International Journal of Ophthalmology
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2026
·Vol. 19
·期 9
·1657
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IF 2
Wen-Xue Guan,Yue Guo,Si-Tong Chen,Zhi-Ming Liu,Yao-Yao Sun,Ming-Wei Zhao
AIM To investigate whether excessive glucocorticoid (GC) exposure disrupts retinal pigment epithelial (RPE) homeostasis through glucocorticoid receptor (GR)-dependent autophagy hyperactivation. METHODS Human retinal pigment epithelial cell line (ARPE-19 cells) were exposed to GC (0–100 µmol/L, 48h). GR subcellular localization was analyzed via mitochondrial fractionation and immunofluorescence. Functional assessments included barrier integrity [zonula occludens-1 (ZO-1) immunostaining], phagocytic capacity (FluoSpheres™-labeled photoreceptor outer segment uptake), and ultrastructural analysis (transmission electron microscopy, TEM). Autophagic flux was quantified using mCherry-green fluorescent protein-microtubule-associated protein 1A/1B-light chain 3 (LC3) B reporters. Molecular mechanisms were probed through AMP-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) pathway activity and autophagic flux assessed by LC3-II levels. GR dependency was confirmed using the antagonist RU486, and cell-type specificity was assessed using mouse photoreceptor (661W) cells. RESULTS GC induced GR upregulation and mitochondrial translocation in a dose- and time-dependent manner, correlating with pathological autophagy activation. Key findings included: 1) tight junction disruption, evidenced by ZO-1 fragmentation, 2) reduction in phagocytic uptake efficiency, 3) mitochondrial shrinkage and autolysosome accumulation (TEM), 4) altered AMPK/mTOR signaling (p-AMPK up, p-mTOR down) associated with autophagosome formation, 5) elevated LC3-II levels confirming excessive autophagic flux. Critically, all GC-induced effects, including GR upregulation, signaling changes, and increased autophagy, were abolished by GR antagonism with RU486. CONCLUSION This study shows that GR-dependent GC exposure induces autophagic flux with ultrastructural evidence suggestive of mitochondria-targeted autophagy and alters AMPK/mTOR signaling, correlating with RPE barrier collapse and phagocytic failure, a possible link to steroid-associated central serous chorioretinopathy (CSC).
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PHYTOTHERAPY RESEARCH
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2025
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IF 6.3
Bingqing Liang,Fengxian Shi,Can Jin,Min Chen,Yuxiao Niu,Anhong Li,Weihua Xu,Zhongping Ning,Fengfeng Xue,Xinming Li,Yuzhong Yan
Curcumin, a highly hydrophobic phenolic compound, has demonstrated potent anticancer activity. However, poor water solubility and a short biological half-life hinder its clinical application. We developed Curcumin-loaded Pluronic F-127 nanoparticles to enhance the bioavailability of Curcumin. It has been reported that excessive autophagy is considered to be the main mechanism of death of various cancer cells. The aim of this study is to investigate whether the Curcumin-loaded Pluronic F-127 nanoparticles exert anti-colon cancer effects by modulating autophagy and explore the specific regulatory mechanism. The proliferative, migratory and apoptotic activity of CT26 cells was assessed by CCK-8 assay, wound healing assay and flow cytometry, respectively. In addition, levels of reactive oxygen species (ROS) were examined by DCFH-DA assay in vitro. ATP levels were detected by the ELISA. The expression levels of autophagy-related proteins and apoptosis-related proteins were visualized by western blotting. Curcumin-loaded Pluronic F-127 nanoparticle inhibited the proliferation of CT26 cells and the growth of colon tumours by promoting cellular autophagy. In addition, Curcumin-loaded Pluronic F-127 nanoparticle reduced mitochondrial membrane potential and impaired mitochondrial function by increasing ROS levels, disrupting ATP biosynthesis. Then the decreased ATP/AMP ratio activated the AMPK/mTOR/ULK1 autophagy signalling pathway and induced autophagy-dependent apoptosis in CT26 cells. Intriguingly, the apoptosis and excessive autophagy induced by Curcumin-loaded Pluronic F-127 nanoparticle were reversed after pretreatment with the antioxidant N-acetyl-L-cysteine. Curcumin-loaded Pluronic F-127 nanoparticle induced autophagy-dependent apoptosis through ROS-AMPK/mTOR/ULK1 signalling in colon cancer cells. Our study offers new insights for colon cancer treatment advancement.
研究领域:
肿瘤学
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纳米医学
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分子生物学
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药理学
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细胞信号转导
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NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY
·
2022
·Vol. 396
·期 4
·683-692
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IF 3.195
Huang Hui,Xue Jie,Xie Tao,Xie Mei-Lin
Osthole is a natural coumarin substance that has an inhibitory effect on hepatic cancer, but its radiosensitization effect on hepatoma cells has not been reported. This study aimed to investigate the effect of osthole. Human HCC-LM3 and SK-Hep-1 hepatoma cells were used and treated with or without osthole, irradiation, or their combination; the cell survival, migration, colony formation, DNA damage repair, intracellular lactic acid content, and glycolysis-related glycogen synthase kinase-3β (GSK-3β), p-GSK-3β, AMP-activated protein kinase (AMPK), p-AMPK, mammalian target of rapamycin (mTOR), p-mTOR, glucose transporter-1 (GLUT-1), GLUT-3, and pyruvate kinase isozyme type M2 (PKM2) protein expressions were determined. Compared with the irradiation group, the osthole plus irradiation group could further decrease the survival rate, migration, colony formation, and DNA damage repair of both hepatoma cells, indicating a synergistic effect of the combination treatment. Moreover, the combination of osthole and irradiation could decrease the content of intracellular lactic acid, ratios of intracellular p-GSK-3β/GSK-3β and p-mTOR/mTOR proteins, and expressions of intracellular GLUT-1/3 and PKM2 proteins, and increase the ratio of intracellular p-AMPK/AMPK proteins. Osthole can increase the radiosensitivity of hepatoma cells, and its radiosensitization mechanisms may be related to glycolytic inhibition by attenuating the GSK-3β/AMPK/mTOR pathway.
研究领域:
癌症生物学
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分子生物学
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药理学
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放射生物学
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CHEMICO-BIOLOGICAL INTERACTIONS
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2023
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IF 5.1
Hefei Wang,Dewei He,Zhe Li,Xiyu Gao,Shuo Yang,Mingchi Cui,Bojian Ye,Bingxu Huang,Shoupeng Fu,Dianfeng Liu
Neuronal apoptosis and neuroinflammation are key factors involved in the pathological changes of Parkinson's disease (PD). Sophoricoside (SOP) has shown anti-inflammatory and anti-apoptosis effects in various diseases. However, the role of SOP in PD has not been reported. In this experiment, we found that oral administration of SOP alleviated weight loss and motor symptoms in 1-Methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP)-injected mice. Further studies revealed that SOP inhibited inflammatory responses and neuronal apoptosis in the midbrain region of MPTP-injected mice. In vitro mechanistic study, we found that SOP exerts neuroprotective effects through a two-sided action. On the one hand, SOP inhibits Lipopolysaccharide (LPS)-induced inflammatory responses in microglia by inhibiting the Nuclear factor kappa-B(NF-κB) pathway. On the other hand, SOP inhibits 1-methyl-4-phenylpyridinium (MPP + )-induced neuronal apoptosis by regulating the Adenosine 5′-monophosphate (AMP)-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) signaling pathway. Thus SOP is expected to be a potential therapeutic agent for PD by targeting neuroinflammation and neuronal apoptosis.
研究领域:
神经科学
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药理学
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神经退行性疾病
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IBRO Neuroscience Reports
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2025
·
IF 2.9
Wei Nong,Xiaoli Chen,Yixin Chen,Xueping Feng,Wen Kong,Rui Chi,Li Yan,Zhiquan Wei
Extracellular β-amyloid protein (Aβ) plaques are prominent pathological feature of Alzheimer's disease (AD). Aβ oligomers and plaques induce sustained microglial activation via the adenosine monophosphate-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR)/interferon regulatory factor 5 (IRF5) signaling pathway. This microglial activation-mediated neuroinflammation can accelerate neuronal cell senescence. Consequently, the regulation of the AMPK/mTOR/IRF5 pathway presents a potential therapeutic target for AD, as it may inhibit neuroinflammation and delay neuronal cell senescence. Mangiferin, a bioactive natural polyphenol extracted from the leaves of Mangifera indica Linn ., has garnered significant attention for its anti-inflammatory properties. However, it remains unclear whether mangiferin can modulate the AMPK/mTOR/IRF5 pathway to inhibit microglial activation-mediated neuroinflammation and delay neuronal cell senescence. This study employed both cellular and animal models of neuronal cell senescence to explore the effects of mangiferin on the regulation of the AMPK/mTOR/IRF5 pathway, aiming to inhibit neuroinflammation and delay neuronal cell senescence in vitro and in vivo . Specifically, SH-SY5Y neuroblastoma cells were subjected to a neuroinflammatory microenvironment induced by Aβ1–42-mediated HMC3 microglial activation to induce neuronal cell senescence in vitro . Additionally, SAMP8 accelerated aging mice were utilized as an aging animal model. The results indicate that mangiferin significantly enhances AMPK phosphorylation in microglial cells, inhibits mTOR activation, and downregulates IRF5 expression. These effects collectively suppress microglial activation and markedly reduce the production of pro-inflammatory cytokines by activated microglia. Consequently, there is a decrease in the proportion of neurons arrested in the G0/G1 phase and a reduction in the number of senescence-associated β-galactosidase (SA-β-gal) positive neurons. Furthermore, mangiferin significantly decreases the expression of neuronal cell senescence markers P16Ink4a and P21Cip1. Collectively, these findings suggest that mangiferin effectively regulates the AMPK/mTOR/IRF5 pathway, inhibits neuroinflammation mediated by microglial activation, and delays neuronal cell senescence. This study underscores the potential of mangiferin for the treatment of neuroinflammation and neurodegenerative diseases.
研究领域:
神经生物学
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药理学
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老年医学
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Virulence
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2026
·
IF 6.8
Xinxian Wang,Shurui Yang,Lichun Xie,Shanshan Qi,Libo Gao,Yongmei Li,Qian Li,Junlong Bi,Jianping Liu,Yongneng Li,Gefen Yin
Classical swine fever virus (CSFV) remains a major threat to the global swine industry, yet the involvement of host miRNAs in its pathogenic mechanisms is not fully understood. In this study, we demonstrate for the first time that miR-17-5p inhibits CSFV replication through an autophagy-dependent mechanism by targeting polycystin-2 (PKD2), a key calcium channel protein that regulates the AMPK/mTOR signaling pathway. Using the PK-15 cell model, we found that CSFV infection significantly upregulates miR-17-5p expression. Functional assays revealed that miR-17-5p exerts antiviral effects by directly binding to the 3’-UTR of PKD2, as confirmed by bioinformatics prediction and dual-luciferase reporter assays. Silencing of PKD2 recapitulated the antiviral effect of miR-17-5p overexpression, while PKD2 reconstitution restored viral replication by activating AMPK signaling and suppressing mTOR activity, thereby significantly enhancing autophagic flux – as evidenced by increased LC3-II/I ratio and decreased p62 levels. Mechanistically, PKD2 regulates intracellular calcium dynamics, modulating the AMPK/mTOR-autophagy axis to promote CSFV proliferation. This work uncovers a novel host antiviral mechanism in which a miRNA controls virus-induced autophagy via calcium signaling. To our knowledge, this is the first report to establish the pivotal role of miRNA-mediated calcium signaling modulation in flavivirus-host interactions. These findings provide a mechanistic framework and potential therapeutic targets for anti-CSFV interventions focused on PKD2 or autophagy regulation.
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Journal of Stroke & Cerebrovascular Diseases
·
2026
·Vol. 35
·期 5
·108628
·
IF 2.1
Zhihong Zhong,Shuhong Wang,Canxin Xu,Qingyun Liu,Xiao Chen,Dong Lin,Liuguan Bian
Background and purpose Intracerebral hemorrhage (ICH) is a devastating acute neurological condition with high mortality and disability. Induced pluripotent stem cell-derived neural progenitor cells (iPSC NPCs) have been shown to promote behavioral recovery by enhancing neural connectivity and providing trophic support. As the adenosine monophosphate-activated protein kinase (AMPK)/ mammalian target of rapamycin (mTOR) signaling pathway is a key regulator of autophagy in stroke, we investigated its role in the context of iPSC NPC transplantation for ICH. Materials and methods The therapeutic effects of iPSC NPC transplantation were evaluated in both in vivo and in vitro ICH models. We analyzed changes in the protein and mRNA expression, along with immunofluorescence, of key markers including glial fibrillary acidic protein (GFAP), AMPK, mTOR, sequestosome 1 (SQSTM1/ P62), and microtubule-associated protein 1 light chain 3 (LC3). Results Our findings demonstrate that iPSC NPCs secrete cytokines that mitigate brain injury and protect astrocytes from autophagy. Specifically, iPSC NPCs promoted astrocyte activation by inhibiting AMPK phosphorylation and promoting mTOR activation in both model systems. The anti-autophagic effect of iPSC NPCs on astrocytes was abolished by an mTOR inhibitor. Conversely, AMPK knockdown with siRNA promoted mTOR phosphorylation and suppressed autophagy in astrocytes. Conclusion This study identifies the interaction between AMPK and mTOR in astrocytes as a critical mechanism underlying the therapeutic benefits of iPSC-NPC transplantation, highlighting it as a promising target for ICH treatment.
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TOXICOLOGY AND APPLIED PHARMACOLOGY
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2025
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IF 3.4
Yanan Xia,Lihua Feng,Yuzhi Lan,Xiangxiang Chen,Xiaomin Tang,Hengyi Xu,Yang Liu
Children's daily exposure to titanium dioxide nanoparticles (TiO₂ NPs) poses significant risks to the developing testes, yet few studies have examined their impact on young testicular growth. Given ghrelin's established antioxidant and testis-protective effects in animal models, we hypothesized that it could mitigate TiO₂ NPs–induced damage. In this first systematic investigation of young testicular responses, three-week-old male rats received oral gavage of TiO₂ NPs (100, 200, or 400 mg/kg), followed 30 min later by intraperitoneal ghrelin (50 mg/kg) for four weeks. Exposure to TiO₂ NPs disrupted seminiferous tubule architecture and reduced serum levels of key developmental and sex hormones, including IGF-1, FSH, LH, and testosterone. Mechanistically, TiO₂ NPs activated the ROS/AMPK/mTOR signaling pathway, resulting in a marked reduction of SOD, CAT, and GSH activities and the induction of oxidative imbalance, while simultaneously upregulating the autophagy protein ULK1 and autophagy-related genes to trigger excessive autophagy, ultimately compromising testicular architecture and function. We further assessed ghrelin's protective efficacy against TiO₂ NPs-induced reproductive injury in young rats, demonstrating that ghrelin inhibited the ROS/AMPK/mTOR signaling pathway, attenuated oxidative stress, and suppressed excessive autophagy, thereby mitigating testicular injury. These findings represent the first evidence of the developing testicular heightened vulnerability to TiO₂ NPs toxicity and underscore ghrelin's potential as a novel protective intervention. Our study provides new insights into the reproductive toxicology of engineered nanoparticles and supports targeted strategies to safeguard pediatric reproductive health.
研究领域:
毒理学
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生殖健康
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纳米生物学
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JOURNAL OF ETHNOPHARMACOLOGY
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2026
·
IF 6.8
Yangdi Chen,Fanggang Bi,Zhong Hua,Jianshe Chen,Chenxi Li,Mingsan Miao,Zixue Sun
Ethnopharmacological relevance Yishen Tongluo Formula (YSTLF) is a modern compound formula derived from the traditional Chinese medicine (TCM) theory of “kidney deficiency and collateral obstruction”, and consists of seven Chinese medicinal herbs. It has been used clinically to treat oligoasthenozoospermia (OAS) for more than two decades, with proven efficacy and a favorable safety profile. However, its precise molecular mechanism has yet to be fully elucidated. Aim of the study The aim was to investigate the therapeutic efficacy and the underlying mechanism of YSTLF in treating OAS associated with the kidney deficiency and collateral obstruction pattern. Materials and methods The chemical constituents of YSTLF were identified by UHPLC-Q-Orbitrap HRMS, and molecular docking was performed between the ten most abundant compounds and AMPK/mTOR. Rat OAS models were established by combined GTW, adrenaline, and ice-water immersion. Pharmacodynamic effects were evaluated through general status, reproductive organ weights, sperm quality, coagulation parameters, and serum sex hormones. Testicular histopathology, ultrastructure, and autolysosomes were examined by HE staining and TEM. Apoptosis was detected by TUNEL staining, and autophagy/apoptosis-related protein expression by IHC. Integrated metabolomics and proteomics with KEGG enrichment were conducted. In GTW-injured GC-1spg cells treated with Compound C or rapamycin, CCK-8 assay assessed viability, flow cytometry evaluated apoptosis, immunofluorescence examined LC3B/cleaved caspase-3 expression and colocalization, and Western blotting/RT-qPCR validated AMPK/mTOR pathway key molecules. Results Among 307 identified compounds (mostly flavonoids), YSTLF improved general status, organ weights, and sperm quality in model rats. The ten most abundant compounds showed binding energies < −7.0 kcal/mol for AMPK/mTOR. Sperm concentration and motility increased dose-dependently. PT and TT were prolonged, FIB decreased, and FSH, LH, T, PRL, and Inh-B were restored. H&E, TEM, and TUNEL revealed alleviated testicular pathology, improved ultrastructure, reduced autolysosomes, and decreased apoptosis. IHC showed downregulated Beclin1 and Bax, and upregulated p62 and Bcl-2. Multi-omics revealed co-enrichment of differential proteins/metabolites in autophagy and mTOR pathways. Western blot/RT-qPCR validated downregulated p-AMPK/AMPK, AMPK mRNA, LC3II, Beclin1, Bax, cleaved caspase-3, and cleaved caspase-3/caspase-3 ratio, alongside upregulated p-mTOR/mTOR, mTOR mRNA, p62, and Bcl-2. In vitro , GTW reduced viability concentration-/time-dependently (stable model: 10%/24 h); YSTLF reversed this (optimal: 15%/24 h), restored viability, reduced apoptosis, and decreased LC3B/cleaved caspase-3 fluorescence/colocalization, while downregulating p-AMPK, LC3II, Bax and upregulating p-mTOR, p62, Bcl-2. Compound C alone mimicked YSTLF's effects without additivity, whereas rapamycin aggravated GTW-induced viability loss, apoptosis, and autophagy/apoptosis co-activation. Conclusion YSTLF improved spermatogenic function in rats with OAS (kidney deficiency and collateral obstruction pattern). Its mechanism of action involves regulation of the AMPK/mTOR signaling pathway and restoration of the balance between autophagy and apoptosis.
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EXPERIMENTAL ANIMALS
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2026
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IF 2
Yang LI,Xinchang FENG,Lingpeng ZHENG
Insulin resistance (IR) and hepatic steatosis are key pathological features of type 2 diabetes mellitus (T2DM). Fraxin, a natural flavonoid with potential metabolic regulatory properties, has been proposed to modulate metabolic disorders. This study aimed to investigate whether fraxin protects against IR and steatosis via Sirt1/AMPK/mTOR-mediated autophagy activation. A T2DM rat model was established using high-fat diet (HFD) feeding combined with streptozotocin (STZ) injection. Rats were treated with fraxin (25 or 50 mg/kg) for 4 weeks, followed by assessment of fasting blood glucose (FBG), insulin (FINS), HOMA-IR index, serum lipid profiles and liver function. Histopathological examination (H&E and Oil Red O staining) evaluated hepatic steatosis. BRL 3A cells exposed to palmitic acid (PA) were treated with fraxin (40 or 80 μM), and glucose uptake, lipid accumulation, and protein expression (IRS-1 phosphorylation, GLUT-2 translocation, autophagy markers and Sirt1/AMPK/mTOR pathway components) were analyzed. The specific autophagy inhibitor chloroquine (CQ) was used to verify whether the regulatory effects of fraxin were dependent on autophagy activation. Fraxin significantly reduced FBG, FINS, HOMA-IR, and dyslipidemia in diabetic rats. In PA-treated BRL 3A cells, fraxin enhanced glucose uptake, reduced lipid droplets, and restored IRS-1 phosphorylation and GLUT-2 membrane localization. Mechanistically, fraxin activated autophagy and modulated the Sirt1/AMPK/mTOR pathway, which were abolished by the Sirt1 inhibitor EX527. In conclusion, fraxin alleviates IR and hepatic steatosis in HFD/STZ-induced diabetic rats by activating autophagy through Sirt1/AMPK/mTOR pathway, suggesting its potential as a therapeutic agent for diabetes-associated metabolic disorders.
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Journal of Integrative Neuroscience
·
2026
·Vol. 25
·期 7
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IF 3.3
Zhihui Li,Qian Wang,Kaixuan Ma,Mengna Yu,Yanyan Wang,Zhongqiao Ge,Peng Lin,Hui Wang,Lexun Lin,Yang Chen,Lina Jia,Heming Li,Zhongqiu Fu,Zhaohua Zhong,Guangtian Wang
Background: Stroke is a major cause of morbidity and mortality, characterized by neuronal damage and complex cell death pathways. This study aimed to investigate the protective role of spermine oxidase (Smox) in ischemic stroke and its effect on neuronal autophagy. Methods: We employed transient middle cerebral artery occlusion (tMCAO) models and oxygen-glucose deprivation/reoxygenation (OGD/R) experiments in HT22 cells to explore the protective effects of Smox knockdown against ischemic injury and to evaluate changes in autophagy. Results: Smox levels were significantly elevated following stroke, and correlated with increased autophagic activity and neuronal apoptosis. In contrast, knockdown of Smox reduced neuronal death and improved neurological function while decreasing autophagy activation. Mechanistically, Smox may regulate autophagy via the phosphorylation of protein kinase B (AKT),AMP-activated protein kinase (AMPK), and mechanistic target of rapamycin (mTOR); Smox knockdown increased AKT and mTOR phosphorylation, while reducing AMPK phosphorylation, suggesting a potential shift in the regulation of neuronal autophagy. Conclusions: Our findings suggest a dual role for Smox in stroke pathology, indicating that it may influence autophagy via the AKT/AMPK/mTOR signaling, which could be critical for neuronal survival after ischemic injury. Targeting Smox may offer a therapeutic strategy for neuronal protection and recovery in stroke management, suggesting the potential importance of autophagy modulation in ischemic brain injury.
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Frontiers in Oncology
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2021
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IF 6.244
Heng Yongqing,Liang Yupei,Zhang Junqian,Li Lihui,Zhang Wenjuan,Jiang Yanyu,Wang Shiwen,Jia Lijun
The neddylation pathway is overactivated in esophageal cancer. Our previous studies indicated that inactivation of neddylation by the NAE inhibitor induced apoptosis and autophagy in cancer cells. Camptothecin (CPT), a well-known anticancer agent, could induce apoptosis and autophagy in cancer cells. However, whether CPT could affect the neddylation pathway and the molecular mechanisms of CPT-induced autophagy in esophageal cancer remains elusive. We found that CPT induced apoptosis and autophagy in esophageal cancer. Mechanistically, CPT inhibited the activity of neddylation and induced the accumulation of p-IkBa to block NF-κB pathway. Furthermore, CPT induced the generation of ROS to modulate the AMPK/mTOR/ULK1 axis to finally promote protective autophagy. In our study, we elucidate a novel mechanism of the NF-κB/AMPK/mTOR/ULK1 pathway in CPT-induced protective autophagy in esophageal cancer cells, which provides a sound rationale for combinational anti-ESCC therapy with CPT and inhibition AMPK/ULK1 pathway.
研究领域:
肿瘤学
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分子生物学
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细胞生物学
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