Biliverdin modulates the Nrf2/A20/eEF1A2 axis to alleviate cerebral ischemia-reperfusion injury by inhibiting pyroptosis DOI Open Access

Wenya Bai,

Siying Huo,

Guilin Zhou

и другие.

Biomedicine & Pharmacotherapy, Год журнала: 2023, Номер 165, С. 115057 - 115057

Опубликована: Июль 1, 2023

This study aimed to examine whether Biliverdin, which is a common metabolite of haem, can alleviate cerebral ischemia reperfusion injury (CIRI) by inhibiting pyroptosis. Here, CIRI was induced middle artery occlusion-reperfusion (MCAO/R) in C57BL/6 J mice and modelled oxygen glucose deprivation/reoxygenation (OGD/R) HT22 cells, it treated with or without Biliverdin. The spatiotemporal expression GSDMD-N infarction volumes were assessed immunofluorescence staining triphenyltetrazolium chloride (TTC), respectively. NLRP3/Caspase-1/GSDMD pathway, central the pyroptosis process, as well Nrf2, A20, eEF1A2 determined Western-blots. interactions verified using dual-luciferase reporter assays, chromatin immunoprecipitation, co-immunoprecipitation. Additionally, role Nrf2/A20/eEF1A2 axis modulating neuroprotective properties Biliverdin investigated A20 gene interference (overexpression and/or silencing). 40 mg/kg could significantly both vivo vitro, promoted activation elevated expression, but decreased expression. Nrf2 bind promoter thereby transcriptionally regulating A20. furthermore interacted through its ZnF4 domain ubiquitinate degrade it, leading downregulation eEF1A2. Our studies have also demonstrated that either knock-down over-expression blunted protective effect Rescue experiments further confirmed regulate NF-κB pathway via axis. In summary, our demonstrates ameliorates findings help identify novel therapeutic targets for treatment CIRI.

Язык: Английский

Self‐Destructive Copper Carriers Induce Pyroptosis and Cuproptosis for Efficient Tumor Immunotherapy Against Dormant and Recurrent Tumors DOI Open Access

Luying Qiao,

Guo‐Qing Zhu, Tengfei Jiang

и другие.

Advanced Materials, Год журнала: 2023, Номер 36(8)

Опубликована: Окт. 11, 2023

Abstract Activating the strong immune system is a key initiative to counteract dormant tumors and prevent recurrence. Herein, self‐destructive multienzymatically active copper‐quinone‐GOx nanoparticles (abbreviated as CQG NPs) have been designed induce harmonious balanced pyroptosis cuproptosis using “Tai Chi mindset” awaken response for suppressing recurrent tumors. This cleverly material can disrupt antioxidant defense mechanism of tumor cells by inhibiting nuclear factor‐erythroid 2‐related factor 2 (NRF2)‐quinone oxidoreductase 1 (NQO1) signaling pathway. Furthermore, combined with its excellent multienzyme activity, it activates NOD‐like receptor protein 3 (NLRP3)‐mediated pyroptosis. Meanwhile, be triggered copper ions released from disintegration NPs sensitivity cancer enhanced through depletion endogenous chelators via Michael addition reaction between glutathione (GSH) quinone ligand, oxygen production catalase‐like reaction, starvation‐induced glucose deficiency. More importantly, NPs‐induced promote immunosuppressive microenvironment (TME) remodeling, enhance infiltration into tumor, activate robust systemic immunity. Collectively, this study provides new strategy resist dormancy, recurrence, improve clinical prognosis

Язык: Английский

Процитировано

83

Signaling pathways and potential therapeutic targets in acute respiratory distress syndrome (ARDS) DOI Creative Commons
Qianrui Huang, Yue Le, Shusheng Li

и другие.

Respiratory Research, Год журнала: 2024, Номер 25(1)

Опубликована: Янв. 13, 2024

Abstract Acute respiratory distress syndrome (ARDS) is a common condition associated with critically ill patients, characterized by bilateral chest radiographical opacities refractory hypoxemia due to noncardiogenic pulmonary edema. Despite significant advances, the mortality of ARDS remains unacceptably high, and there are still no effective targeted pharmacotherapeutic agents. With outbreak coronavirus disease 19 worldwide, has increased correspondingly. Comprehending pathophysiology underlying molecular mechanisms may thus be essential developing therapeutic strategies reducing mortality. To facilitate further understanding its pathogenesis exploring novel therapeutics, this review provides comprehensive information from presents therapeutics. We first describe that involve dysregulated inflammation, alveolar-capillary barrier dysfunction, impaired alveolar fluid clearance oxidative stress. Next, we summarize signaling pathways related above four aspects pathophysiology, along latest research progress. Finally, discuss emerging show exciting promise in ARDS, including several pharmacologic therapies, microRNA-based therapies mesenchymal stromal cell highlighting pathophysiological basis influences on signal transduction for their use.

Язык: Английский

Процитировано

22

S100A9-/- alleviates LPS-induced acute lung injury by regulating M1 macrophage polarization and inhibiting pyroptosis via the TLR4/MyD88/NFκB signaling axis DOI Open Access
Gong Chen,

Ji Ma,

Ya Deng

и другие.

Biomedicine & Pharmacotherapy, Год журнала: 2024, Номер 172, С. 116233 - 116233

Опубликована: Фев. 2, 2024

Acute lung injury (ALI) is characterized by pulmonary diffusion abnormalities that may progress to multiple-organ failure in severe cases. There are limited effective treatments for ALI, which makes the search new therapeutic avenues critically important. Macrophages play a pivotal role pathogenesis of ALI. The degree macrophage polarization closely related severity and prognosis S100A9 promotes M1 macrophages. present study assessed effects S100A9-gene deficiency on acute injury. Our cohort showed plasma S100A8/A9 levels had significant diagnostic value pediatric pneumonia primarily correlated with monocyte-macrophages neutrophils. We established lipopolysaccharide (LPS)-induced mouse model demonstrated knockout gene mitigated inflammation suppressing secretion pro-inflammatory cytokines, reducing number inflammatory cells bronchoalveolar lavage fluid, inhibiting cell apoptosis, ameliorated mice. vitro vivo mechanistic studies inhibited reduced chemotactic factors cytokines TLR4/MyD88/NF-κB signaling pathway reversing expression NLRP3 pyroptosis pathway, death. In conclusion, alleviated LPS-induced via TLR4/MyD88/NFκB suggests potential strategy treatment

Язык: Английский

Процитировано

19

NLRP3 Inflammasome: A key contributor to the inflammation formation DOI

Wen-Juan Zhang,

Kejun Li,

Lan Yi

и другие.

Food and Chemical Toxicology, Год журнала: 2023, Номер 174, С. 113683 - 113683

Опубликована: Фев. 20, 2023

Язык: Английский

Процитировано

37

The role of neutrophil extracellular traps in sepsis and sepsis-related acute lung injury DOI

Shujing Zou,

Hongyu Jie, Xinai Han

и другие.

International Immunopharmacology, Год журнала: 2023, Номер 124, С. 110436 - 110436

Опубликована: Сен. 7, 2023

Язык: Английский

Процитировано

32

Baicalin inhibits influenza A (H1N1)‐induced pyroptosis of lung alveolar epithelial cells via caspase‐3/GSDME pathway DOI

Zhenqiao Wei,

Rui Gao, Zhen Sun

и другие.

Journal of Medical Virology, Год журнала: 2023, Номер 95(5)

Опубликована: Май 1, 2023

Abstract Baicalin (7‐ d ‐glucuronic acid‐5, 6‐dihydroxyflavone) derived from the root of Scutellaria baicalensis used as Traditional Chinese Medicine (TCM) has been revealed to exert potential antiviral activity via various pathways, while molecular mechanisms have not fully understood. Pyroptosis, an inflammatory form programmed cell death (PCD), is reported play a crucial role in host fate during viral infection. In this study, transcriptome analysis mice lung tissue reveals that baicalin reverses alterations mRNA levels PCD‐associated genes upon H1N1 challenge, with concomitant decrease population H1N1‐induced propidium iodide (PI) + and Annexin Ⅴ cells. Intriguingly, we find contributes survival infected alveolar epithelial cells partly through its inhibition pyroptosis, which manifested by reduced bubble‐like protrusion lactate dehydrogenase (LDH) release. Moreover, antipyroptosis effect response infection found be mediated repression on caspase‐3/Gasdermin E (GSDME) pathway. Cleaved caspase‐3 N‐terminal fragment GSDME (GSDME‐N) are detected H1N1‐infected lines tissues, markedly reversed treatment. Furthermore, caspase‐3/GSDME pathway inhibitor or siRNA exerts equal treatment A549 BEAS‐2B cells, indicating pivotal activities baicalin. Conclusively, for first time, demonstrate could effectively suppress pyroptosis both vitro vivo.

Язык: Английский

Процитировано

25

Targeting ferroptosis using Chinese herbal compounds to treat respiratory diseases DOI Creative Commons

Mengjiao Xu,

Di Zhang, Jun Yan

и другие.

Phytomedicine, Год журнала: 2024, Номер 130, С. 155738 - 155738

Опубликована: Июнь 1, 2024

Respiratory diseases pose a grave threat to human life. Therefore, understanding their pathogenesis and therapeutic strategy is important. Ferroptosis novel type of iron-dependent programmed cell death, distinct from apoptosis, necroptosis, autophagy, characterised by iron, reactive oxygen species, lipid peroxide accumulation, as well glutathione (GSH) depletion GSH peroxidase 4 (GPX4) inactivation. A close association between ferroptosis the onset progression respiratory diseases, including chronic obstructive pulmonary disease, acute lung injury, bronchial asthma, fibrosis, cancer, has been reported. Recent studies have shown that traditional Chinese medicine (TCM) compounds exhibit unique advantages in treatment owing natural properties potential efficacy. These can effectively regulate modulating several key signalling pathways such system Xc

Язык: Английский

Процитировано

11

Advances in nanomaterial-targeted treatment of acute lung injury after burns DOI Creative Commons
Shuo Zhang, Xinyu Zhao,

Yuhao Xue

и другие.

Journal of Nanobiotechnology, Год журнала: 2024, Номер 22(1)

Опубликована: Июнь 18, 2024

Abstract Acute lung injury ( ALI ) is a common complication in patients with severe burns and has complex pathogenesis high morbidity mortality rates. A variety of drugs have been identified the clinic for treatment ALI, but they toxic side effects caused by easy degradation body distribution throughout body. In recent years, as understanding mechanism underlying improved, scholars developed new nanomaterials that can be safely effectively targeted ALI. Most these methods involve such lipids, organic polymers, peptides, extracellular vesicles or cell membranes, inorganic nanoparticles other nanomaterials, which are to reach tissues perform their functions through active targeting passive targeting, process involves cells organelles. this review, first, mechanisms pathophysiological features occurrence after burn reviewed, potential therapeutic targets summarized, existing classified, possible problems challenges discussed provide reference development

Язык: Английский

Процитировано

11

Advances on adaptive immune responses affected by infectious bursal disease virus in chicken DOI Creative Commons
Tao Zhang,

Suyan Wang,

Yongzhen Liu

и другие.

Frontiers in Immunology, Год журнала: 2024, Номер 14

Опубликована: Янв. 10, 2024

Infectious bursal disease (IBD) is an acute, highly infectious, and immunosuppressive caused by the infectious virus (IBDV), which interferes with immune system, causes hypoimmunity seriously threatens healthy development of poultry industry. Adaptive response, important defense line host resistance to pathogen infection, host-specific response mainly mediated T B lymphocytes. As in poultry, IBDV infection closely related injury adaptive system. In this review, we focus on recent advances influenced especially damage organs, as well effect humoral cellular hoping provide a theoretical basis for further exploration molecular mechanism immunosuppression induced establishment novel prevention control measures IBD.

Язык: Английский

Процитировано

9

LL-37 improves sepsis-induced acute lung injury by suppressing pyroptosis in alveolar epithelial cells DOI
Quanzhen Wang, Wei Wen,

Lei Zhou

и другие.

International Immunopharmacology, Год журнала: 2024, Номер 129, С. 111580 - 111580

Опубликована: Фев. 3, 2024

Язык: Английский

Процитировано

9