BRITISH JOURNAL OF PHARMACOLOGY
·
2026
·
IF 7.5
Chang Liu,Zhuoqun Wang,Linxin Zhang,Di Yang,Zhihong Zhang,Xiaoli Cui,Ali H. Eid,Mengyang Wang
Background and Purpose Fangchinoline (FAN), a bioactive bisbenzylisoquinoline alkaloid from Stephania tetrandra , shows protective potential against angiotensin II (Ang II)-induced hypertensive heart failure (HF), particularly involving mitophagy and ferroptosis, remain unclear. We investigated the effects of FAN on Ang II-induced cardiac remodelling and HF. Experimental Approach A hypertensive heart failure model was established in C57BL/6 mice via 4-week Ang II infusion. FAN was administered during the final 2 weeks. Cardiac function was assessed by echocardiography and pathological remodelling was evaluated by histological staining. RNA sequencing of cardiac tissue was performed to investigate the mechanism of anti-heart failure action of FAN. The potential binding proteins of FAN were verified by molecular docking, drug affinity response target stability (DARTS), cellular thermal shift assay (CETSA) and surface plasmon resonance assay (SPR). In vitro , neonatal rat ventricular myocytes (NRVMs) were used to investigate the effects of FAN on cellular hypertrophy, mitophagy and ferroptosis. Key Results In vivo , FAN treatment significantly ameliorated cardiac hypertrophy, dysfunction and fibrosis. These protective effects were independent of blood pressure-lowering actions. Mechanistically, FAN activates PGC-1α to enhance mitophagy and suppress STAT6-PPARγ signalling, thereby inhibiting ferroptosis and restoring redox homeostasis. In vitro , FAN reduced Ang II-induced NRVM hypertrophy, ROS production and mitochondrial membrane potential depolarisation, and confirmed the modulation of mitophagy and ferroptosis markers. Conclusions and Implications We demonstrate that FAN alleviates Ang II-induced HF through a mechanism involving the activation of PGC-1α-mediated mitophagy and regulation of the STAT6-PPARγ pathway, ultimately suppressing cardiomyocyte ferroptosis. These results offer new perspectives for HF treatment. Graphical FAN mitigates HF by engaging PGC-1α-mediated mitophagy and STAT6-PPARγ to counteract ferroptosis.
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Cells
·
2021
·Vol. 10
·期 6
·1359
·
IF 6.6
Nashwa Amin,Shijia Chen,Qiannan Ren,Xiaoning Tan,Benson O. A. Botchway,Zhiying Hu,Fengpei Chen,Shan Ye,Xiaoxue Du,Zuobing Chen,Marong Fang
Hypoxia-inducible factor 1 can sufficiently control the progress of neurological symptoms after ischemic stroke owing to their actions associated with its downstream genes. In this study, we evaluated the role of HIF-1α in attenuating brain damage after endothelin-1 injection. Focal cerebral ischemia in mice were induced by endothelin-1 microinjection. Hypoxia-inducible factor 1 activator, dimethyloxalylglycine (DMOG), and HIF-1α inhibitor, acriflavine (ACF), were used to evaluate the hypoxia-inducible factor 1 activity during cerebral ischemia. The expression levels of HIF-1α, glial fibrillary acidic protein (GFAP), interleukin-10 (IL-10), inducible nitric oxide synthase (iNOS), phosphorylated I-kappa-B-alpha/total I-kappa-B-alpha (p-IκBα/IκBα) and nuclear factor kappa B (NF-kB) were assessed. Besides, mRNA levels of IL-10, tumor necrosis factor- alpha (TNF-α), and NF-kB were also analyzed. Results showed a noticeable increase in hypoxia-inducible factor 1 and IL-10 levels in the DMOG group with a decline in iNOS, TNF-α, and NF-kB levels, implying the anti-inflammatory role of hypoxia-inducible factor 1 activator following stroke. These findings were further corroborated by GFAP immunostaining that showed astrocytic activation to be inhibited 12 days post-ischemia, as well as histological and TEM analyses that demonstrated hypoxia-inducible factor 1 induction to alleviate neuronal soma damage and cell death. Based on our study, HIF-1α could be a potential therapeutic target for ischemic stroke.Keywords:endothelin-1;hypoxia-inducible factor-1;interleukin 10;astrocyte;dimethyloxalylglycine;acriflavine;proinflammatory cytokines
研究领域:
神经科学
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药理学
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分子生物学
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BIOORGANIC & MEDICINAL CHEMISTRY
·
2021
·
IF 3.641
Zichen Xu,Bin Zhang,Zhixin Liao,Shaohua Gou
Hypoxia is one of the unique features of tumor physiology. Hypoxia inducible factor (HIF-1α), as a major transcription factor in response to hypoxia, has been considered as a promising tumor-specific target for anticancer therapy. The formation of a hypoxic microenvironment in tumors can decrease the curative effect of cytotoxic chemotherapeutic drugs. To promote the antitumor efficacy of chemotherapy by suppressing hypoxia, we designed and prepared a novel gemcitabine-based drug conjugate ( GEM -5 ) containing a HIF-1α inhibitor (YC-1). As expected, GEM -5 showed excellent antiproliferative activity (IC 50 = 0.03 μΜ under hypoxia) and remarkably induced the apoptosis of A2780 cells in vitro . Additionally, western blot analysis demonstrated that GEM -5 significantly down-regulated the expression of HIF-1α and up-regulated the expression of tumor suppressor p53. More importantly, GEM -5 effectively inhibited tumor growth in the A2780 xenograft mouse model and significantly ameliorated tumor hypoxia in vivo . This novel, simple, and effective strategy for overcoming tumor hypoxia and enhancing the antitumor effect of chemotherapeutic drugs has great potential in cancer therapy.
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JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
·
2025
·Vol. 29
·期 8
·e70566
·
IF 4.2
Ying‐jie Ren,Tian‐qi Sun,Yu Lu,Dan‐Li Liu,Rui Gao,Ting Li,Min Guo,Qing‐hua Liu,Hai‐long Wang,Min Pang
Chronic obstructive pulmonary disease (COPD) is a widespread lung disease marked by alveolar wall damage, leading to inflammation and fibrosis. Key risk factors include age, smoking, sex, and education, with smoking being the most crucial. These factors are globally consistent and linked with aging. Club cell secretory protein 16 (CC16), primarily secreted by non‐ciliated bronchial epithelial cells, is crucial for pulmonary health, offering anti‐inflammatory and antioxidant benefits. CC16 levels are notably reduced in COPD, suggesting its enhancement as a potential treatment. In this study, cellular senescence of BEAS‐2B cells was stimulated using cigarette smoke extract (CSE) and the function of recombinant human CC16 protein (rhCC16) in cellular senescence was assessed by detecting the levels of β‐galactosidase, p16, p21, ROS and the underlined mechanism was revealed by measuring mitochondrial biogenesis and metabolism. Additionally, COPD mice were prepared, and rhCC16's role on the cellular senescence of lung tissues was examined. Our findings showed that rhCC16 ameliorated cellular senescence in BEAS‐2B cells and lung tissues of COPD mice accompanied by lower levels of β‐galactosidase, p16, p21 and ROS. Mechanically, rhCC16 mitigated senescence via triggering PGC‐1α expression through the AMPK/SIRT1 pathway and fostering mitochondrial biogenesis and metabolism to reduce the levels of ROS. Furthermore, the results also indicated that rhCC16 exerted its effect via both integrin α4β1 and clathrin‐mediated endocytosis. Collectively, rhCC16 suppresses cellular senescence and ameliorates COPD‐like symptoms by activating the AMPK/Sirt1‐PGC‐1‐α‐TFAM pathway to foster mitochondrial function.
研究领域:
医学
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生物学
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呼吸系统疾病
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分子生物学
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eLife
·
2021
·
IF 8.146
Chunbo Zhang,Tianyu Zhong,Yuanyuan Li,Xianfeng Li,Xiaopeng Yuan,Linlin Liu,Weilin Wu,Jing Wu,Ye Wu,Rui Liang,Xinhua Xie,Chuanchuan Kang,Yuwen Liu,Zhonghong Lai,Jianbo Xiao,Zhixian Tang,Riqun Jin,Yan Wang,Yongwei Xiao,Jin Zhang,Jian Li,Qian Liu,Zhongsheng Sun,Jianing Zhong
Ten-eleven translocation methylcytosine dioxygenase 1 (TET1) is involved in multiple biological functions in cell development, differentiation, and transcriptional regulation. Tet1 deficient mice display the defects of murine glucose metabolism. However, the role of TET1 in metabolic homeostasis keeps unknown. Here, our finding demonstrates that hepatic TET1 physically interacts with silent information regulator T1 (SIRT1) via its C-terminal and activates its deacetylase activity, further regulating the acetylation-dependent cellular translocalization of transcriptional factors PGC-1α and FOXO1, resulting in the activation of hepatic gluconeogenic gene expression that includes PPARGC1A, G6PC, and SLC2A4. Importantly, the hepatic gluconeogenic gene activation program induced by fasting is inhibited in Tet1 heterozygous mice livers. The adenosine 5’-monophosphate-activated protein kinase (AMPK) activators metformin or AICAR—two compounds that mimic fasting—elevate hepatic gluconeogenic gene expression dependent on in turn activation of the AMPK-TET1-SIRT1 axis. Collectively, our study identifies TET1 as a SIRT1 coactivator and demonstrates that the AMPK-TET1-SIRT1 axis represents a potential mechanism or therapeutic target for glucose metabolism or metabolic diseases.
研究领域:
分子生物学
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代谢学
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药理学
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CURRENT NEUROVASCULAR RESEARCH
·
2022
·Vol. 19
·期 1
·61-72
·
IF 2.294
Xu Shu-Ying,Zeng Chun-Li,Ni Si-Ming,Peng Yong-Jun
Background: Acupuncture has been recommended as an alternative and complementary therapy for preventing and treating cerebral ischemia by the World Health Organization (WHO) for years. However, the mechanisms remain unclear. Accumulating evidence has shown that acupuncture can promote
angiogenesis to attenuate brain damage after ischemic stroke. In recent years, exosome- carried microRNAs (miRNAs) activated by acupuncture have proven effective in regulating pathological changes. We, therefore, investigated whether electro-acupuncture (EA) enhanced angiogenesis in cerebral
stroke via exosome-carried miR-210. Methods: We extracted and identified the exosomes from the serum of MCAO with EA treatment and injected them into MCAO rats for further observation. Simultaneously, miR-120 siRNA and HIF-1α inhibitor were transfected. Then, we evaluated the volume
of infarction, pathological changes, and expression levels of angiogenic related factors of each group of rats by TTC and HE staining, transmission electron microscope (TEM), western blot, and quantitative PCR (qPCR). Results: Compared with the MCAO group, EA-Exosome (EA-EXO) treatment
significantly decreased the infarct volume and the pathological damage, but miR-210 siRNA or HIF-1α inhibitor reversed the protective outcomes induced by EA-EXO. Moreover, EA-EXO treatment upregulated miR-210 and increased CD34, HIF-1α, VEGF, Notch1 protein, and mRNA expressions
compared to the MCAO group. MiR-210 siRNA or HIF-1α inhibitor treatments both down-regulated those angiogenic related proteins and mRNAs. Conclusion: EA treatment could activate the HIF-1α/VEGF/Notch 1 signal pathway to facilitate angiogenesis after ischemic stroke via exosomal
miR-210.
研究领域:
神经科学
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分子生物学
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中医药学
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中风研究
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Acta Biomaterialia
·
2026
·
IF 10.4
Jiakun Guo,Jintao Huang,Yan Wang,Juan Sun,Shang Liu,Chao Deng,Jian Lu,Zhiyuan Zhong
Transarterial chemoembolization (TACE) is a primary treatment option for unresectable hepatocellular carcinoma (HCC). Its clinical efficacy is, however, challenged by hypoxic and immunosuppressive tumor microenvironment. Herein, we report that absorbable microspheres (Asphere) with sustained co-delivery of hypoxia-inducible factor 1 (HIF-1) inhibitor, acriflavine (ACF), effectively reverse tumor hypoxia and boost TACE therapy of advanced HCC. Interestingly, Asphere demonstrates nearly quantitative loading of both epirubicin (EPI) and ACF within 1 min, while achieving sustained release of the dual drugs over 8 weeks. EPI/ACF-loaded Aspheres (EA@Asphere) greatly inhibit hypoxia-associated proteins and augment immunogenic cell death in HCC cells under hypoxic conditions, which in turn triggers maturation of dendritic cells (DCs) and secretion of pro-inflammatory cytokines. In H22 murine hepatoma model, EA@Asphere markedly boosts DC maturation, CD8 + T cell infiltration, and macrophage polarization from M2 to M1, achieving complete tumor regression in 2 out of 7 mice. EA@Asphere further blocks tumor vasculature in orthotopic VX2 liver tumor in rabbits, alleviates hypoxia, and suppresses tumor progression and metastasis. Thus, Asphere co-delivering HIF-1 inhibitors holds significant translational potential to boost TACE therapy in advanced HCC. Statement of significance This work introduces an approach to enhance transarterial chemoembolization (TACE) for advanced hepatocellular carcinoma (HCC) by co-delivering HIF-1 inhibitor acriflavine (ACF) and epirubicin (EPI) via absorbable microspheres (Asphere). Asphere demonstrates swift dual drug loading, sustained 8-week release, and simultaneous reversal of hypoxia and immunosuppression, addressing critical challenges of current TACE therapy. In preclinical studies, EA@Asphere significantly suppresses hypoxia-associated protein expression, enhances immunogenic cell death, promotes dendritic cell maturation, and reprograms tumor microenvironment, achieving significant inhibition of the tumor progression and metastasis. These findings offer transformative potential to improve clinical outcomes in advanced HCC, holding broad interest for researchers and clinicians in oncology and drug delivery.
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Chinese Medicine
·
2026
·Vol. 21
·期 1
·146
·
IF 7.4
Yang Junfa,Shu Min,Fang Hui,Yang Fan,Li Jiahe,Sun Yuansong,Li He,Xu Tao
Background Liver fibrosis is a representative scarring response that can ultimately lead to liver cancer. However, relevant antifibrotic drugs for the effective treatment of liver fibrosis in humans have not yet been identified. 6-Shogaol is derived from natural products and exhibits multiple biological activities, including anti-inflammatory and antioxidant properties; however, its efficacy and potential mechanism of action against liver fibrosis remains unclear. This study aimed to examine the anti-fibrotic properties and potential mechanisms of action of 6-Shogaol. Methods Two liver fibrosis mouse models (carbon tetrachloride (CCl 4 ) and bile duct ligation (BDL)) were constructed to evaluate the anti-fibrotic properties of 6-Shogaol in vivo . Transforming growth factor-β1 (TGF-β1)-induced human hepatic stellate cells (HSCs) LX-2 cells were used as in vitro models. Network pharmacology analysis was introduced to explore the key targets of 6-Shogaol regarding the mechanisms on liver fibrosis. Molecular docking, molecular dynamics simulations, drug affinity reactivity target stability (DARTS) and isothermal titration calorimetry (ITC) were used to detect the affinity and binding between 6-Shogaol and its target. Additionally, we invested the mechanism of 6-Shogaol through RNA sequencing combined with Western blotting, oxygen consumption rate (OCR), extracellular acidification rate (ECAR), immunofluorescence co-localization, histopathology, immunohistochemical staining and RT-qPCR. Results The results showed that 6-Shogaol remarkably alleviated CCl 4 - and BDL-induced liver fibrosis in mice, including observations of improved liver function, decreased activity of HSCs, and decreased extracellular matrix (ECM) deposition. In an in vitro model, 6-Shogaol suppressed TGF-β1-induced LX-2 activation. Mechanistically, RNA sequence analysis revealed that the effect of 6-Shogaol on liver fibrosis is linked to glycolytic reprogramming. 6-Shogaol suppressed HSCs glycolysis by decreasing glycolytic enzymes (HK2, PKM2, and GLUT1) and glycolytic metabolite levels (lactic acid and pyruvic acid). Furthermore, network pharmacology suggested HIF-1α as a potential 6-Shogaol target. Molecular docking, molecular dynamics simulations, DARTS, and ITC confirmed that 6-Shogaol could directly bind to HIF-1α. Interestingly, we demonstrated that HIF-1α knockout significantly inhibited HSCs glycolysis and activation, whereas the overexpression of HIF-1α increased HSCs glycolysis and activation. Moreover, specific knockout of HIF-1α did not enhance the suppressive effect of 6-Shogaol on HSCs activation or fibrosis-associated protein expression in vivo . Conclusion These findings showed that 6-Shogaol ameliorated liver fibrosis by modulating the expression of HIF-1α associated with glycolysis reprogramming and validate 6-Shogaol as a promising therapeutic strategy for liver fibrosis. Graphical
The alternative text for this image may have been generated using AI.
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JOURNAL OF NANOBIOTECHNOLOGY
·
2026
·Vol. 24
·期 1
·391
·
IF 15
Chen Ying,Peng De-Wei,Jiang Sheng-Rui,Shao Qian-Chun,Zhang Yi-Cong,Chi Zai-Long
Objective Retinal neovascularization is a leading cause of irreversible blindness worldwide. Chinese herbal medicines have unique therapeutic properties, such as antioxidant, anti-inflammatory, and neuroprotective effects. This study aims to investigate the therapeutic effects and underlying mechanisms of the Chinese medicinal herb Curcuma longa -derived extracellular vesicle-like particles (CL-EVLPs) in a mouse model of retinal neovascularization. Methods CL-EVLPs were extracted from fresh Curcuma longa rhizomes through differential centrifugation and sucrose density gradient centrifugation and characterized by transmission electron microscopy (TEM), and nanoparticle tracking analysis (NTA), and western blot analysis of EVLP-associated protein markers. CL-EVLPs were administered to oxygen-induced retinopathy (OIR) model mice via intravitreal injection. The therapeutic effects were evaluated using retinal flat mounts, fundus fluorescein angiography (FFA), and reactive oxygen species (ROS) staining. The underlying molecular mechanisms were explored through metabolomics, transcriptomics, and network pharmacology analyses, and the expression levels of relevant factors were quantified using real-time polymerase chain reaction (PCR) or western blotting. In vitro experiments were conducted using human retinal microvascular endothelial cells (hRMECs) and BV2 microglia. Results CL-EVLPs exhibited typical EV-like characteristics, including a saucer‑ or cup‑shaped morphology, a mean diameter of 140.7 nm, and enrichment of the EV‑related protein ARF1. CL-EVLPs effectively inhibited neovascularization in the OIR model, as evidenced by reduced pathological neovascular tufts and avascular zones and decreased vascular permeability and tortuosity. Furthermore, CL-EVLPs significantly decreased ROS production in the retinas of OIR mice. Mechanistically, CL-EVLPs inhibited HIF-1α/VEGF/ERK signaling and activated the NRF2/HO-1 antioxidant pathway. In vitro experiments confirmed that CL-EVLPs inhibited endothelial cell viability and alleviated oxidative stress in microglia. Integrated network pharmacology and metabolomics analyses proved that the cargo molecules of CL-EVLPs, such as curcumin and its derivatives, auraptene, and triptophenolide, exhibit regulatory antioxidant and anti-inflammatory effects and modulate multiple signaling pathways associated with retinal neovascular diseases. Conclusion CL-EVLPs effectively suppress retinal neovascularization by inhibiting the HIF-1α/VEGFA/ERK axis and activating the NRF2/HO-1 pathway. This study suggests that CL-EVLPs, as a multitarget therapeutic strategy, hold promising clinical translational potential for the treatment of retinal neovascular diseases. Graphical abstract The alternative text for this image may have been generated using AI.
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Antioxidants
·
2026
·Vol. 15
·期 5
·652
·
IF 8.2
Haoyang Dai,Qinqin Zhang,Pei Chen,Suiqing Chen
The pathogenesis of acute liver injury (ALI) involves the loss of hepatic detoxification function, massive death of liver parenchymal cells within a short period, and excessive inflammatory responses. Studies have shown that Esculetin (Esc) possesses potent anti-inflammatory, antioxidant, and anti-tumor properties. In this study, we investigate whether Esc has a protective effect against ALI in mice and its potential mechanism. Esculetin markedly decreased ROS, MitoSOX, and apoptosis levels in AML12 cells and restored MMP. H&E staining demonstrated that Esc alleviated hepatic histopathological injury, and its intervention reduced serum ALT and AST levels. Moreover, Esc diminished ROS and apoptosis levels in the liver. Hepatic proteomic profiling identified the AMPK signaling pathway. Esc reduced the protein levels of p-AMPK/AMPK, PGC-1α, p-SIRT1/SIRT1, and BAX and upregulated the levels of Bcl-2 in liver tissue. Concomitantly, we added inhibitor Compound C (CC) to the AML12 cells to assess whether Esc acted through the AMPK pathway. The results showed that CC exacerbated the degree of liver injury, whereas Esc was able to reverse these phenomena, thus exerting an anti-liver injury effect. These findings provide mechanistic insights into the protective effects of Esc against ALI and support its potential as a therapeutic candidate for ALI.
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Journal of Ginseng Research
·
2026
·
IF 7.5
Chongyang Zhang,Yuning chen,Wei Liu,Rong-chang Chen
Background Ginsenoside RK3 was first isolated from heat-processed ginseng. Our study aimed to explore the underlying mechanism of RK3 in combating isoproterenol (ISO)-induced heart failure (HF) in mice. Methods HF was induced in mice by subcutaneous injection of ISO (80mg/kg/d) 1 hour after intraperitoneal administration of RK3 (10 and 20 mg/kg/d) for 28 days. Cardiac function and heart injury were assessed and comprehensive metabolic alterations in the serum were profiled. Western blot analysis was conducted. In vitro experiments, H9c2 cells were pretreated with RK3 before hypoxia exposure. Cell viability and LDH release were determined. Results In vivo experiments demonstrated that RK3 treatment prevented ISO-induced myocardial damage. Additionally, RK3 reduced serum inflammatory factors and levels of myocardial fibrosis. Metabolomics data indicated that RK3 mitigated the ISO-induced increase in glycolytic intermediates, including 3-phenyllactic acid, D-glucose-6-phosphate, D-glucose-1-phosphate, and D-fructose-6-phosphate and the decrease in intermediates of the TCA cycle, such as citric acid. Treatment with RK3 also inhibited the expression of MCT4 while enhancing the expression of MPC2, PGC-1α, Sirt1, and p-AMPK in heart tissues. In vitro investigations revealed that the protective effect of RK3 on H9c2 cells was abolished by AMPK inhibition. Conclusions Our study, for the first time, confirmed that RK3 protects against ISO-induced HF, which may be related to the restoration of balance in the pyruvate-lactate axis through the activation of the AMPK/Sirt1/PGC1 pathway.
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CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY
·
2026
·Vol. 53
·期 9
·e70153
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IF 2.5
Renchuang Cao,Qingying Meng,Gengyuan Li,Shumei Yuan,Chunmei Li,Xin Zhao,Dongmei Zhang
Heat shock factor 2 (HSF2) and hypoxia‐inducible factor 1α are activated by angiotensin II (ANGII) in cardiomyocytes. The endoplasmic reticulum (ER) stress plays a critical role in cardiac hypertrophy. Moreover, HIF‐1α is known to be regulated by HSF2 in tumour cells. In this study, we hypothesised and clarified whether HSF2 trans‐activated HIF‐1α through initiation of ER stress in hypertrophic cardiomyocytes. Myocardial hypertrophy was induced by the treatment of ANGII. Expression of the gene or protein was assessed by applying RT‐PCR, WB, ICC and IHC. Luciferase and CHIP were applied to detect the transcription of HIF‐1α by HSF2. Both in vitro and in vivo, the expression of HIF‐1α, ER stress markers and HSF2 was increased in ANGII‐treated hypertrophic cardiomyocytes. Blocking ER stress suppressed the expression of HSF2 and HIF‐1α in ANGII‐treated cardiomyocytes. Silencing HSF2 inhibited HIF‐1α, thereby reducing hypertrophy but had no effect on ER stress. Similarly, silencing HIF‐1α reduced hypertrophy without affecting ER stress or HSF2 expression. HSF2 transcriptionally activated HIF‐1α. We concluded that ER stress induced by ANGII activates HSF2, which then trans‐activates HIF‐1α, promoting cardiac hypertrophy.
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