生理学报最新文献

{"title":"[Research progress on the role of the microbiota-gut-liver axis immune pathway in metabolic dysfunction-associated steatotic liver disease].","authors":"Shun-Ling Yuan, Yuan-Qi Huang, Chuang-Tao Li, Di-Qun Xu, Xi Zheng","doi":"10.13294/j.aps.2025.0075","DOIUrl":"10.13294/j.aps.2025.0075","url":null,"abstract":"<p><p>Metabolic dysfunction-associated steatotic liver disease (MASLD) is a widely prevalent chronic liver disease that presents significant challenges to public health and medical care worldwide, yet its underlying mechanisms remain incompletely understood. The gut microbiome plays a crucial role in MASLD. Liver inflammation is a key factor in the onset and progression of this disease, and the gut microbiota significantly influences the liver's immune system and inflammatory responses. This article aims to review how both pro-inflammatory and anti-inflammatory gut microbes regulate liver inflammation by activating liver immunity and enhancing liver immune protection, respectively, through the microbiota-gut-liver axis. This review seeks to provide valuable insights for the improvement and treatment of MASLD.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 3","pages":"579-591"},"PeriodicalIF":0.0,"publicationDate":"2026-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148325348","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}

{"title":"[ERβ-mediated estrogen signaling promotes the alleviation of inflammation and myofiber repair in cardiotoxin-induced acute skeletal myositis in mice].","authors":"Jun-Yi Xie, Qi-Hui Cai, Xiao-Lu Niu, Nan Wang, Xin-Yu Hu, Xiao-Lei Huang, Rui-Xue Wang, Zhe Chen, Zhao-Hong Liao","doi":"10.13294/j.aps.2026.0049","DOIUrl":"10.13294/j.aps.2026.0049","url":null,"abstract":"&lt;p&gt;&lt;p&gt;Traumatic stress often leads to abnormalities in sex hormone levels, among which elevated estrogen levels are associated with improved patient prognosis. However, the mechanism by which estrogen affects the inflammatory response and repair process in acute skeletal myositis remains unclear. This study aimed to investigate the effects of estradiol (E&lt;sub&gt;2&lt;/sub&gt;) signaling on the resolution of acute skeletal myositis and muscle fiber repair in mice induced by cardiotoxin (CTX). An acute skeletal myositis model was established in C57BL/6 mice. Endogenous E&lt;sub&gt;2&lt;/sub&gt; levels were reduced by ovariectomy (OVX) in female mice, and interventions were performed with β-Estradiol or the estrogen receptor β (ERβ)-specific antagonist 4-[2-phenyl-5,7-bis(trifluoromethyl)pyrazolo[1,5-a]pyrimidin-3-yl]phenol (PHTPP). Differentiated C2C12 myotubes were treated with interferon γ (IFN-γ) in combination with β-Estradiol or PHTPP. Serum E&lt;sub&gt;2&lt;/sub&gt; levels were measured by ELISA. Inflammatory cell infiltration in injured muscle was assessed by HE staining. Immunofluorescence staining was used to detect the expression levels of ERβ, embryonic myosin heavy chain (eMHC), CD45, myogenic determining factor (MyoD) and myogenin. Proportion of CD45&lt;sup&gt;+&lt;/sup&gt; inflammatory cells in injured muscle was detected by flow cytometry. Western blot was used to detect protein expression levels of mouse major histocompatibility complex class I molecules (MHC-I) H-2K&lt;sup&gt;b&lt;/sup&gt;, major histocompatibility complex class II molecules (MHC-II) H2-Eα, Toll-like receptor 3 (TLR3), and ERβ in differentiated myotubes. RT-qPCR was used to measure mRNA expression levels of ERα, ERβ, G protein-coupled receptor 30 (GPR30), interleukin-1β (IL-1β), IL-6, IL-10, and monocyte chemoattractant protein-1 (MCP-1) in injured muscle and differentiated myotubes. The results showed that, in acute skeletal myositis, injured muscle of female mice exhibited milder inflammation compared to male mice, and serum E&lt;sub&gt;2&lt;/sub&gt; levels were significantly higher in the female mice. Meanwhile, expression of ERβ was significantly up-regulated in injured muscle and inflammatory myotubes, whereas no significant changes were observed in ERα and GPR30. OVX decreased serum E&lt;sub&gt;2&lt;/sub&gt; level, exacerbated inflammation, and increased infiltration of CD45&lt;sup&gt;+&lt;/sup&gt; inflammatory cells in injured muscle, whereas these effects were reversed by β-Estradiol treatment. The effects of PHTPP were the same as those of OVX, except that it didn't affect serum E&lt;sub&gt;2&lt;/sub&gt; levels. In inflammatory myotubes, β-Estradiol up-regulated the protein expression level of ERβ, down-regulated the expression levels of immune molecules H-2K&lt;sup&gt;b&lt;/sup&gt;, H2-Eα, TLR3, and pro-inflammatory factors IL-1β, IL-6, MCP-1, up-regulated the expression of anti-inflammatory factor IL-10, and up-regulated the expression of MyoD and myogenin. The effects of PHTPP were opposite to those of β-Estradiol. The expression of eMHC in the injured muscle of OVX m","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 3","pages":"631-641"},"PeriodicalIF":0.0,"publicationDate":"2026-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148325071","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}

{"title":"[Ischemic post-conditioning alleviates I/R lung injury by activating PI3K/AKT pathway in rats].","authors":"Wang-Xin Yan, Yuan Cheng, Man Huang, Jun-Peng Xu, Zhen-Zhen Luo, Shu-Yuan Wang, Yong-Yue Dai, Li-Yi You, Wan-Tie Wang","doi":"10.13294/j.aps.2026.0050","DOIUrl":"10.13294/j.aps.2026.0050","url":null,"abstract":"<p><p>The present study aimed to investigate whether ischemic post-conditioning (I-post-C) could reduce lung ischemia/reperfusion injury (LIRI) by activating PI3K/AKT pathway in rats. Male Sprague-Dawley (SD) rats aged 6-8 weeks were randomly divided into four groups: control group, ischemia/reperfusion (I/R) group, I-post-C group, and I-post-C+PI3K inhibitor (I-post-C+LY294002) group. The left pulmonary hilum of rats in the I/R group was clamped for 30 min with a miniature arterial clip and then released, followed by reperfusion for 1 h; the left pulmonary hilum of rats in the I-post-C group was blocked for 30 min, followed by reperfusion for 30 s, and this process was repeated three times before reperfusion for 1 h; rats in the I-post-C+LY294002 group were intraperitoneally injected with LY294002 (10 mg/kg) once a day for 3 d before surgery, and the subsequent treatment was the same as that of the I-post-C group. Lung tissue injury was assessed using HE staining and calculation of total lung water content (TLW), index of quantitative assessment (IQA), and lung wet-to-dry weight ratio (W/D). TUNEL assay was used to detect the level of apoptosis in lung tissue. Western blot was used to detect the activation level of Caspase 3 (cleaved Caspase 3/pro-Caspase 3 ratio) and the phosphorylation levels of phosphatidylinositol 3-kinase (PI3K), protein kinase B (PKB/AKT) and glycogen synthase kinase 3β (GSK-3β) in lung tissue. Mitochondrial membrane potential was measured by JC-1 staining. The results showed that compared with the control group, the I/R group exhibited significant lung tissue damage, a significant decrease in mitochondrial membrane potential, significantly elevated cleaved Caspase 3/pro-Caspase 3 ratio and cell apoptosis level, as well as decreased phosphorylation levels of PI3K/AKT/GSK-3β. I-post-C significantly reversed the aforementioned changes in lung tissue of the I/R group and exerted a protective effect on lung tissue. The PI3K inhibitor LY294002 partially eliminated this lung protective effect of I-post-C. These results suggest that I-post-C activates the PI3K/AKT pathway to inactivate GSK-3β, inhibits mitochondrial membrane potential decline, antagonizes lung tissue cell apoptosis, and thereby alleviates LIRI.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 3","pages":"705-712"},"PeriodicalIF":0.0,"publicationDate":"2026-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148325066","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}

{"title":"[Lactate clearance is positively correlated with peripheral blood monocyte counts after high-intensity exercise].","authors":"Su-Jie Mao, Fan Xia, Jing-Feng Wang, Zhuang-Li Pan","doi":"10.13294/j.aps.2025.0083","DOIUrl":"10.13294/j.aps.2025.0083","url":null,"abstract":"<p><p>This study aimed to explore the relationship between lactate clearance and immune function in elite athletes, providing a theoretical basis for optimizing training loads and immune monitoring. In this cross-sectional observational study, 31 high-level athletes were recruited. Blood lactate concentrations were measured at 3, 5, 7, and 9 min after high-intensity exercise, whereas immune cell counts were assessed at rest (pre-exercise baseline). The results showed that lactate clearance at 3-5 min and 3-7 min was significantly and positively correlated with rest total white blood cell count and monocyte count (<i>P</i> < 0.05). Stepwise regression further identified rest monocyte count as the only significant predictor of lactate clearance at 3-7 and 3-9 min, suggesting that higher monocyte levels are associated with faster lactate removal. These findings suggest that the immune system may play a supportive role in the early phase of lactate clearance following intense exercise. The time-dependent association between monocytes and lactate clearance points to a potential interaction between immune activity and metabolic recovery. This study provides new insights that may help guide the adjustment of training loads and the development of personalized recovery strategies for elite athletes.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 3","pages":"677-692"},"PeriodicalIF":0.0,"publicationDate":"2026-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148325150","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}

{"title":"[Reshaping glycometabolic reprogramming to suppress M1 macrophage polarization for diabetic wound therapy].","authors":"Yue-Yu Xiang, Ai-Tian Zheng, Biao-Liang Wu","doi":"10.13294/j.aps.2026.0047","DOIUrl":"10.13294/j.aps.2026.0047","url":null,"abstract":"<p><p>Diabetic chronic wounds, a severe diabetic complication, are closely linked to macrophage metabolic reprogramming. Under hyperglycemic conditions, macrophage metabolism shifts from oxidative phosphorylation to aerobic glycolysis, triggering increased lactate production, activation of the nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome, and imbalance in macrophage polarization, ultimately leading to difficult wound healing. Metabolic imbalance also results in an altered wound microenvironment characterized by inhibited angiogenesis, aberrant matrix remodeling, and compromised stem cell function. Key metabolites like lactate and pyruvate exacerbate oxidative stress and epigenetic disruption via receptor-mediated signals or chromatin modifications, creating a \"metabolism-inflammation\" vicious cycle. Metabolism-based therapeutic strategies for diabetic wounds include: 1) targeting lactate dehydrogenase A (LDHA) to inhibit lactate production; 2) modulating monocarboxylate transporter (MCT) to maintain intracellular pH homeostasis; 3) stabilizing pyruvate kinase M2 (PKM2) tetramers to restore pyruvate metabolism; 4) applying mitochondria-targeted antioxidants to intervene in oxidative stress; and 5) utilizing specific small molecule inhibitors (including dichloroacetate as a pyruvate dehydrogenase kinase 4 inhibitor, dimethyl malonate as a succinate dehydrogenase inhibitor, and tanshinone IIA). These strategies provide novel approaches for restoring metabolic-immune balance.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 3","pages":"487-500"},"PeriodicalIF":0.0,"publicationDate":"2026-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148325302","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}

{"title":"[Skeletal muscle-specific knockdown of ACSL1 gene ameliorates cisplatin-induced skeletal muscle atrophy].","authors":"Huan Wang, Hao-Zhe Wang, Jiang-Ping Xie, Hao Wang, Wen-Jun Fang, Men-Qian Li, Pei-Shan Chen, Wen-Bi He, Lin Zhu, Xiao-Guang Liu","doi":"10.13294/j.aps.2025.0093","DOIUrl":"10.13294/j.aps.2025.0093","url":null,"abstract":"<p><p>The aim of this study was to explore the role of long-chain acyl-CoA synthetase 1 (ACSL1) in cisplatin-induced skeletal muscle atrophy and the underlying mechanism. Wild-type mice were divided into cisplatin group and control group. The results of fluorescence quantitative PCR and sequencing of reference transcriptome showed that ACSL1 gene was significantly up-regulated in the skeletal muscle of cisplatin group compared with the control group, suggesting that ACSL1 may play a key role in cisplatin-induced skeletal muscle atrophy. To further investigate ACSL1's function and potential mechanism, the present study constructed an adeno-associated virus to achieve muscle-specific ACSL1 knockdown and established a cisplatin-induced skeletal muscle atrophy model. The results of immunofluorescence staining showed that compared with mice only receiving cisplatin intervention, mice receiving ACSL1 gene knockdown and cisplatin intervention had significantly increased muscle fiber cross-sectional area, maximum diameter, minimum diameter, and average diameter in their skeletal muscles. The results of RT-qPCR and immunohistochemical staining showed that knockdown of the ACSL1 gene in skeletal muscle down-regulated the mRNA expression levels of atrophy related gene 1 (Atrogin-1) and autophagy-related factors such as autophagy related protein 16 like protein 1 (Atg16L1), Atg12, and Atg7 in cisplatin-induced skeletal muscle atrophy, up-regulated the protein expression level of myogenin, and down-regulated Toll-like receptor 4 (TLR4) protein expression level, but had no significant effect on the mRNA expression levels of ferroptosis-related factors (except for cyclooxygenase-2) and inflammation-related factors such as stimulator of interferon genes (STING), Toll-like receptor 4 (TLR4) and TLR9 in cisplatin-induced skeletal muscle atrophy. These results suggest that specific knockdown of ACSL1 gene in skeletal muscle may alleviate cisplatin-induced skeletal muscle atrophy by down-regulating the expression of Atrogin-1, TLR4 and autophagy-related factors.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 3","pages":"616-630"},"PeriodicalIF":0.0,"publicationDate":"2026-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148325359","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}

{"title":"[The development trend of microRNA patents from the perspective of the Nobel Prize].","authors":"Qiang-Yu Xiang, Zong-Zhen Wu, Lu Zhang, Huan Liu","doi":"10.13294/j.aps.2026.0056","DOIUrl":"10.13294/j.aps.2026.0056","url":null,"abstract":"<p><p>The 2024 Nobel Prize in Physiology or Medicine has been awarded to Victor Ambros and Gary Ruvkun for their discovery of the central role of microRNA (miRNA) in gene regulation. Based on the Derwent Innovation patent database and combined with the Derwent Data Analyzer tool, this study conducted a multidimensional analysis of 57232 patent entries in the field of miRNA, revealing the global technological innovation pattern and dynamic evolution trend in this field. Analysis shows that miRNA technology has entered a rapid growth stage since 2002, and reached the peak of patent applications in 2022, and its research hotspots are concentrated in the fields of tumor therapy, gene therapy, molecular diagnosis and nucleic acid drug development. In the global patent distribution, China and the United States occupy the dominant position, and universities, scientific research institutions and enterprises constitute the main force of technological innovation. Network analysis of patentees and inventors reveals the importance of collaborative innovation and interdisciplinary collaboration in driving technological development. In addition, the analysis of patent keywords and classification code shows that miRNA technology has significant potential in the research and development of cancer-related biomarkers and the mining of therapeutic targets, while delivery technology and nucleic acid modification have become the key directions to break the technical bottleneck. In the future, miRNA technology will be more widely used in precision medicine, nucleic acid drug delivery and gene therapy. Delivery technologies such as lipid nanoparticles and extracellular vesicles, as well as AI-driven target mining, will significantly accelerate the clinical application of miRNA drugs. From the perspective of patents, this study provides important theoretical basis and data support for basic research and industrial development in the field of miRNA.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 3","pages":"665-676"},"PeriodicalIF":0.0,"publicationDate":"2026-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148325346","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}

{"title":"[Qizhiweitong particles improve the contractile phenotype of gastric smooth muscle cells in the Parkinson's disease rats with gastroparesis].","authors":"Yue Zhang, Xiao-Lin Xiu, Qian-Ying Shen, Zi-Ming Liu, Yu-Li Sun, Xiao-Li Zhang, Jin-Xia Zhu, Li-Fei Zheng","doi":"10.13294/j.aps.2025.0104","DOIUrl":"10.13294/j.aps.2025.0104","url":null,"abstract":"<p><p>Parkinson's disease (PD) is often accompanied by symptoms of gastric dysmotility, such as gastroparesis. Gastroparesis not only seriously affects the life quality of PD patients, but also causes fluctuations in drug absorption rate, exacerbating the motor symptoms of PD. The previous studies of our laboratory have shown that PD model rats also exhibit gastroparesis, with increased pro-inflammatory cytokines in the gastric muscularis. The markers of related neurons were abnormal. Additionally, the contractile protein markers, as well as their transcriptional regulators, were reduced in smooth muscle cells (SMCs). Continuous gastric feeding of Qizhiweitong particles (QZWT) for seven days improved gastric motility in PD rats with gastroparesis by suppressing inflammation. However, whether QZWT can restore neurons in the gastric muscularis and the differentiated phenotype of SMCs remains to be further investigated. In this study, we detected expressions of neuronal markers in the gastric muscularis and contractile markers of SMCs by immunofluorescence staining, Western blotting, and real-time quantitative PCR, and observed the ultrastructure of SMCs by transmission electron microscopy techniques, aiming to explore the potential mechanisms underlying the improvement effect of QZWT on gastric dysmotility in PD rats and provide new ideas for the treatment of PD gastroparesis. Our results showed that after QZWT administration, there was no change in neuronal markers tyrosine hydroxylase, choline acetyltransferase, and neuronal nitric oxide synthase in the muscular layer of gastric corpus of the PD gastroparesis rats. However, compared to the PD rats, the protein and mRNA expression levels of myosin heavy chain 11 and myosin light chain 20 were significantly up-regulated in the smooth muscle layer of gastric corpus of PD rats with QZWT treatment. Furthermore, the protein and mRNA expression levels of serum response factor (SRF), which regulates the transcription of SMC contractile protein genes, as well as the mRNA level of the transcription related cofactor myocardin (MYOCD), were significantly up-regulated. In addition, the ultrastructure feature of gastric corpus showed that the morphology of SMCs in the PD rats with QZWT treatment was improved, displaying clear dense patches and dense bodies. The vacuoles in the SMCs disappeared. These results suggest that QZWT treatment up-regulates the expression of SRF and MYOCD, which may be associated with its effect of inhibiting inflammation, and further increases the expression of contractile proteins and restores the morphology of the SMCs, promoting gastric smooth muscle contractions in PD gastroparesis rats, thereby leading to improved gastric motility.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 3","pages":"605-615"},"PeriodicalIF":0.0,"publicationDate":"2026-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148325353","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}

{"title":"Pathophysiology of cilia in cardiovascular diseases.","authors":"Lin-Sen Wang, Dan Zhou, Xiao Ma, Zhi-Hua Wang","doi":"10.13294/j.aps.2026.0046","DOIUrl":"10.13294/j.aps.2026.0046","url":null,"abstract":"<p><p>Cilia are organelles on the surface of eukaryotic cells, characterized by complex microtubule structures and diverse physiological functions. By sensing external environmental changes, cilia play critical roles in cell movement, signal transduction, and molecule transport. Ciliary dysfunction has been associated with pathogenesis of human diseases. Primary cilia in the cardiovascular system sense blood flow shear stress, fluid dynamics, and external signals, and regulate cellular processes such as proliferation, differentiation and movement. Dysfunction of cilia has been closely linked to the onset of cardiovascular diseases, including hypertension, myocardial fibrosis, atherosclerosis and congenital heart disease. This relationship emphasizes the role of cilia in maintaining cardiovascular health and their potential in both prevention and therapeutic strategies. By exploring the regulatory mechanisms of cilia in the cardiovascular system and their involvement in disease pathogenesis, this review aims to provide a theoretical basis for cilia-related research and highlight their potential in early diagnosis and treatment.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 3","pages":"463-475"},"PeriodicalIF":0.0,"publicationDate":"2026-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148325324","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}

{"title":"[Spermine induces ferroptosis-related phenotype in acute myeloid leukemia cells through reactive oxygen species].","authors":"Lu Wang, Dong-Wei Guan, Yao-Ying Long, Xiao-Wei Ning, Yong-Long Yu, Shi-Jie Yang, Xi Zhang","doi":"10.13294/j.aps.2026.0053","DOIUrl":"10.13294/j.aps.2026.0053","url":null,"abstract":"<p><p>Polyamines, including putrescine, spermidine, and spermine, are widely involved in various physiological processes <i>in vivo</i>. Their metabolic alterations are closely associated with tumor development, and interfering with polyamine metabolism has become a therapeutic strategy under investigation for cancer. However, studies have also demonstrated that spermine can inhibit the growth of castration-resistant prostate cancer, indicating its antitumor effects. This study aimed to investigate the effects of spermine on acute myeloid leukemia (AML) cells. CCK8 assay, cell counting, and lactate dehydrogenase release assay demonstrated that spermine reduced the viability of MOLM-13 and HL-60 cells, inhibited their proliferation, and induced cytotoxicity. Flow cytometry analysis of Annexin V and 7-AAD binding in MOLM-13 cells revealed an increase in the proportion of Annexin V⁺ cells and Annexin V⁺7-AAD⁺ late apoptotic cells as spermine concentration increased. Proteomic and transcriptomic analyses revealed altered expression of ferroptosis pathway-related proteins and genes in MOLM-13 cells following spermine treatment. Using Liperfluo, BDP 581/591 C11, and FerroOrange probes to detect cellular lipid peroxidation and intracellular free Fe²⁺ levels, combined with transmission electron microscopy to observe cell ultrastructure, it was confirmed that spermine induced ferroptosis-related phenotype in MOLM-13 cells; CM-H₂DCFDA and MitoSO^TM Red probes further detected elevated levels of intracellular and mitochondrial reactive oxygen species (ROS), and Western blot showed that spermine caused changes in the expression of ferroptosis-related proteins. Ferroptosis inhibitor liproxstatin-1 partially reversed the spermine-induced ferroptosis-related phenotype in MOLM-13 cells, but did not reverse the decline in cell viability. In contrast, the ROS scavenger N-acetylcysteine completely reversed both the ferroptosis-related phenotype and the reduction in cell viability. These results suggest that spermine induces ferroptosis-related phenotype in AML cells, and its mechanism is associated with ROS generation.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 3","pages":"693-704"},"PeriodicalIF":0.0,"publicationDate":"2026-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148325333","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}