PHYTOMEDICINE
·
2025
·
IF 8.3
Simin Tian,Guang Xin,Kun Zhang,Ao Wen,Xiuxiang Yu,Chengyang Ni,Yijiang Liu,Xiaojuan Li,Yu Cao,Wen Huang
Background Acute pancreatitis (AP) is an inflammatory disease of the pancreas marked by inflammation and acinar cell necrosis. Scutellariae Barbata (S. Barbata), a traditional Chinese herb for inflammation, has unclear efficacy for AP. Purpose This study examined the mechanism of eriodictyol, an active component of S. Barbata decoction, targeting pancreatic necrosis and inflammation for the first time. Study Design This study firstly evaluated the pharmacological effects of S. Barbata on AP. Transcriptomic analysis and pharmacological screening were performed to identify essential genes linked to pancreatic necrosis and specific bioactive compounds in S. Barbata. These candidates underwent thorough validation with multiple assays. Our findings strongly demonstrate effectiveness of S. Barbata in combating pancreatic necrosis and reveal the underlying mechanisms involved. Methods Animal experiments were conducted to assess the effects of S. Barbata on AP. Analysis of bulk and single-cell RNA-seq data identified PANoptosis. The protein-protein interaction network and Cytoscape were used to identify AP targets based on PANoptosis. The ConnectivityMap database was used to filter potential compounds from S. Barbatae based on specific targets. After quantifying eriodictyol, its binding to ZBP1 was confirmed through molecular docking, dynamic simulation, cellular thermal shift assay, mtDNA analysis, and ZBP1 overexpression in 266-6 cells. Experiments in vivo and in vitro assessed the effects of eriodictyol on AP. Results S. Barbata decoction reduced pancreatic inflammation and necrosis. Gene Set Enrichment Analysis of PANoptosis revealed that Zbp1, Nlpr3, Ripk1, Casp8, Gsdmd , and Mlkl are ZBP1-dependent targets for AP. Eriodictyol, the active compound in S. Barbata showed a strong affinity for ZBP1. Eriodictyol may enhance pancreatic conditions and reduce ZBP1-dependent protein expression, with minimal impact on mtDNA levels. Conclusion This study broadened the traditional use of S. Barbata suggested eriodictyol as a potential AP treatment candidate via ZBP1-dependent signaling.
研究领域:
药理学
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分子生物学
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中医药学
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DOI
PubMed
高影响因子
Discover Oncology
·
2024
·Vol. 15
·期 1
·1-13
·
IF 2.8
Yin Xiaoyan,Zhang Haizhong,Wang Jingmiao,Bian Yanrui,Jia Qiaojing,Yang Zhichao,Shan Chunguang
In this study, we investigated the role of the newly discovered lncRNA FLJ20021 in laryngeal cancer (LC) and its resistance to cisplatin treatment. We initially observed elevated lncRNA FLJ20021 levels in cisplatin-resistant LC cells (Hep-2/R). To explore its function, we transfected lncRNA FLJ20021 and cyclin-dependent kinase 1 (CDK1) into Hep-2/R cells, assessing their impact on cisplatin sensitivity and PANoptosis. Silencing lncRNA FLJ20021 effectively reduced cisplatin resistance and induced PANoptosis in Hep-2/R cells. Mechanistically, lncRNA FLJ20021 primarily localized in the nucleus and interacted with CDK1 mRNA, thereby enhancing its transcriptional stability. CDK1, in turn, promoted panapoptosis in a ZBP1-dependent manner, which helped overcome cisplatin resistance in Hep-2/R cells. This study suggests that targeting lncRNA FLJ20021 can be a promising approach to combat cisplatin resistance in laryngeal cancer by regulating CDK1 and promoting PANoptosis via the ZBP1 pathway. These findings open up possibilities for lncRNA-based therapies in the context of laryngeal cancer.
研究领域:
肿瘤学
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分子生物学
·
癌症治疗
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DOI
PubMed
高影响因子
PHYSIOLOGICAL RESEARCH
·
2024
·Vol. 73
·期 5
·779
·
IF 1.9
Lu BAI,Qian CHEN,Yanqing LI,Fen WU,Mingzhe JIN,Yuhong CHEN,Xu TENG,Sheng JIN,Huanfang FAN,Yuming WU
Trimethylamine N-oxide (TMAO), a bioactive metabolite of gut microbes, plays a pivotal role in the pathogenesis of kidney diseases by activating programmed cell death (PCD) pathways. However, whether trimethylamine (TMA) contributes to chronic kidney injury and which kind of PCD is involved in TMA-induced chronic kidney injury has not been previously evaluated. To observe the effect of TMA, male C57BL/6J mice were randomly divided into two groups: the Control group and the TMA group. The mice in the TMA group were intraperitoneally injected with 100 μmol/kg/day TMA for three months, whereas the mice in the Control group were injected with normal saline for the same period. After three months, plasma creatinine and blood urea nitrogen levels, indicators of kidney function, increased significantly in the TMA group as compared with those in the Control group. Furthermore, Masson staining assay showed that TMA treatment led to a larger area of fibrosis than the Control group. TMA treatment did not change the Bax/Bcl-2 ratio, RIP1, RIP3 and MLKL phosphorylation, or iron and malondialdehyde levels in kidney tissues, indicating that apoptosis, ferroptosis and necroptosis were not involved in TMA-induced chronic kidney injury. However, compared with the Control group, TMA treatment significantly upregulated NLRP3, Caspase-1, IL-1β, cleaved-Caspase 8, Caspase-8, and ZBP1 protein expression in kidney tissues. These results indicated that the ZBP1-NLRP3 inflammasome pathway was involved in TMA-induced chronic kidney injury. In conclusion, our studies revealed that the ZBP1-NLRP3 inflammasome may take part in the progression of TMA induced chronic kidney injury.
研究领域:
肾脏病学
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免疫学
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微生物学
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分子生物学
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病理学
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DOI
高影响因子
ACTA PHARMACOLOGICA SINICA
·
2024
·
IF 6.9
You Yi-ping,Yan Liang,Ke Hua-yu,Li Ya-ping,Shi Zi-jian,Zhou Zhi-ya,Yang Hai-yan,Yuan Tao,Gan Ying-qing,Lu Na,Xu Li-hui,Hu Bo,Ou-Yang Dong-yun,Zha Qing-bing,He Xian-hui
PANoptosis is an emerging form of regulated cell death (RCD) characterized by simultaneous activation of pyroptotic, apoptotic, and necroptotic signaling that not only participates in pathologies of inflammatory diseases but also has a critical role against pathogenic infections. Targeting PANoptosis represents a promising therapeutic strategy for related inflammatory diseases, but identification of inhibitors for PANoptosis remains an unmet demand. Baicalin (黄芩苷) is an active flavonoid isolated from Scutellaria baicalensis Georgi (Huangqin), a traditional Chinese medicinal herb used for heat-clearing and detoxifying. Numerous studies suggest that baicalin possesses inhibitory activities on various forms of RCD including apoptosis/secondary necrosis, pyroptosis, and necroptosis, thereby mitigating inflammatory responses. In this study we investigated the effects of baicalin on PANoptosis in macrophage cellular models. Primary macrophages (BMDMs) or J774A.1 macrophage cells were treated with 5Z-7-oxozeaenol (OXO, an inhibitor for TAK1) in combination with TNF-α or LPS. We showed that OXO plus TNF-α or LPS induced robust lytic cell death, which was dose-dependently inhibited by baicalin (50−200 μM). We demonstrated that PANoptosis induction was accompanied by overt mitochondrial injury, mitochondrial DNA (mtDNA) release and Z-DNA formation. Z-DNA was formed from cytosolic oxidized mtDNA. Both oxidized mtDNA and mitochondrial Z-DNA puncta were co-localized with the PANoptosome (including ZBP1, RIPK3, ASC, and caspase-8), a platform for mediating PANoptosis. Intriguingly, baicalin not only prevented mitochondrial injury but also blocked mtDNA release, Z-DNA formation and PANoptosome assembly. Knockdown of ZBP1 markedly decreased PANoptotic cell death. In a mouse model of hemophagocytic lymphohistiocytosis (HLH), administration of baicalin (200 mg/kg, i.g., for 4 times) significantly mitigated lung and liver injury and reduced levels of serum TNF-α and IFN-γ, concomitant with decreased levels of PANoptosis hallmarks in these organs. Baicalin also abrogated the hallmarks of PANoptosis in liver-resident macrophages (Kupffer cells) in HLH mice. Collectively, our results demonstrate that baicalin inhibits PANoptosis in macrophages by blocking mitochondrial Z-DNA formation and ZBP1-PANoptosome assembly, thus conferring protection against inflammatory diseases. PANoptosis is a form of regulated cell death displaying simultaneous activation of pyroptotic, apoptotic, and necroptotic signaling. This study shows that induction of PANoptosis is linked to mitochondrial dysfunction and mitochondrial Z-DNA formation. Baicalin inhibits PANoptosis in macrophages in vitro via blocking mitochondrial dysfunction and the mitochondrial Z-DNA formation and thereby impeding the assembly of ZBP1-associated PANoptosome. In a mouse model of hemophagocytic lymphohistiocytosis (HLH), baicalin inhibits the activation of PANoptotic signaling in liver-resident macrophages (Kupffer cells) in vivo, thus mitigating systemic inflammation and multiple organ injury in mice.
研究领域:
免疫学
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细胞生物学
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药理学
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炎症
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调控性细胞死亡
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DOI
PubMed
高影响因子
MOLECULAR CELL
·
2025
·
IF 16.6
Jianfeng He,Yongyi Zhu,Zichao Tian,Mengqin Liu,Anmin Gao,Wangmi Fu,Fei Lu,Yutong Sun,Yajun Guo,Rongqing Pan,Yuchen Ji,Jianxiang Chen,Huasong Lu,Juan Lin,Xingguo Liang,Chun Kim,Chun Zhou,Huipeng Jiao
Z-DNA-binding protein 1 (ZBP1; also known as DAI or DLM-1) regulates cell death and inflammation by sensing left-handed double-helical nucleic acids, including Z-RNA and Z-DNA. However, the physiological conditions that generate Z-form nucleic acids (Z-NAs) and activate ZBP1-dependent signaling pathways remain largely elusive. In this study, we developed a probe, Zα-mFc, that specifically detected both Z-DNA and Z-RNA. Utilizing this probe, we discovered that inhibiting spliceosome causes nuclear accumulation of Z-RNA:DNA hybrids, which are sensed by ZBP1 via its Zα domains, triggering apoptosis and necroptosis in mammalian cells. Furthermore, we solved crystal structures of the human or mouse Zα1 domain complexed with a 6-bp RNA:DNA hybrid, revealing that the RNA:DNA hybrid adopts a left-handed conformation. Our findings demonstrate that the spliceosome acts as a checkpoint preventing accumulation of Z-RNA:DNA hybrids, which potentially function as endogenous ligands activating ZBP1-dependent cell death pathways.
研究领域:
分子生物学
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免疫学
·
细胞生物学
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DOI
PubMed
高影响因子
PHYSIOLOGICAL RESEARCH
·
2026
·Vol. 75
·期 1
·89
·
IF 2.8
Qian CHEN,Zhaoxu QIU,Yaobo ZHAO,Lu BAI,Yuhong CHEN,Sheng JIN,Fenfen MA,Jing DAI
The present study was aimed to investigate whether trimethylamine-N-oxide (TMAO) contributed to kidney aging by activating necroptosis. Male C57BL/6J mice were randomly divided into Control group (3 months old) and Old group (18 months old), compared to 3-month-old controls, 18-month-old male C57BL/6J mice showed significant increases in plasma creatinine (Cre) and blood urea nitrogen (BUN) ( P <0.05), enhanced renal fibrosis ( P <0.001), elevated plasma TMAO ( P <0.01), and upregulation of senescence markers p53, p21, and p16 ( P <0.05, P <0.01, and P <0.001, respectively). In order to investigate the effects of TMAO on kidney aging, the mice were intraperitoneally injected with TMAO for one to three months, mice showed time-dependent increases in Cre and BUN ( P <0.05, respectively), progressive fibrosis, and gradual upregulation of senescence markers, ZBP1, and phosphorylation of RIPK3 and MLKL ( P <0.05, respectively). In addition, three months of DMB treatment (inhibitor for TMAO formation) significantly reduced the plasma Cre and BUN levels ( P <0.001 and P <0.05), downregulated the senescence markers expression, and improved kidney fibrosis ( P <0.001 or P <0.05, respectively). In conclusion, our studies revealed that TMAO induced kidney aging by activating ZBP1-mediated necroptosis. Moreover, the inhibition of TMAO generation might be a potential treatment for kidney aging.
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DOI
PubMed
高影响因子
PHYSIOLOGICAL RESEARCH
·
2026
·
IF 2.8
Q Chen,Z Qiu,Y Zhao,L Bai,Y Chan,S Jin,F Ma,J Dai
The present study was aimed to investigate whether trimethylamine-N-oxide (TMAO) contributed to kidney aging by activating necroptosis. Male C57BL/6J mice were randomly divided into Control group (3 months old) and Old group (18 months old), compared to 3-month-old controls, 18-month-old male C57BL/6J mice showed significant increases in plasma creatinine (Cre) and blood urea nitrogen (BUN) (P<0.05), enhanced renal fibrosis (P<0.001), elevated plasma TMAO (P<0.01), and upregulation of senescence markers p53, p21, and p16 (P<0.05, P<0.01, and P<0.001, respectively). In order to investigate the effects of TMAO on kidney aging, the mice were intraperitoneally injected with TMAO for one to three months, mice showed time-dependent increases in Cre and BUN (P<0.05, respectively), progressive fibrosis, and gradual upregulation of senescence markers, ZBP1, and phosphorylation of RIPK3 and MLKL (P<0.05, respectively). In addition, three months of DMB treatment (inhibitor for TMAO formation) significantly reduced the plasma Cre and BUN levels (P<0.001 and P<0.05), downregulated the senescence markers expression, and improved kidney fibrosis (P<0.001 or P<0.05, respectively). In conclusion, our studies revealed that TMAO induced kidney aging by activating ZBP1-mediated necroptosis. Moreover, the inhibition of TMAO generation might be a potential treatment for kidney aging. Key words Kidney aging " Trimethylamine-N-oxide " ZBP1 " Necroptosis " DMB.
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PubMed
高影响因子
EXPERIMENTAL AND MOLECULAR MEDICINE
·
2025
·
IF 12.9
Wu Jin,Guo Zixiang,Wang Long,Shen Yue,Li Xiang,Zhang Zhewei,Han Xiao,Zhang Jianlan,Cai Kunzhan,Tang Chunbo
Periodontitis is an oral immunoinflammatory disease, and macrophages play a crucial role in its pathophysiology. However, macrophage death during antibacterial activities will exacerbate inflammation and tissue damage. Porphyromonas gingivalis is a major constituent of subgingival biofilm plaques in periodontitis, but the effects and precise molecular mechanisms by which it triggers macrophage death remain unknown. Here we found that P. gingivalis infection notably activated multiple death pathways in bone-marrow-derived macrophages, including pyroptosis, apoptosis and necrosis. Furthermore, using RNA sequencing, we identified that P. gingivalis infection markedly increased the expression of Z-DNA binding protein 1 (Zbp1) in bone-marrow-derived macrophages. Initially identified as an interferon-induced tumor-associated protein, Zbp1 serves as an upstream sensor that regulates cell death by activating PANoptosis. Mechanistically, P. gingivalis induced a mitochondrial stress response, prompting the release of mitochondrial DNA. This mitochondrial DNA then interacted with Zbp1, consequently augmenting its downstream PANoptosis signals. In addition, P. gingivalis stimulated macrophage Zbp1 expression through the Tlr2/4–JNK–Stat3/5 pathway, exacerbating macrophage death. Importantly, blocking the biosynthesis of endogenous Zbp1 by pharmacological delivery with microneedles improved the survival of P. gingivalis -infected macrophages and inhibited periodontal tissue destruction. These findings highlight Zbp1 as a potential therapeutic target for P. gingivalis -induced periodontitis.
研究领域:
免疫学
·
口腔医学
·
分子生物学
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DOI
PubMed
高影响因子
BIOMATERIALS
·
2025
·
IF 12.9
Derui Xu,Tong Xu,Yunxiang Zhang,Yanjun Su,Xinmiao Hou,Yating Cui,Qian Liu,Lingxia Liu,Xiaotao Zhou,Haixu Xu,Xinghua Jin,Xichuan Li
Tumor immune microenvironment reconstruction and regulated cell death promotion synergistically enhance treatment outcomes in immunosuppressive non-small-cell lung cancer (NSCLC). PANoptosis, a newly identified form of immunogenic cell death that integrates the essential molecular components of pyroptosis, apoptosis, and necroptosis, elicits robust antitumor immunity via damage-associated molecular pattern (DAMP)-mediated immune activation. Nevertheless, strategies to induce PANoptosis remain underexplored, presenting a critical gap in leveraging its therapeutic potential. Herein, we engineered a multifunctional nanoreactor (Bi@SiO 2 @COP@AQ4N&PTX@hybrid-membrane, BSCAPM) as a PANoptosis inducer by integrating photothermal, photodynamic, chemotherapy, and SiO 2 -mediated biological effects. The nanoreactor features a bismuth-based core for photothermal functionality, in conjunction with a SiO 2 layer and a drug-loaded covalent organic polymer (COP) nanoplatform that synergistically disrupts mitochondrial homeostasis. In addition, the bioactive nanoparticles mediate co-delivery of paclitaxel and phenoxyanthraquinone, concurrently compromising nuclear DNA superhelical integrity and triggering profound mitochondrial stress culminating in PANoptosome assembly and ZBP1-dependent PANoptosis. In vitro and in vivo studies demonstrated that BSCAPM effectively targeted tumor sites, initiated ZBP1-dependent PANoptosis and elicited a robust immunogenic response, leading to enhanced tumor elimination and lung metastasis restraints. This study not only elucidates the mechanistic basis of BSCAPM-induced PANoptosis but also provides a new strategy for the precise treatment of NSCLC.
研究领域:
肿瘤学
·
免疫治疗
·
纳米医学
·
细胞死亡机制
·
生物医学工程
·
癌症免疫学
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产品关联
DOI
PubMed
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
·
2026
·
IF 6.8
Yonghu Chen,Linying Hu,Qiang Fu,Hongzhen Chen,Zhe Jiang,Xuezheng Li
Ethnopharmacological relevance Pulmonary fibrosis (PF) is a progressive interstitial lung disease characterized by alveolar epithelial injury, inflammation, and excessive extracellular matrix deposition, yet current therapeutic options remain limited. Panax ginseng C.A. Meyer, a renowned qi-tonifying herb in traditional Chinese medicine, has long been used to enhance spleen and lung function by replenishing qi. However, the mechanism of action of its primary active component, ginseng stem and leaf saponins (GSLS), in pulmonary fibrosis remains incompletely understood. Aim of the study : This study aims to elucidate the protective role of GSLS against pulmonary fibrosis by investigating how GSLS regulates mitochondrial transcription factor A (TFAM)–mtDNA homeostasis and suppresses PANoptosis in alveolar epithelial cells. Materials and methods The major constituents of GSLS were identified using UHPLC–Q Exactive HFX. A BLM-induced mouse model of pulmonary fibrosis and an MLE-12–primary fibroblast co-culture system were established to evaluate the therapeutic effects of GSLS. Surface plasmon resonance (SPR) and cell thermal shift assays (CETSA) were performed to assess the direct interaction and thermal stability between GSLS and TFAM. Co-immunoprecipitation (Co-IP), RT-qPCR, and immunofluorescence were used to evaluate PANoptosome assembly, cytosolic double-stranded DNA (dsDNA) leakage, and fibrotic marker expression. Results GSLS was found to contain multiple active ginsenosides, including Rk2, CK, Rk3, and Rf. In vivo , GSLS markedly alleviated BLM-induced lung pathological injury, reduced collagen deposition, and decreased oxidative stress. In vitro , GSLS directly bound to TFAM and enhanced its thermal stability. RT-qPCR and immunofluorescence analyses further demonstrated that GSLS effectively suppressed abnormal cytosolic dsDNA leakage, reduced MLE-12 cell death, and ameliorated mitochondrial dysfunction. Moreover, GSLS inhibited the assembly of the PANoptosome complex, suppressed epithelial PANoptosis, and decreased the expression of fibrosis-related proteins. Conclusion GSLS mitigates BLM-induced pulmonary fibrosis by stabilizing TFAM, maintaining mtDNA homeostasis, and suppressing PANoptosis. This clarifies the potential mechanism of GSLS therapy for PF.
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PubMed
高影响因子
JOURNAL OF NUTRITIONAL BIOCHEMISTRY
·
2026
·
IF 5.2
Yuting Dong,Xiaodan Wang,Shize Wang,Kang Yang,Tong Xu,Hongjin Lin
DEHP induces thymus injury in chickens by activating the NF-κB/TNF-α pathway, triggering oxidative stress and PANoptosis. • QUE can alleviate the activation of the NF-κB/TNF-α pathway, oxidative stress and PANoptosis induced by DEHP in chickens. • QUE exerts a targeted effect on NF-κB, thereby mitigating DEHP-induced thymus injury in chickens. Quercetin (Que), a natural dietary flavonoid, possesses significant antioxidative and immunoregulatory properties. Di(2-ethylhexyl) phthalate (DEHP), a pervasive environmental endocrine-disrupting chemical, triggers oxidative stress (OS) and elicits immunotoxic effects in various species. However, whether Que can target NF-κB to alleviate DEHP-induced OS and PANoptosis in the chicken thymus remains unclear to date. To investigate the mechanism of thymus damage induced by DEHP and the intervention effect of Que, we established an in vivo chicken model treated with DEHP and/or Que. Based on the results of network pharmacology, molecular docking, molecular dynamics simulations, and Cell Thermal Shift Assay (CETSA), we predicted that NF-κB is the key target for the protective effect of Que. Subsequently, through H&E staining, CCK-8, immunofluorescence, Western blot and other techniques, we verified the effects of DEHP and/or Que on OS, the assembly of PANoptosome, and cellular PANoptosis in chicken thymus tissue and chicken lymphocyte cell line (MSB-1). Meanwhile, to clarify the key role of NF-κB in the above regulatory process, we conducted reverse validation experiments by introducing the NF-κB activator Act1 in cellular experiments. The results demonstrated that DEHP exposure markedly induces the upregulation of NF-κB and TNF-α(P<0.05), leading to a pronounced burst of reactive oxygen species (ROS) and consequent OS within the chicken thymus. This process further activates the ZBP1-mediated PANoptosis pathway, ultimately causing damage to chicken thymus tissue. Que intervention effectively suppresses NF-κB activation, blocking the transmission of the NF-κB/TNF-α/ROS signaling axis, thereby reversing DEHP-induced ZBP1-mediated PANoptosis in chicken thymus. Download: Download high-res image (290KB) Download: Download full-size image
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PubMed
高影响因子
Frontiers in Immunology
·
2022
·
IF 8.786
Zhang Nan,Gao Xiaochen,Zhang Weijia,Xiong Junyao,Cao Xiaojian,Fu Zhen F.,Cui Min
Japanese encephalitis virus (JEV) is one of the most important members of the flavivirus family. It is a typical zoonotic pathogen that has caused substantial social and economic losses worldwide. The relation between JEV-induced immunosuppression and inflammatory responses has not been thoroughly investigated. In this study, cells infiltrating the brain tissue of JEV-infected mice were mainly identified as monocytic myeloid-derived suppressor cells (M-MDSCs), which subsequently differentiated into CD3+ macrophages. Co-culture with T cells showed that both splenic M-MDSCs and brain infiltrated M-MDSCs isolated from JEV-infected mice inhibited T cell proliferation through ARG1 and iNOS. The splenectomy model revealed that JEV-induced M-MDSCs were mainly derived from bone marrow and migrated to the spleen and central nervous system (CNS). The results of the transcriptome analysis and IRF7-deficient mice indicated that the ZBP1-IRF7 signaling pathway stimulated by JEV RNA played a central role in the induction of M-MDSCs. M-MDSCs migrated into the CNS through the chemokine CCL2/N-CCL2 derived from astrocytes and brain infiltrated M-MDSCs differentiated into CD3+ macrophages through a mechanism mediated by M-CSF, IL-6 and IFN-γ in the brain microenvironment. These findings provide evidence for the mechanism that JEV regulates the differentiation of M-MDSCs and thereby exacerbates pathogenicity, which represents a potential therapeutic target for Japanese encephalitis (JE).
研究领域:
免疫学
·
神经病毒学
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病毒学
·
致病机制
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DOI
PubMed
高影响因子
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