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The protective effects and mechanism of myricetin in liver diseases (Review).
IF 3.4 3区 医学 Q2 MEDICINE, RESEARCH & EXPERIMENTAL Pub Date : 2025-04-01 Epub Date: 2025-02-07 DOI: 10.3892/mmr.2025.13452
Mi Chen, Shengnan Zhang, Xingqiong Huang, Dandan Zhang, Dan Zhu, Changhan Ouyang, Yankun Li

Liver diseases have become one of the significant threats to global health. However, there is a lack of effective targeted therapeutic drugs in this field and the existing drugs used for liver disease treatment usually have side‑effects. Traditional Chinese medicine (TCM) has the distinctive advantages of multi‑target and low side‑effects. As a flavonoid with various pharmacological activities such as anti‑tumour, anti‑oxidant, anti‑inflammatory and anti‑bacterial, the TCM myricetin has been widely used in liver disease research. The present work focuses on the role and molecular mechanism of myricetin in liver diseases such as acute liver injury, fatty liver, liver fibrosis and hepatocellular carcinoma. It is a promising reference for further research and application of myricetin in the treatment of liver diseases.

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引用次数: 0
Identification and validation of biomarkers related to mitophagy in chronic obstructive pulmonary disease.
IF 3.4 3区 医学 Q2 MEDICINE, RESEARCH & EXPERIMENTAL Pub Date : 2025-04-01 Epub Date: 2025-02-14 DOI: 10.3892/mmr.2025.13458
Jie Chen, Xiaofeng Zhang, Gengyun Sun

Mitophagy plays significant roles in chronic obstructive pulmonary disease (COPD). The present study aimed to screen and validate mitophagy‑related genes in COPD by using bioinformatic analysis and experimental validation. The original data were downloaded from Gene Expression Omnibus datasets and 29 mitophagy‑related genes sets were acquired from the Molecular Signatures Database. The differentially expressed mitophagy‑related genes (DEMRGs) were screened using the Wilcoxon test. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analysis were conducted for the identification of DEMRGs. In addition, clustering analysis was used to assess the differential expression characteristics of DEMRGs in patients with COPD. Least absolute shrinkage and selection operator (LASSO) regression analysis was performed to identify signature genes with COPD diagnostic significance; these genes were validated using the test dataset. In addition, the degree of infiltration of 28 immune cells in COPD and control samples was assessed. Finally, cigarette smoke extract (CSE)‑treated bronchial epithelial cells were employed to verify the role of signature genes in regulating mitophagy in vitro using molecular biology approaches. A total of 14 DEMRGs were identified, which were mainly involved in mitophagy‑related processes and pathways. Clustering analysis indicated the expression levels of 14 DEMRGs except for microtubule‑associated protein 1 light chain‑3β, which was significantly different. Moreover, combination with LASSO, receiver operating characteristic curve and the validation dataset resulted in the identification of the mitochondrial transcription termination factor 3 (MTERF3). The infiltrating abundance of the majority of the immune cells was higher in COPD samples than that noted in the control samples; MTERF3 demonstrated the optimal correlation with macrophages, myeloid‑derived suppressor cells, regulatory T cells and activated cluster of differentiation 8 T cells. Further analysis revealed that MTERF3 expression was increased in CSE‑treated 16HBE cells and knockdown of MTERF3 expression promoted mitophagy. These findings provide novel insights into the role of mitophagy in COPD and identify novel targets for COPD diagnosis and treatment.

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引用次数: 0
[Retracted] lncRNA FGD5‑AS1 promotes breast cancer progression by regulating the hsa‑miR‑195‑5p/NUAK2 axis.
IF 3.4 3区 医学 Q2 MEDICINE, RESEARCH & EXPERIMENTAL Pub Date : 2025-04-01 Epub Date: 2025-02-14 DOI: 10.3892/mmr.2025.13457
Kun Fang, Zheng-Jie Xu, Su-Xiao Jiang, De-Sheng Tang, Chang-Sheng Yan, You-Yuan Deng, Fu-Ying Zhao

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the cell migration and invasion assay data shown in Fig. 2C and D on p. 4 were strikingly similar to data that had already been published in different form in other articles written by different authors from different research institutes, some of which have now been retracted. Owing to the fact that the contentious data in the above article had already been published prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a satisfactory reply.  The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 23: 460, 2021; DOI: 10.3892/mmr.2021.12099].

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引用次数: 0
CIP2A promotes bronchiolitis obliterans by activating the NF‑κB pathway.
IF 3.4 3区 医学 Q2 MEDICINE, RESEARCH & EXPERIMENTAL Pub Date : 2025-04-01 Epub Date: 2025-02-28 DOI: 10.3892/mmr.2025.13473
Xu Zhou, Xingyou Zhao, Yanning Li, Baoqing Zhang

Bronchiolitis obliterans (BO) is a destructive fibrotic lung disease, which can be partly induced by 2,3‑butanedione [also known as diacetyl (DA)]; however, the mechanism underlying the effects of DA on BO is not clear. In the present study, a bioinformatics analysis was performed using DA‑treated or untreated lung tissues of rats, and it was observed that cell proliferation regulating inhibitor of protein phosphatase 2A (CIP2A) was significantly increased in samples from the DA group. CIP2A is associated with inflammation and epithelial‑mesenchymal transition (EMT), and facilitates lung injury; however, its effect on DA‑induced BO and the underlying mechanism remain unknown. To solve these issues, DA‑treated models of BO were established in rats and cells, and ethoxysanguinarine (a CIP2A inhibitor) was administered to induce a decrease in CIP2A. The pathological changes were detected by hematoxylin and eosin, Masson and Giemsa staining. Reverse transcription‑quantitative PCR, western blotting, immunohistochemistry, immunofluorescence and enzyme‑linked immunosorbent assay were used to measure CIP2A expression and levels of pathology‑related markers. Notably, inhibition of CIP2A ameliorated the pathological features of BO, including reduced intraluminal occlusion, inflammatory infiltration and fibrosis. The expression of inflammation, fibrosis and EMT markers was also decreased in samples with CIP2A inhibition. Furthermore, CIP2A inhibition was revealed to work through the nuclear factor‑κB (NF‑κB) pathway; phosphorylation of NF‑κB inhibitor α and nuclear translocation of p65 were reduced. In summary, these results demonstrated that CIP2A may promote BO development by increasing inflammation, fibrosis and EMT through activating the NF‑κB signaling pathway. Therefore, inhibition of CIP2A may be considered a potential strategy for BO treatment.

闭塞性支气管炎(Bronchiolitis obliterans,BO)是一种破坏性肺纤维化疾病,2,3-丁二酮(又称双乙酰(DA))可诱发部分BO;然而,DA对BO的影响机制尚不清楚。本研究利用经 DA 处理或未经 DA 处理的大鼠肺组织进行了生物信息学分析,结果发现 DA 组样本中细胞增殖调节蛋白磷酸酶 2A 抑制剂(CIP2A)显著增加。CIP2A与炎症和上皮-间质转化(EMT)有关,并促进肺损伤;然而,它对DA诱导的BO的影响及其潜在机制仍不清楚。为了解决这些问题,我们在大鼠和细胞中建立了DA处理的BO模型,并施用乙氧胰鸟苷(一种CIP2A抑制剂)来诱导CIP2A的减少。病理变化通过苏木精、伊红、Masson 和 Giemsa 染色法检测。逆转录-定量 PCR、Western 印迹、免疫组织化学、免疫荧光和酶联免疫吸附试验被用来检测 CIP2A 的表达和病理相关标记物的水平。值得注意的是,抑制 CIP2A 能改善 BO 的病理特征,包括减少管腔内闭塞、炎症浸润和纤维化。在抑制了CIP2A的样本中,炎症、纤维化和EMT标记物的表达也有所下降。此外,研究还发现 CIP2A 抑制剂是通过核因子-κB(NF-κB)途径发挥作用的;NF-κB 抑制剂 α 的磷酸化和 p65 的核转位均有所减少。总之,这些结果表明,CIP2A 可通过激活 NF-κB 信号通路,增加炎症、纤维化和 EMT,从而促进 BO 的发展。因此,抑制 CIP2A 可被视为治疗 BO 的一种潜在策略。
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引用次数: 0
Hydroxychloroquine: A double‑edged sword (Review).
IF 3.4 3区 医学 Q2 MEDICINE, RESEARCH & EXPERIMENTAL Pub Date : 2025-04-01 Epub Date: 2025-02-21 DOI: 10.3892/mmr.2025.13467
Rongxiu Huo, Chengcheng Wei, Yanting Yang, Jinying Lin, Xinxiang Huang

Hydroxychloroquine (HCQ) is an antimalarial drug that has historically been used to treat and prevent malaria. However, its mechanism of action has not yet been fully elucidated. HCQ affects various cellular and molecular pathways through different mechanisms. HCQ has also been shown to be a disease‑improving agent for the treatment of rheumatic diseases, including systemic lupus erythematosus, antiphospholipid syndrome, rheumatoid arthritis and primary Sjögren's syndrome. Although generally considered safe, adverse reactions have been reported with the use of HCQ and clinicians should carefully monitor patients with rheumatism when prescribing these drugs. The purpose of the present review is to strengthen the clinical use of HCQ for autoimmune diseases while highlighting the adverse effects that may occur during treatment.

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引用次数: 0
[Retracted] Tan IIA inhibits H1299 cell viability through the MDM4‑IAP3 signaling pathway. 【撤回】Tan IIA通过MDM4‑IAP3信号通路抑制H1299细胞活力。
IF 3.4 3区 医学 Q2 MEDICINE, RESEARCH & EXPERIMENTAL Pub Date : 2025-03-01 Epub Date: 2025-01-17 DOI: 10.3892/mmr.2025.13435
Yukun Zu, Jianning Wang, Wei Ping, Wei Sun

Following the publication of the above paper, it was drawn to the Editors' attention by a concerned reader that certain of the western blotting data shown in Fig. 1C and D on p. 2386 were strikingly similar to data appearing in different form in a pair of other articles written by different authors at a different research institute that had already been published elsewhere prior to the submission of this paper to Molecular Medicine Reports. Moreover, some of the data featured in Fig. 6A and C were strikingly similar, also suggesting that the data in this figure had been misassembled. In view of the fact that the abovementioned data had already apparently been published previously, the Editor of Molecular Medicine Reports has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 17: 2384‑2392, 2018; DOI: 10.3892/mmr.2017.8152].

在上述论文发表后,一位关心的读者提请编辑注意,2386页图1C和D中所示的某些western blotting数据与另一家研究机构的不同作者所写的其他两篇文章中以不同形式出现的数据惊人地相似,这些文章在提交给《分子医学报告》之前已经在其他地方发表过。此外,图6A和图C中的一些数据惊人地相似,也表明该图中的数据是错误组装的。鉴于上述数据显然已经在之前发表过,《分子医学报告》编辑决定从期刊上撤回这篇论文。作者被要求对这些担忧作出解释,但编辑部没有收到答复。对于由此给读者带来的不便,本刊编辑深表歉意。[分子医学报告]17:2384‑2392,2018;DOI: 10.3892 / mmr.2017.8152]。
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引用次数: 0
Preconditioning with acteoside ameliorates myocardial ischemia‑reperfusion injury by targeting HSP90AA1 and the PI3K/Akt signaling pathway.
IF 3.4 3区 医学 Q2 MEDICINE, RESEARCH & EXPERIMENTAL Pub Date : 2025-03-01 Epub Date: 2025-01-31 DOI: 10.3892/mmr.2025.13442
Jing Li, Yuxin Guo, Yang Yang, Qing Xue, Hong Cao, Guangyuan Yang, Linlin Jia, Haibo Yu

The present study aimed to investigate the cardioprotective effects of acteoside (AC) on myocardial ischemia‑reperfusion injury (MIRI). To meet this aim, a network pharmacological analysis was conducted to search for key genes and signaling pathways associated with AC and MIRI. The infarct size of the rat heart was evaluated using 2,3,5‑triphenyltetrazolium chloride staining, and the serum levels of creatine kinase MB isoenzyme, cardiac troponin I, malondialdehyde and superoxide dismutase were subsequently detected in an in vivo experiment. The inhibitory effect of AC on oxidative stress was further confirmed by assessing the intracellular accumulation of reactive oxygen species (ROS). Hematoxylin and eosin staining was subsequently carried out to observe cardiac histopathological damage. The anti‑apoptotic effects of AC were determined using terminal deoxynucleotidyl‑transferase‑mediated dUTP nick end labeling assay and Hoechst 33342 staining, and the expression levels of apoptosis‑associated proteins in the myocardial tissue were assessed using immunohistochemical analysis. In addition, cell viability was determined using a Cell Counting Kit‑8 assay, and the expression levels of key target proteins associated with AC and MIRI were detected by western blot analysis. The results suggested that pretreatment with AC could mitigate MIRI‑induced myocardial damage, oxidative stress and apoptosis. The anti‑apoptotic effects of AC were associated with elevated Bcl‑2 levels, and reduced caspase‑3 and Bax expression levels in myocardial tissue. In vitro, AC pretreatment both led to an increased rate of cell survival and alleviated oxidative stress, as demonstrated by a decreased level of intracellular ROS accumulation. Moreover, guided by the network pharmacological analysis, heat‑shock protein 90AA1 (HSP90AA1) and the phosphoinositide 3‑kinase (PI3K)/serine‑threonine protein kinase (Akt) signaling pathway emerged as key targets for the action of AC against MIRI. Furthermore, the western blot analysis results showed that pretreatment with AC led to a significant increase in the activity of the PI3K/Akt signaling pathway, in addition to increased expression levels of glycogen synthase kinase‑3β and HSP90AA1. Taken together, the findings of the present study revealed that AC may exert cardioprotective effects on MIRI through suppressing apoptosis and oxidative stress by regulating the expression and activity of key proteins.

{"title":"Preconditioning with acteoside ameliorates myocardial ischemia‑reperfusion injury by targeting HSP90AA1 and the PI3K/Akt signaling pathway.","authors":"Jing Li, Yuxin Guo, Yang Yang, Qing Xue, Hong Cao, Guangyuan Yang, Linlin Jia, Haibo Yu","doi":"10.3892/mmr.2025.13442","DOIUrl":"10.3892/mmr.2025.13442","url":null,"abstract":"<p><p>The present study aimed to investigate the cardioprotective effects of acteoside (AC) on myocardial ischemia‑reperfusion injury (MIRI). To meet this aim, a network pharmacological analysis was conducted to search for key genes and signaling pathways associated with AC and MIRI. The infarct size of the rat heart was evaluated using 2,3,5‑triphenyltetrazolium chloride staining, and the serum levels of creatine kinase MB isoenzyme, cardiac troponin I, malondialdehyde and superoxide dismutase were subsequently detected in an <i>in vivo</i> experiment. The inhibitory effect of AC on oxidative stress was further confirmed by assessing the intracellular accumulation of reactive oxygen species (ROS). Hematoxylin and eosin staining was subsequently carried out to observe cardiac histopathological damage. The anti‑apoptotic effects of AC were determined using terminal deoxynucleotidyl‑transferase‑mediated dUTP nick end labeling assay and Hoechst 33342 staining, and the expression levels of apoptosis‑associated proteins in the myocardial tissue were assessed using immunohistochemical analysis. In addition, cell viability was determined using a Cell Counting Kit‑8 assay, and the expression levels of key target proteins associated with AC and MIRI were detected by western blot analysis. The results suggested that pretreatment with AC could mitigate MIRI‑induced myocardial damage, oxidative stress and apoptosis. The anti‑apoptotic effects of AC were associated with elevated Bcl‑2 levels, and reduced caspase‑3 and Bax expression levels in myocardial tissue. <i>In vitro</i>, AC pretreatment both led to an increased rate of cell survival and alleviated oxidative stress, as demonstrated by a decreased level of intracellular ROS accumulation. Moreover, guided by the network pharmacological analysis, heat‑shock protein 90AA1 (HSP90AA1) and the phosphoinositide 3‑kinase (PI3K)/serine‑threonine protein kinase (Akt) signaling pathway emerged as key targets for the action of AC against MIRI. Furthermore, the western blot analysis results showed that pretreatment with AC led to a significant increase in the activity of the PI3K/Akt signaling pathway, in addition to increased expression levels of glycogen synthase kinase‑3β and HSP90AA1. Taken together, the findings of the present study revealed that AC may exert cardioprotective effects on MIRI through suppressing apoptosis and oxidative stress by regulating the expression and activity of key proteins.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 3","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11795246/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143066698","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Prospects for potential therapy targeting immune‑associated factors in endometriosis (Review). 针对子宫内膜异位症免疫相关因子的潜在治疗前景(综述)。
IF 3.4 3区 医学 Q2 MEDICINE, RESEARCH & EXPERIMENTAL Pub Date : 2025-03-01 Epub Date: 2024-12-24 DOI: 10.3892/mmr.2024.13422
Wenwen Zhang, Kang Li, Aiwen Jian, Guanran Zhang, Xiaoli Zhang

Endometriosis (EM) is a chronic inflammatory disease that is one of the most common causes of gynecological systemic lesions in women before menopause. The most representative histological feature of EM is that the endometrium appears outside of the uterine cavity, often in the ovary. Although it is generally accepted that the epithelial and stromal cells of the ectopic endometrium are not malignant, they still have numerous similarities to malignant tumors, including considerable changes to the immune microenvironment (immune monitoring disorder), the creation of a specific hormone environment, high levels of oxidative stress, chronic inflammation and abnormal immune cell regulation. The pathogenesis of EM is not fully understood, which makes it difficult to identify specific biomarkers and potential therapeutic targets for early disease diagnosis and effective treatment. However, considerable progress has been made in this field over the past few decades. The purpose of the present review is to summarize the confirmed and potential biomarkers for EM, and to identify potential therapeutic targets based on changes in immunological factors (including natural killer cells, macrophages, the complement system, miRNA and P‑selectin) in the ectopic endometrial tissue. It is hoped that this work can be used as the basis for identifying accurate diagnostic markers for EM and developing personalized immune‑targeted therapy.

子宫内膜异位症(EM)是一种慢性炎症性疾病,是绝经前妇女妇科系统病变最常见的原因之一。EM最具代表性的组织学特征是子宫内膜出现在子宫腔外,常在卵巢内。虽然人们普遍认为异位子宫内膜的上皮细胞和基质细胞不是恶性的,但它们与恶性肿瘤仍有许多相似之处,包括免疫微环境的显著改变(免疫监测障碍)、特定激素环境的产生、高水平的氧化应激、慢性炎症和免疫细胞调节异常。EM的发病机制尚不完全清楚,这使得难以确定特异性的生物标志物和潜在的治疗靶点,从而进行疾病的早期诊断和有效治疗。然而,在过去的几十年里,这一领域取得了相当大的进展。本综述的目的是总结EM的确认和潜在的生物标志物,并根据异位子宫内膜组织中免疫因子(包括自然杀伤细胞、巨噬细胞、补体系统、miRNA和P -选择素)的变化确定潜在的治疗靶点。希望这项工作可以作为确定EM准确诊断标记物和开发个性化免疫靶向治疗的基础。
{"title":"Prospects for potential therapy targeting immune‑associated factors in endometriosis (Review).","authors":"Wenwen Zhang, Kang Li, Aiwen Jian, Guanran Zhang, Xiaoli Zhang","doi":"10.3892/mmr.2024.13422","DOIUrl":"10.3892/mmr.2024.13422","url":null,"abstract":"<p><p>Endometriosis (EM) is a chronic inflammatory disease that is one of the most common causes of gynecological systemic lesions in women before menopause. The most representative histological feature of EM is that the endometrium appears outside of the uterine cavity, often in the ovary. Although it is generally accepted that the epithelial and stromal cells of the ectopic endometrium are not malignant, they still have numerous similarities to malignant tumors, including considerable changes to the immune microenvironment (immune monitoring disorder), the creation of a specific hormone environment, high levels of oxidative stress, chronic inflammation and abnormal immune cell regulation. The pathogenesis of EM is not fully understood, which makes it difficult to identify specific biomarkers and potential therapeutic targets for early disease diagnosis and effective treatment. However, considerable progress has been made in this field over the past few decades. The purpose of the present review is to summarize the confirmed and potential biomarkers for EM, and to identify potential therapeutic targets based on changes in immunological factors (including natural killer cells, macrophages, the complement system, miRNA and P‑selectin) in the ectopic endometrial tissue. It is hoped that this work can be used as the basis for identifying accurate diagnostic markers for EM and developing personalized immune‑targeted therapy.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 3","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11715623/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142882564","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Quercetin attenuates the symptoms of osteoarthritis in vitro and in vivo by suppressing ferroptosis via activation of AMPK/Nrf2/Gpx4 signaling. 槲皮素通过激活AMPK/Nrf2/Gpx4信号抑制铁下垂,在体外和体内减轻骨关节炎的症状。
IF 3.4 3区 医学 Q2 MEDICINE, RESEARCH & EXPERIMENTAL Pub Date : 2025-03-01 Epub Date: 2024-12-24 DOI: 10.3892/mmr.2024.13425
Shiyu Dong, Xiaoliang Li, Genrong Xu, Liming Chen, Jiyang Zhao

Osteoarthritis (OA) is a common joint disorder involving the cartilage and other joint tissues. Quercetin (QCT) serves a protective role in the development of OA. However, to the best of our knowledge, the regulatory mechanisms of QCT in the progression of OA have not yet been fully elucidated. In order to mimic a model of OA in vitro, IL‑1β was used to stimulate chondrocytes. Furthermore, an in vivo animal model of OA was induced by anterior cruciate ligament transection (ACLT). 5‑Ethynyl‑2'‑deoxyuridine assays, TUNEL assays, ELISAs, western blotting and immunohistochemical assays were conducted to assess the chondroprotective properties of QCT in the development of OA. The results revealed that 100 µM QCT significantly promoted the proliferation, reduced the apoptosis and inflammation, and inhibited the extracellular matrix (ECM) degradation in IL‑1β‑stimulated chondrocytes. Additionally, QCT attenuated the IL‑1β‑induced ferroptosis of chondrocytes, as demonstrated by the reduced lipid reactive oxygen species and Fe2+ levels. Conversely, the inhibitory effects of QCT on the apoptosis and inflammatory responses were reversed by the activation of ferroptosis by erastin in IL‑1β‑stimulated chondrocytes. Furthermore, QCT significantly elevated the level of phosphorylated (p‑)5' AMP‑activated protein kinase (AMPK) and the levels of two negative regulators of ferroptosis [nuclear factor erythroid 2‑related factor 2 (Nrf2) and glutathione peroxidase 4 (Gpx4)] in IL‑1β‑stimulated chondrocytes. The AMPK inhibitor compound C notably reversed the promoting effects of QCT on phosphorylated‑AMPK, Nrf2 and Gpx4 expression in IL‑1β‑stimulated chondrocytes. Additionally, QCT markedly ameliorated the destruction and degradation of articular cartilage, and elevated the p‑AMPK, Nrf2 and Gpx4 levels in the mouse model of ACLT‑induced OA. Overall, the present study demonstrated that QCT inhibited the development of OA by suppressing ferroptosis via the activation of the AMPK/Nrf2/Gpx4 signaling pathway. These findings provide novel insights into the regulatory mechanisms of QCT for the treatment of patients with OA.

骨关节炎(OA)是一种常见的关节疾病,涉及软骨和其他关节组织。槲皮素(QCT)在OA的发生发展中起保护作用。然而,据我们所知,QCT在OA进展中的调控机制尚未完全阐明。为了在体外模拟OA模型,使用IL - 1β刺激软骨细胞。采用前交叉韧带横断法(ACLT)建立骨关节炎动物模型。采用5‑乙炔‑2‑脱氧尿苷法、TUNEL法、elisa法、western blotting法和免疫组化法评估QCT在骨性关节炎发展中的软骨保护作用。结果显示,100µM QCT能显著促进IL - 1β刺激的软骨细胞增殖,减少细胞凋亡和炎症,抑制细胞外基质(ECM)降解。此外,通过降低脂质活性氧和Fe2+水平,QCT可以减弱IL - 1β诱导的软骨细胞铁下垂。相反,QCT对凋亡和炎症反应的抑制作用被IL - 1β刺激的软骨细胞中erastin激活的铁凋亡逆转。此外,QCT显著提高了IL - 1β刺激的软骨细胞中磷酸化(p -)5' AMP激活的蛋白激酶(AMPK)水平和两种铁凋亡负调节因子[核因子-红细胞2相关因子2 (Nrf2)和谷胱甘肽过氧化物酶4 (Gpx4)]的水平。AMPK抑制剂化合物C显著逆转了QCT对IL - 1β刺激的软骨细胞中磷酸化AMPK、Nrf2和Gpx4表达的促进作用。此外,在ACLT诱导的OA小鼠模型中,QCT显著改善了关节软骨的破坏和退化,并提高了p - AMPK、Nrf2和Gpx4的水平。总体而言,本研究表明,QCT通过激活AMPK/Nrf2/Gpx4信号通路抑制铁下垂,从而抑制OA的发展。这些发现为QCT治疗OA患者的调控机制提供了新的见解。
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引用次数: 0
Adiponectin targets the AMPK/mTOR signaling pathway to alleviate cognitive impairment in epilepsy. 脂联素靶向AMPK/mTOR信号通路减轻癫痫患者的认知障碍。
IF 3.4 3区 医学 Q2 MEDICINE, RESEARCH & EXPERIMENTAL Pub Date : 2025-03-01 Epub Date: 2025-01-03 DOI: 10.3892/mmr.2025.13429
Yaoyuan Zhang, Zhenzhen Qu, Zhuofeng Mao, Hu Liu, Weiping Wang, Lijing Jia

Among patients with chronic epilepsy, 70‑80% have cognitive impairment. To investigate the relationship between adiponectin (ADPN) and the cognitive level in epilepsy and its mechanism, 20 epileptic patients and 20 healthy controls were included for the assessment of the cognitive level. An ELISA was used to evaluate the serum ADPN level. An epileptic rat model was established and treated with AdipoRon, an ADPN receptor (AdipoR) agonist, which binds to AdipoR1 and AdipoR2. The Morris water maze test was used to assess the cognitive function of rats, and the expression levels of the synapsis‑associated proteins postsynaptic density protein 95 (PSD95), synaptosomal associated protein 25 (SNAP25) and synaptophysin (SYP), as well as AMP‑activated protein kinase (AMPK), mTOR, phosphorylated (p‑)AMPK and p‑mTOR were determined by immunoblotting. Serum ADPN levels were positively correlated with the Montreal cognitive assessment score. AdipoRon improved the cognitive function of epileptic rats, maintained the structural integrity of hippocampal neurons and reduced neuronal damage. It also promoted the mRNA expression of AdipoR1 and AdipoR2 in the hippocampus. Furthermore, AdipoRon increased the expression of the synapsis‑associated proteins PSD95, SNAP25 and SYP by activating the AMPK/mTOR signaling pathway. ADPN improved cognitive impairment in epilepsy by targeting the AMPK/mTOR signaling pathway, providing novel insights for the treatment of epilepsy.

在慢性癫痫患者中,70 - 80%存在认知障碍。为探讨脂联素(ADPN)与癫痫患者认知水平的关系及其机制,选取20例癫痫患者和20例健康对照进行认知水平评估。ELISA法检测血清ADPN水平。建立癫痫大鼠模型,并用ADPN受体(AdipoR)激动剂AdipoRon治疗,AdipoRon与AdipoR1和AdipoR2结合。采用Morris水迷宫法评估大鼠认知功能,免疫印迹法检测突触相关蛋白突触后密度蛋白95 (PSD95)、突触体相关蛋白25 (SNAP25)、突触素(SYP)以及AMP活化蛋白激酶(AMPK)、mTOR、磷酸化(p -)AMPK和p - mTOR的表达水平。血清ADPN水平与蒙特利尔认知评估评分呈正相关。AdipoRon改善癫痫大鼠认知功能,保持海马神经元结构完整性,减轻神经元损伤。促进海马组织中AdipoR1和AdipoR2 mRNA的表达。此外,AdipoRon通过激活AMPK/mTOR信号通路增加突触相关蛋白PSD95、SNAP25和SYP的表达。ADPN通过靶向AMPK/mTOR信号通路改善癫痫患者的认知障碍,为癫痫治疗提供了新的见解。
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