR4 knockdown reversed these effects. Moreover, METTL3-high macrophages promoted EC cell proliferation and migration, up-regulated PD-L1, and inhibited apoptosis. METTL3 is up-regulated in EC-associated macrophages, promotes M2 polarization via m6A modification of CXCR4, and thereby accelerates EC malignant progression.","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"78 2","pages":"136-141"},"PeriodicalIF":1.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12989231/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147467899","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}

引用次数: 0

The role of senescence indicators in the linkage between high-glycemic food intake and lung cancer: a Mendelian randomization study. 衰老指标在高血糖食物摄入与肺癌之间的关联中的作用：一项孟德尔随机研究。

IF 1.9 4区医学

Journal of Clinical Biochemistry and Nutrition Pub Date : 2026-03-01 Epub Date: 2025-12-04 DOI: 10.3164/jcbn.25-208

Yunzhi Ma, Shuping Huang, Xiaoyan Huang, Zhaoke Wen, Yifan Zhou, Zhenniu Lei, Ronglin Li, Shucong Peng, Junqi Qin, Shengjing Liang, Yonglong Zhong

{"title":"The role of senescence indicators in the linkage between high-glycemic food intake and lung cancer: a Mendelian randomization study.","authors":"Yunzhi Ma, Shuping Huang, Xiaoyan Huang, Zhaoke Wen, Yifan Zhou, Zhenniu Lei, Ronglin Li, Shucong Peng, Junqi Qin, Shengjing Liang, Yonglong Zhong","doi":"10.3164/jcbn.25-208","DOIUrl":"10.3164/jcbn.25-208","url":null,"abstract":"High-sugar food intake is linked with elevated lung cancer (LC) risk. Accelerated biological senescence is a risk factor for various diseases. This study probes the role of senescence indicators in the genetic causality between high-sugar food intake and LC risk. Using GWAS data and Mendelian randomization, we found that the intake of sugar added in tea exhibited a significant positive causal association with overall LC risk (OR = 1.310, 95% CI: 1.024-1.675, p = 0.031) and lung squamous cell carcinoma risk (OR = 1.616, 95% CI: 1.089-2.398, p = 0.017). Artificial sweetener intake in cereals was positively linked with small cell lung cancer risk (OR = 4.042, 95% CI: 1.153-14.170, p = 0.029). GrimAge acceleration was significantly correlated with LC risk (p = 0.047), and Hannum age acceleration showed a positive linkage with small cell lung cancer risk (p = 0.002). The intake of sugar added to tea was positively causally linked to both GrimAge (p = 0.045) and Hannum age acceleration (p = 0.025). Mediation analysis indicated that GrimAge acceleration mediated 9.64% of the effect of sugar added to tea on LC risk. In conclusion, high-sugar food intake exhibits a genetic causal linkage with LC risk, partially mediated by biological senescence.","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"78 2","pages":"126-135"},"PeriodicalIF":1.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12989228/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147468169","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}

引用次数: 0

The effect of SIRT1 knockdown on the gene expression of CoQ10 biosynthetic enzymes. SIRT1敲低对辅酶q10生物合成酶基因表达的影响。

IF 1.9 4区医学

Journal of Clinical Biochemistry and Nutrition Pub Date : 2026-03-01 Epub Date: 2026-01-10 DOI: 10.3164/jcbn.24-239

Rena Okuizumi, Satsuki Maruyama, Mizuho Okamoto, Akio Fujisawa, Yorihiro Yamamoto, Misato Kashiba

{"title":"The effect of SIRT1 knockdown on the gene expression of CoQ10 biosynthetic enzymes.","authors":"Rena Okuizumi, Satsuki Maruyama, Mizuho Okamoto, Akio Fujisawa, Yorihiro Yamamoto, Misato Kashiba","doi":"10.3164/jcbn.24-239","DOIUrl":"10.3164/jcbn.24-239","url":null,"abstract":"Coenzyme Q10 is a lipid-soluble antioxidant essential for the mitochondrial electron transport chain. Its concentration in the body decreases with age. The biosynthesis of coenzyme Q10 involves enzymes coq1 (PDSS1, PDSS2) through coq9, though the regulatory mechanisms of their gene expression and enzyme activities are unknown. SIRT1, an anti-aging gene, regulates various transcription factors. This study investigates the impact of SIRT1 knockdown on the gene expression of coenzyme Q10 biosynthetic enzymes and coenzyme Q10 levels in MDA-MB-231 and HepG2 cells. SIRT1 knockdown significantly increased coq4 gene expression in MDA-MB-231 cells, while coq6 and coq7 expression decreased. In HepG2 cells, coq4 expression also increased, but coq6 and coq7 expression remained unchanged. Coenzyme Q10 levels increased in both cell lines. Further experiments with PGC-1α and NRF1 knockdown, downstream factors of SIRT1, in MDA-MB-231 cells showed no change in coq4 expression, while coq6 and coq7 expression decreased, and coenzyme Q10 levels remained unchanged. These findings suggest that the increase in coenzyme Q10 levels following SIRT1 knockdown may be attributed to coq4, indicating a pathway distinct from PGC-1α and NRF1.","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"78 2","pages":"89-97"},"PeriodicalIF":1.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12989230/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147468138","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}

引用次数: 0

Morroniside in Cornus officinalis Sieb. et Zucc. protects renal tubular epithelial cells from hypoxia/reoxygenation damage by inhibiting oxidative stress and ferroptosis. 山茱萸中的Morroniside。调查。通过抑制氧化应激和铁下垂保护肾小管上皮细胞免受缺氧/再氧化损伤。

IF 1.9 4区医学

Journal of Clinical Biochemistry and Nutrition Pub Date : 2026-03-01 Epub Date: 2025-12-17 DOI: 10.3164/jcbn.25-124

Xiang Wang, Fei Huang

{"title":"Morroniside in Cornus officinalis Sieb. et Zucc. protects renal tubular epithelial cells from hypoxia/reoxygenation damage by inhibiting oxidative stress and ferroptosis.","authors":"Xiang Wang, Fei Huang","doi":"10.3164/jcbn.25-124","DOIUrl":"10.3164/jcbn.25-124","url":null,"abstract":"Acute kidney injury (AKI) is a critical condition with high morbidity and mortality, often caused by ischemia/reperfusion (I/R) injury. Morroniside (MOR), derived from Cornus officinalis, has anti-inflammatory and antioxidant properties. This study investigates its effects on AKI induced by hypoxia/reoxygenation (H/R) in renal tubular epithelial cells. H/R-induced HK-2 cells were treated with MOR (0.5, 1.0, and 2.0 ‍μM). Cell viability was assessed using CCK-8, and oxidative stress was evaluated via reactive oxygen species (ROS), superoxide dismutase (SOD), glutathione (GSH), and malondialdehyde (MDA) levels. Ferroptosis was examined through GPX4 and ACSL4 expression. The Nrf2/HO-1 signaling pathway was analyzed by Western blotting. Results show that MOR alleviates H/R-induced cell damage and oxidative stress by increasing cell viability, reducing lactate dehydrogenase (LDH) release, ROS, and MDA levels, while enhancing SOD and GSH activities. It also inhibits ferroptosis by upregulating GPX4 and downregulating ACSL4. Additionally, MOR activates the Nrf2/HO-1 signaling pathway. These findings suggest that MOR protects renal tubular epithelial cells from H/R injury by reducing oxidative damage and inhibiting ferroptosis, potentially through the Nrf2/HO-1 pathway.","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"78 2","pages":"121-125"},"PeriodicalIF":1.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12989224/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147468083","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}

引用次数: 0

Antioxidant polymer nanoparticles ameliorate cancer cachexia via intestinal ROS scavenging. 抗氧化聚合物纳米颗粒通过清除肠道活性氧改善癌症恶病质。

IF 1.9 4区医学

Journal of Clinical Biochemistry and Nutrition Pub Date : 2026-03-01 Epub Date: 2025-11-15 DOI: 10.3164/jcbn.25-179

Yutaka Ikeda, Yukio Nagasaki

{"title":"Antioxidant polymer nanoparticles ameliorate cancer cachexia via intestinal ROS scavenging.","authors":"Yutaka Ikeda, Yukio Nagasaki","doi":"10.3164/jcbn.25-179","DOIUrl":"10.3164/jcbn.25-179","url":null,"abstract":"Cancer cachexia affects approximately 80% of patients with advanced cancer, leading to anorexia, weight loss, and severe muscle wasting that negatively impacts survival. Despite its clinical significance, no effective therapies have been approved worldwide. Inflammatory cytokines, particularly interleukin-6 (IL-6), are known to play a key role in the pathogenesis of cachexia and represent promising therapeutic targets. In this study, we explored the role of intestinal oxidative stress in regulating systemic inflammation associated with cancer cachexia. We orally administered antioxidant polymer nanoparticles (siSMAPoTN), designed to localize in the intestinal lumen and selectively scavenge reactive oxygen species (ROS), to tumor-bearing cancer cachexia model mice. As a result, siSMAPoTN treatment suppressed plasma IL-6 elevation, mitigated muscle protein degradation signaling, and effectively prevented muscle atrophy. Notably, the intestinally localized action of antioxidant nanoparticles led to systemic therapeutic effects, thereby significantly alleviating cancer cachexia. These findings highlight that increased oxidative stress contributes to the systemic inflammatory cascade of cachexia, and demonstrate the therapeutic potential of intestinally acting antioxidant nanoparticles as a novel non-invasive strategy for cancer cachexia management.","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"78 2","pages":"98-101"},"PeriodicalIF":1.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12989226/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147467952","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}

引用次数: 0

A novel rapid technique for quantifying serum oxidized albumin in a mouse model of chronic kidney disease. 一种新的快速定量慢性肾脏疾病小鼠模型血清氧化白蛋白的技术。

IF 1.9 4区医学

Journal of Clinical Biochemistry and Nutrition Pub Date : 2026-03-01 Epub Date: 2025-12-17 DOI: 10.3164/jcbn.25-154

Beibei Liu, Danyang Tian, Jianlong Dong, Bing-Feng Li

{"title":"A novel rapid technique for quantifying serum oxidized albumin in a mouse model of chronic kidney disease.","authors":"Beibei Liu, Danyang Tian, Jianlong Dong, Bing-Feng Li","doi":"10.3164/jcbn.25-154","DOIUrl":"10.3164/jcbn.25-154","url":null,"abstract":"Oxidative stress serves as both a precursor to and consequence of numerous pathological conditions; however, its assessment remains technically challenging and often imprecise. In the current investigation, we established a rapid high-performance liquid chromatography (HPLC)-based method for quantifying serum oxidized albumin in a murine model of chronic kidney disease (CKD). We optimized the HPLC protocol specifically for measuring oxidized albumin in mice. To validate our methodology, C57BL/6J mice underwent 5/6 nephrectomy (5/6Nx) and were randomly allocated to one of three dietary regimens: standard diet, high-salt diet, or high-salt diet supplemented with Tempol (4-hydroxy-2,2,6,6-tetramethylpiperidine-N-oxyl), a superoxide dismutase mimetic. Following an 8-week intervention period, serum oxidized albumin levels were quantitatively assessed. The key findings were as follows: (i) Our optimized oxidized albumin assay demonstrates excellent intra-day and inter-day reproducibility with a rapid analysis time of 9.5 ‍min; (ii) Oxidized albumin concentrations were significantly increased in high-salt diet-fed animals relative to normal-diet controls, an effect that was attenuated by Tempol administration; (iii) Significant positive correlations were observed between oxidized albumin levels and both urinary protein excretion and 8-isoprostane concentrations. Collectively, we have developed a robust and efficient HPLC-based analytical approach for measuring oxidized albumin in murine serum. This methodology demonstrates both rapid processing capabilities and comparable performance compared to conventional techniques, suggesting substantial utility for investigating oxidative stress in animal models.","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"78 2","pages":"142-149"},"PeriodicalIF":1.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12989225/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147467921","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}

引用次数: 0

Ultrasonic exposure enhances the body's antioxidant capacity. 超声波可以增强人体的抗氧化能力。

IF 1.9 4区医学

Journal of Clinical Biochemistry and Nutrition Pub Date : 2026-03-01 Epub Date: 2026-01-16 DOI: 10.3164/jcbn.25-210

Ryousuke Niwa, Hiroshi Ichikawa, Haruka Shimada, Hiroko P Indo, Yukiko Minamiyama, Hideyuki J Majima, Shigeru Oowada, Iwaki Akiyama

{"title":"Ultrasonic exposure enhances the body's antioxidant capacity.","authors":"Ryousuke Niwa, Hiroshi Ichikawa, Haruka Shimada, Hiroko P Indo, Yukiko Minamiyama, Hideyuki J Majima, Shigeru Oowada, Iwaki Akiyama","doi":"10.3164/jcbn.25-210","DOIUrl":"10.3164/jcbn.25-210","url":null,"abstract":"Reactive oxygen species (ROS) are deeply involved in aging and the onset of various diseases, and enhancing the body's antioxidant capacity is considered effective for prevention. This study investigated the effects of ultrasound (US) exposure as a novel non-invasive intervention on the body's antioxidant capacity. First, a single US exposure to the rat back transiently increased the scavenging activities of multiple radicals, including hydroxyl radical (•OH), superoxide radical (O2 •-), and singlet oxygen (1O2). Next, upon performing cyclic US exposure, the increase in antioxidant capacity persisted for over 24 ‍h, with the most multifaceted and pronounced effects observed at medium intensity (ISPTA = 0.11 ‍W/cm2). Furthermore, long-term exposure for approximately one month revealed that biological antioxidant capacity was maintained at a high level. These results suggest that US exposure induces an oxidative stress response similar to exercise stimulation and may promote long-term adaptations such as antioxidant enzyme expression. This study is the first in the world to demonstrate enhanced antioxidant capacity in vivo through non-invasive intervention using US.","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"78 2","pages":"150-157"},"PeriodicalIF":1.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12989223/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147468165","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}

引用次数: 0

Erratum. 勘误表。

IF 1.7 4区医学

Journal of Clinical Biochemistry and Nutrition Pub Date : 2026-03-01 DOI: 10.3164/jcbn.24-58_Erratum

引用次数: 0