EUROPEAN JOURNAL OF MEDICINAL CHEMISTRY
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2023
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IF 6.7
Xiaoxiao Yang,Zhigang Liu,Mengyuan Fang,Tingfeng Zou,Zhen Zhang,Xianshe Meng,Tianxiang Wang,Huawen Meng,Yuanli Chen,Yajun Duan,Qingshan Li
Pterostilbene is a demethylated resveratrol derivative with attractive anti-inflammatory, anti-tumor and anti-oxidative stress activities. However, the clinical use of pterostilbene is limited by its poor selectivity and druggability. Heart failure is a leading cause of morbidity and mortality worldwide, which is closely related to enhanced oxidative stress and inflammation. There is an urgent need for new effective therapeutic drugs that can reduce oxidative stress and inflammatory responses. Therefore, we designed and synthesized a series of novel pterostilbene chalcone and dihydropyrazole derivatives with antioxidant and anti-inflammatory activities by the molecular hybridization strategy. The preliminary anti-inflammatory activities and structure-activity relationships of these compounds were evaluated by nitric oxide (NO) inhibitory activity in lipopolysaccharide (LPS)-treated RAW264.7 cells, and compound E1 exhibited the most potent anti-inflammatory activities. Furthermore, pretreatment with compound E1 decreased reactive oxygen species (ROS) generation both in RAW264.7 and H9C2 cells by increasing the expression of nuclear factor erythroid 2-related factor 2 (Nrf2), as well as downstream antioxidant enzymes superoxide dismutase 1 (SOD1), catalase (CAT) and glutathione peroxidase 1 (GPX1). In addition, compound E1 also significantly inhibited LPS or doxorubicin (DOX)-induced inflammation in both RAW264.7 and H9C2 cells through reducing the expression of inflammatory cytokines by inhibiting nuclear factor-κB (NF-κB) signaling pathway . Moreover, we found that compound E1 improved DOX-induced heart failure by inhibiting inflammation and oxidative stress in mouse model, which is mediated by the potential of antioxidant and anti-inflammatory activities. In conclusion, this study demonstrated the novel pterostilbene dihydropyrazole derivative E1 was identified as a promising agent for heart failure treatment.
研究领域:
药理学
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心脏病学
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分子生物学
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生物化学
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高影响因子
PHYTOMEDICINE
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2026
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IF 8.3
XiaoYang Qu,LiJuan Chen,JiangHua He,YuFei Fang,Jing Sun,ZhiYing Yu,Zhen Yang,ZiJing Zhang,JianBo Chen,Ling Dong
Background Epilepsy is a prevalent neurological disorder characterized by recurrent seizures and has limited effectiveness of available clinical treatments. Ferroptosis of neurons is one of the main mechanisms of epilepsy. Arisaema Cum Bile (ACB) is a traditional Chinese medicine that is prepared by fermenting animals bile with Rhizoma Arisaematis rhizomes, has demonstrated therapeutic effects on epilepsy and other nervous system diseases. Furthermore, the active components responsible for the anti-epileptic effects of ACB and the intrinsic mechanisms are still unclear. Purpose This study aims to clarify the principal bioactive constituents of ACB and their mechanisms in the treatment of epilepsy. It also seeks to provide data support for its clinical application in antiepileptic combination therapy. Method Pentylenetetrazol injections were used to induce epilepsy in rats. ACB and brain metabolites were identified via UPLC-Q-Exactive Orbitrap MS/MS, and active components were predicted through bioinformatics analysis. In vivo , ACB and hyodeoxycholic acid (HDCA) were administered by gavage, and the effects on oxidative stress, inflammation, and cognitive impairment were evaluated. Additionally, ferroptosis-related protein and gene expression were analyzed using western blot, PCR, immunofluorescence, and flow cytometry. In vitro , using primary neurons and HT22 cells, with electrophysiology employed to assess neuronal activity and glutamate used to induce ferroptosis in HT22 cells, in order to explore how HDCA alleviates epilepsy by inhibiting neuronal ferroptosis. Result A total of 37 chemical components were identified from the ACB, of which 10 active constituents can cross the blood-brain barrier, including steroids and terpenoids. Bioinformatics analysis suggests that HDCA may be one of the key active components responsible for ACB anti-epileptic effects and ferroptosis may represent a crucial underlying therapeutic mechanism. Studies in animals have demonstrated that treatment with ACB and HDCA reduced the frequency and severity of seizures in epileptic rats, mitigated hippocampal neuronal damage, improved post-epileptic cognitive learning capacity, alleviated neuroinflammatory injury and decreased markers of ferroptosis. This neuroprotective effect likely occurs through activation of the p53/Nrf2/GPX4 signaling pathway. Further in vitro cell experiments demonstrated that HDCA can inhibit the generation of action potentials in primary hippocampal neurons, protects HT22 neurons from glutamate-induced cell death, an effect that is reduced by Nrf2 inhibitors. These findings corroborate earlier bioinformatics analyses, confirming that the neuroprotective effects of HDCA are closely linked to Nrf2-mediated ferroptosis pathways. Conclusion HDCA is a key component of ACB anti-epileptic effects, potentially inhibiting ferroptosis through the p53/Nrf2/GPX4 pathway to reduce epilepsy.
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FREE RADICAL BIOLOGY AND MEDICINE
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2026
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IF 8
Zhan Wang,Cheng Zheng,Wenzhen Li,Kaung Myat Kyaw,Yunmin Zhu,Yihan Lin,Zhen Lin,Di Wu,Zhiqi Hu,Yang Sun,Kaitao Li
Introduction Androgenetic alopecia (AGA), the most common form of hair loss, lacks ideal therapies due to the limitations of current drugs. Natural compounds with low toxicity and good biocompatibility present promising alternatives. Ginkgolide B (GB), a bioactive component of Ginkgo biloba , possesses multiple biological activities, yet its efficacy and mechanism against AGA remain unexplored. Objectives This study aimed to investigate the hair growth-promoting effect of GB in a dihydrotestosterone (DHT)-induced hair loss model and to elucidate the underlying molecular mechanism. Additionally, a novel detachable microneedle delivery system was developed and evaluated to overcome GB's poor transdermal permeability, thereby enhancing its therapeutic efficacy. Methods The AGA microenvironment was first simulated using DHT-stimulated human dermal papilla cells (HDPCs) in vitro. The molecular mechanism by which GB improves the secretory function of HDPCs was investigated through network pharmacology, western blot, transmission electron microscopy, and immunofluorescence. Subsequently, a detachable microneedle system was designed, in which GB was encapsulated in poly (lactic-co-glycolic acid) (PLGA) microspheres and integrated with the sulfobutylether-β-cyclodextrin (SCD)-based matrix (GB@MS-MN). The therapeutic efficacy of this system was evaluated in a DHT-induced hair loss model. Results GB rescued DHT-induced dysfunction in HDPCs, reversing the aberrant secretion of hepatocyte growth factor (HGF) and dickkopf-1 (DKK1). Mechanistically, GB alleviated DHT-induced endoplasmic reticulum stress (ERS) in HDPCs by activating the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway. And GB promoted hair growth in DHT-induced hair loss mice. The GB@MS-MN system demonstrated excellent mechanical properties and targeted follicular delivery and showed superior hair growth promotion compared to free GB and minoxidil. It effectively suppressed follicular ERS, with no observed systemic toxicity. Conclusion In summary, this study confirms that GB protects HDPCs function by suppressing DHT-induced ERS through activation of the Nrf2/HO-1 pathway. Furthermore, a detachable microneedle delivery system based on a PLGA-SCD composite effectively overcomes the transdermal barrier of GB and demonstrates superior hair-promoting efficacy.
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JOURNAL OF THE SCIENCE OF FOOD AND AGRICULTURE
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2026
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IF 4
Haixia Han,Juanjuan Gao,Quan Sun,Dandan Tong,Jian Liu,Xiuli Yang,Jingjing Sun,Yue Cui,Juan Wang,Zuoshan Feng,Mingxi Jia
BACKGROUND Acrylamide (ACR), an environmental neurotoxicant prevalent in thermally processed foods, contributes to brain injury via oxidative stress and neuroinflammation. The cumulative effects of long-term low-dose exposure are particularly alarming. As a traditional food ingredient, the inflorescence of Coreopsis tinctoria Nutt. is rich in polyphenolic compounds that exhibit significant anti-inflammatory and antioxidant properties. This study systematically evaluated the neuroprotective potential of Coreopsis tinctoria Nutt. polyphenols (CTNP) against chronic low-dose ACR exposure in mice. RESULTS Behavioral analyses demonstrated that CTNP (0.25–1.00 g kg −1 ) significantly ameliorated ACR-induced gait abnormalities and restored voluntary activity. CTNP mitigated neuronal misalignment and loss of synaptic density in the hippocampal CA1/CA3 regions and markedly reduced serum levels of brain injury markers MBP and GFAP by 30.6% and 41.7%, respectively. Mechanistic investigations revealed that CTNP attenuated oxidative damage via activation of the Nrf2/HO-1 pathway, leading to decreased brain reactive oxygen species and malondialdehyde levels while enhancing catalase, superoxide dismutase and glutathione peroxidase activities. Furthermore, CTNP suppressed MAPK pathway-mediated neuroinflammation, reducing pro-inflammatory factors such as COX-2, TNF- α and IL-1 β . CONCLUSION These findings demonstrate that CTNP, as diet-derived bioactives, mitigate ACR neurotoxicity through coordinated modulation of Nrf2/HO-1 antioxidant and MAPK anti-inflammatory pathways, supporting their potential as a functional food component for preventing environmental toxicant-associated neural damage. © 2026 Society of Chemical Industry.
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PHYTOMEDICINE
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2026
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IF 11.3
Chunge Zhang,Shuai Huang,Wenxin Zhang,Hongbo Teng,Yuna Shao,Yihua Zhang,Shihang Ren,Qi Wu,Yan Zhao,Zhaowei Yan
Background Acanthopanax sessiliflorus ( A. sessiliflorus ) extract has been used in various traditional Chinese medicines and compound preparations for the treatment of arrhythmia. Our preliminary studies have demonstrated that A. sessiliflorus extract exerts significant protective effects against arrhythmia induced by barium chloride. The present study aims to elucidate the bioactive components of A. sessiliflorus and to investigate the underlying mechanisms by which it mitigates barium chloride-induced arrhythmia. Methods Network pharmacology was employed to predict the pharmacological profiles of chemical constituents from A. sessiliflorus, followed by a systematic screening of their biological activities. Subsequently, a barium chloride-induced arrhythmia model was established, and the potential therapeutic mechanisms were analyzed using transcriptomics. Functional and histopathological analyses of the rat hearts were performed. Western blot was used to detect the expression levels of the Nrf2/HO-1 axis, connexins, ion channels, and autophagy-related proteins in myocardial tissue and NRVMs. Subsequently, PCR, immunofluorescence, co-immunoprecipitation, and molecular docking were employed to verify the involvement of the targets in the intervention of arrhythmia. Results The results showed that after treatment with divaroside, the arrhythmia and redox system imbalance induced by BaCl₂ in rats were significantly restored. Divaroside can inhibit calcium overload by regulating the expression levels of RyR2 and SERCA2a in the sarcoplasmic reticulum, serving as a means to alleviate arrhythmia. In addition, we have confirmed that autophagy plays a crucial role in arrhythmia, and divaroside can activate autophagy, thereby protecting cardiomyocytes from BaCl₂-induced damage. Finally, it was confirmed that divaroside can weaken the interaction between the Keap1-Nrf2 complex and promote the nuclear translocation of Nrf2, activating the Nrf2/HO-1 axis and regulating the aforementioned pathways to counteract arrhythmia. Conclusion This study suggests that divaroside prevents the occurrence of arrhythmia by activating autophagy and reducing abnormal calcium ion homeostasis through the Nrf2/HO-1 axis.
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BIOCHEMICAL PHARMACOLOGY
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2026
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IF 6.5
Yu-jia Huo,Miao Wei,Xiao Fan,Li-wen Peng,Jing-chang Yuan,Si-si Tan,Xiao-chen Wang,Ruo-tong Ou-yang,Yi-jing Zhou,Yan-yu Pu,Xi Gao,Jun-qin Lei,Hong Li
Glaucoma is a prominent global cause of irreversible vision loss, fundamentally driven by the continuous degeneration and ultimate death of retinal ganglion cells (RGCs), in which persistent oxidative stress plays a pivotal role. While selenium (Se) offers robust endogenous antioxidant defense, the severe toxicity and narrow therapeutic window of inorganic selenium strictly limit its application. To overcome this critical bottleneck, chitosan-functionalized selenium nanoparticles (CS-SeNPs) are engineered. This strategic nanomodification effectively shields the inherent toxicity of free selenium while conferring improved colloidal stability and biocompatibility. Clinically, systemic Se levels in patients with primary open-angle glaucoma (POAG) are found to be significantly diminished compared to healthy controls. Mechanistically, transcriptome sequencing reveals that CS-SeNPs function through the phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) pathway to upregulate the downstream nuclear factor erythroid 2-related factor 2/heme oxygenase-1 (Nrf2/HO-1) antioxidant axis, reducing intracellular oxidative stress and apoptosis. In vivo, an intravitreal administration strategy for CS-SeNPs is established. In a rat model of acute ocular hypertension (AOH), this targeted local delivery reduces oxidative damage, preserves retinal hierarchical architecture, and restores visual electrophysiological function. These findings identify systemic Se deficiency as a clinical hallmark of POAG and demonstrate that intravitreal CS-SeNPs offer a promising, intraocular pressure-independent nanotherapeutic strategy for glaucomatous neuroprotection.
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MOLECULAR AND CELLULAR BIOCHEMISTRY
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2026
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IF 4.7
Liu Xiang,Sun Jing-Jing,Mao Chang-Kun,Cao Yong-Sheng,Deng Qi-Fei,Li Guang-Yuan
Cryptorchidism, characterized by the failure of one or both testes to descend into the scrotum, is the most prevalent urogenital malformation in male infants and an important risk element of male infertility and testicular cancer. The purpose of this study was to investigate the molecular mechanisms underlying cryptorchidism-induced testicular damage, with a focus on the role of USP35. Here we established a unilateral experimental cryptorchidism model of Sprague-Dawley rats by resetting the left testis to the abdominal cavity and suturing the inguinal canal, thus preventing its natural descent. The findings indicated that apoptosis and oxidative stress (OS) levels were increased in the undescended testis (UDT) compared to the descended testis (DT) group. Subsequent mRNA sequencing of DT and UDT tissues revealed that ubiquitin specific peptidase 35 (USP35) expression was downregulated in the UDT, implying that USP35 may be an important factor in the pathogenesis of cryptorchidism. To further investigate, an oxidative damage model was constructed using H 2 O 2 -treated GC-1 spermatogonia. USP35 expression was reduced in H 2 O 2 -exposed cells, while overexpression of USP35 attenuated H 2 O 2 -induced oxidative damage by inhibiting apoptosis and OS. Mechanistically, USP35 interacted with nuclear factor erythroid 2-related factor 2 (NRF2) and stabilized its protein expression via deubiquitination. Impairment of NRF2 function abolished the protective effect of USP35 against oxidative damage in H 2 O 2 -treated GC-1 spermatogonia. Overall, these results highlight the significance of the USP35-NRF2 axis in protecting spermatogonia from oxidative injury, suggesting that USP35 may be a potential therapeutic target against cryptorchidism-induced early germ cell damage.
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JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
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2026
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IF 6.7
Yufei Cao,Yiqiang Zhang,Boran Zhou,Yingxue Zhang,Xu Han,Xinyuan Luan,Yu Wang,Hongjing Zhao
Zearalenone (ZEN) is a mycotoxin that induces hepatic oxidative injury by promoting ROS accumulation and compromising antioxidant defenses. Transcriptomic profiling revealed xanthine oxidase (XOD) as a key mediator. Structure-based molecular docking identified polydatin (PD) from Polygonum cuspidatum as a potent XOD inhibitor with strong binding affinity. Biochemical assays confirmed PD’s XOD inhibition. In vitro and in vivo studies demonstrated that PD significantly attenuated ZEN-induced oxidative stress, reduced ROS generation, and improved pathological markers of liver injury, with optimal efficacy at low concentrations. Molecular dynamics simulations revealed PD forms a stable complex with XOD. Concurrently, PD activated the Nrf2/HO-1 pathway, enhancing SOD and GSH-Px expression while reducing lipid peroxidation. These findings demonstrate that PD mitigates ZEN hepatotoxicity through dual mechanisms: direct XOD inhibition and enhancement of endogenous antioxidant capacity, supporting its therapeutic potential.
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ANTIOXIDANTS & REDOX SIGNALING
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2025
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IF 6.1
Xian-Dong Li,Yue-Xin Ning,Yi-Feng Pei,Jing-Yuan Niu,Jian Luo,Yi-Na Zhang,Zi-Ai Zhao,Xiao-Wen Hou,Qian-Kun Zhao,Tian-Ce Xu,Hui-Sheng Chen
Aims: Cathodal transcranial direct current stimulation (C-tDCS), a noninvasive physical therapy, has potential neuroprotective effects in acute ischemic stroke. However, the rational timing of its application and the underlying mechanisms remain inadequately understood. This study aims to investigate its neuroprotective effects and the involved mechanisms.Results: Our in vivo results indicated that C-tDCS applied during the reperfusion phase but not during the ischemic phase significantly improved neurological outcomes, reduced infarct volume, and mitigated histopathological damage in middle cerebral artery occlusion/reperfusion rats. C-tDCS during the reperfusion phase suppressed ferroptosis, activated nuclear factor erythroid 2-related factor 2 (Nrf2), and inhibited mitophagy. In vitro, the ferroptosis inducer RSL3 negated the protective effects of cathodal direct current stimulation on HT22 neuronal cells subjected to oxygen-glucose deprivation/reoxygenation injury. Furthermore, the Nrf2 inhibitor ML385 and the mitophagy activator FCCP reversed the inhibitory effects of C-tDCS on ferroptosis, with FCCP also affecting Nrf2 activation by C-tDCS.Innovation and Conclusions: These results demonstrate that C-tDCS during reperfusion attenuates cerebral ischemia-reperfusion injury by coordinating mitophagy inhibition and Nrf2 activation to counteract ferroptosis, which provides new evidence for its potential translational clinical applications. Antioxid. Redox Signal. 00, 000–000.
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Frontiers in Bioscience-Landmark
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2025
·Vol. 30
·期 6
·36615
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IF 3.1
Shanli Wu,Gun Yang,Xiaosha Wen,Yi Lin,Shenglong Wang,Jing Wang,Quan Liu,Dixian Luo
Background:Aldo-keto reductase 1B10 (AKR1B10) is expressed in various malignant tissues. Several studies have highlighted the essential function of AKR1B10 in lipid metabolism and in the detoxification of lipid peroxides. The aim of this research was to explore the role of AKR1B10 in the susceptibility of MDA-MB-231 cells to ferroptosis. These cells serve as a model for triple-negative breast cancer (TNBC).Methods:Lentiviral transfection was used to establish stable cell lines with high or low expression of AKR1B10. Our model of ferroptosis used the ferroptosis activator RSL3, and the specific ferroptosis inhibitor ferrostatin-1 (Fer-1) to rescue cell death. Stable cell lines were treated with the specific inhibitor OSU-T315 directed against phosphorylation of Ser473 in protein kinase B (AKT) and Ser9 in glycogen synthase kinase 3 beta (GSK3β), either alone or in combination with RSL3. A fatty acid stress model was established using palmitic acid (PA) or arachidonic acid (AA), either in the presence or absence of serum starvation and with or without co-treatment with RSL3. Cell viability was evaluated with the cell counting kit-8 (CCK8) assay and lipid peroxidation levels by flow cytometry after staining with C11 BODIPY 581/591. Exploration of the underlying mechanisms was conducted through RNA sequencing and bioinformatics analysis. Western blotting was performed to evaluate protein levels, and quantitative real-time polymerase chain reaction (qPCR) was used to evaluate transcript levels.Results:Western blot and qPCR analyses validated the successful establishment of stable MDA-MB-231 cell lines with and without AKR1B10 overexpression. Cell viability and lipid reactive oxygen species (ROS) assays showed that AKR1B10 suppressed ferroptosis in the RSL3-induced cell death model. Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Set Enrichment Analysis (GSEA) analyses indicated the phosphatidylinositol 3-kinase (PI3K)-AKT pathway was likely to play a role in the underlying mechanisms. AKR1B10 increased the expression of glutathione peroxidase 4 (GPX4), thus potentially implicating the AKT/GSK3β/nuclear factor erythroid 2-related factor 2 (NRF2)/GPX4 pathway in the mechanism. These changes in protein levels were also observed by Western blot analysis after 6 h of RSL3 treatment. Under the influence of RSL3, the transcript levels of NRF2-related genes including GPX4, ferritin heavy chain 1 (FTH1), heme oxygenase 1 (HO-1), and NAD(P)H quinone dehydrogenase 1 (NQO-1) were significantly elevated in the AKR1B10 overexpression cell line, whereas that of prostaglandin-endoperoxide synthase 2 (PTGS2) was significantly reduced. Similar changes were observed after treatment with OSU-T315. AKR1B10 was found to suppress the sensitivity to ferroptosis induced by treatment with OSU-T315, PA, or AA. These phenomena were rescued by the ferroptosis inhibitor Fer-1.Conclusions:AKR1B10 appears to be an important mechanism protecting MDA-MB-231 cells from ferroptosis, possibly through the AKT Ser473/GSK3β Ser9/NRF2/GPX4 pathway. AKR1B10 may be a key factor underlying the therapeutic effect of RSL3 under different exogenous fatty acid microenvironments.
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FITOTERAPIA
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2025
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IF 2.6
Liyuan Shen,Jingwen Xu,Yihai Wang,Jiaming Yao,Xiangjiu He
Chronic myeloid leukemia (CML) is a myeloproliferative tumor, which is prone to drug resistance during treatment. Previous studies have indicated that Ficus altissima Blume exhibits potential antitumor properties, with 5,7,2′-trihydroxy-4′-methoxy-6-(3-hydroxy-3-methylbutyl)-isoflavone (TMI) as its main active component. However, the antitumour activity of TMI and its underlying mechanisms remain unexplored. This study investigated the anti-proliferative effects of TMI on adriamycin (ADR)-resistant leukemia K562 cells (K562/ADR cells) and the mechanism of overcoming multidrug resistance (MDR). The findings demonstrated that TMI significantly downregulated P-glycoprotein (P-gp) and breast cancer resistance protein (BCRP) expression. It was confirmed that TMI triggered caspase-dependent apoptosis in K562/ADR and K562 cells. While reactive oxygen species accumulation and PI3K/AKT/mTOR mediated TMI's effect in K562 cells, these pathways were irrelevant to its apoptosis induction and MDR overcoming in K562/ADR cells. Further research found that the nuclear factor erythroid 2-related factor 2 (Nrf2) expression was significantly suppressed by TMI treatment. In contrast, exposure to the Nrf2 agonist tert-butylhydroquinone resulted in upregulation of P-gp and BCRP protein levels in K562/ADR cells. This suggests that TMI's overcoming of K562/ADR cell drug resistance is associated with Nrf2 degradation. Finally, molecular docking analysis and cellular thermal shift assay experiments showed that TMI exerted anti-drug resistance effect by directly binding to Nrf2 protein. Collectively, TMI overcomes K562/ADR cell resistance primarily through targeting and inhibiting Nrf2 protein and decreasing drug efflux protein expression, ultimately promoting cell death. These results highlight TMI's potential as a drug-resistant leukemia therapy, while also suggesting that developing Nrf2-targeted inhibitors may represent a novel strategy for overcoming tumor drug resistance.
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JOURNAL OF MOLECULAR HISTOLOGY
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2025
·Vol. 56
·期 6
·1-14
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IF 2.2
Liang Jia-Jun,Liu Hong-Xia,Yan Jian-Gang,Xie Guo,Liu Wen-Li,Lin Jia-Hui,Li Xiao-Min,Mao Xin-Liang
The specific hepatoprotective mechanism of Fermented Panax ginseng C.A. Meyer extract (FGE) has not yet been fully elucidated. In this study, an AAPH-induced liver injury model was established to investigate the hepatoprotective effects of FGE. The hepatoprotective effects of FGE may involve the mediation of the NRF2 pathway by rare ginsenosides such as 20(R)-Rh1, 20(S)-Rg2, Rg5, 20(R)-Rg2, and 20(S)-Rh1. The results showed that FGE effectively improved pathological damage and liver dysfunction, increased SOD and GPx expression in the liver, and inhibited excessive ROS generation both in vivo and in vitro. Mechanistically, FGE regulated the mRNA and protein expression of KEAP1, HO-1, and NQO1, while enhancing NRF2 protein expression and promoting its nuclear translocation. In conclusion, the NRF2 signaling pathway activated by FGE may inhibit AAPH-induced oxidative stress and alleviate the resulting liver injury. Graphical abstract
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