ACTA PHARMACOLOGICA SINICA
·
2013
·Vol. 34
·期 7
·939-950
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IF 2.354
Peng Yan-min,Zheng Jian-bin,Zhou Yu-bo,Li Jia
Aim: Curcumin has shown promising anticancer activity, which relies on its inhibition on NF-κB pathway. In this study, we characterized the pharmacological profile of a novel curcumin analog P1 and elucidate the related mechanisms. Methods: HEK293/NF-κB cells, stably transfected with an NF-κB-responsive luciferase reporter plasmid, were generated for high-throughput screen (HTS). Eight cancer cell lines, including PC3, COLO 205, HeLa cells etc . were tested. Cell viability was assessed using the sulforhodamine B (SRB) assays. Cell apoptosis was evaluated using FACS, immunocytochemistry, and Western blotting. H 2 -DCFDA and MitoSOX Red were used to detect cellular and mitochondrial reactive oxygen species (ROS). The mitochondrial function was evaluated using mitochondrial oxygen consumption assay. Results: P1, a tropinone curcumin, was found in HTS targeting the NF-κB pathway. Its IC 50 value in inhibition of TNF-α-induced NF-κB activation was 0.8 μmol/L, whereas its IC 50 values in inhibiting the growth of A549 and HeLa cells were 1.24 and 0.69 μmol/L, respectively, which was 20- to 30-fold more potent than curcumin. The inhibition of P1 on the NF-κB pathway was further addressed in HeLa cells. The compound up to 10 μmol/L did not affect the binding of NF-κB to DNA, but markedly inhibited NF-κB nuclear translocation, IκB degradation and IκB kinase phosphorylation. The compound (1 and 3 μmol/L) concentration-dependently induced ROS generation, whereas curcumin up to 20 μmol/L had no effect. P1-induced ROS generation was mainly localized in mitochondria, and reversed by NAC. Moreover, the compound significantly enhanced TNF-α-induced apoptosis. Conclusion: P1 is a novel curcumin analog with potent anticancer activities, which exerts a distinct inhibition on the NF-κB pathway.
研究领域:
药理学
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肿瘤学
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细胞生物学
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分子生物学
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JOURNAL OF MOLECULAR HISTOLOGY
·
2026
·Vol. 57
·期 4
·229
·
IF 2.6
Chen Pei-sheng,Xu Liu-fei,Wang Bo,Zhang Sheng-ping,Luo Yi-yu,Wang Xiang-peng
Glioblastoma (GBM) is a highly malignant brain tumor with a poor prognosis. Long noncoding RNAs (lncRNAs) significantly influence GBM pathogenesis. Although lncRNA MIR4435-2HG is known to promote tumorigenesis in various cancers, its regulatory role in GBM remains undefined. We quantified MIR4435-2HG and miR-181d-5p expression using quantitative reverse transcription polymerase chain reaction. The functional impact of the MIR4435-2HG/miR-181d-5p/MALT1/NF-κB axis was assessed in A172 and U87 MG cells through cell counting kit-8 (CCK-8), wound healing, Transwell, flow cytometry, Terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL), western blot, and immunofluorescence assays. Interactions between miR-181d-5p, MIR4435-2HG, and MALT1 were confirmed by dual-luciferase reporter, fluorescence in situ hybridization, RNA immunoprecipitation, and RNA pulldown experiments. Finally, a xenograft tumor model in C57BL/6 mice, combined with hematoxylin and eosin staining, immunohistochemistry, and TUNEL staining, was used to investigate the role of MIR4435-2HG in vivo. The results demonstrated that both MIR4435-2HG and MALT1 were upregulated in GBM tissues and cell lines, whereas the expression of miR-181d-5p was reduced. MIR4435-2HG promoted GBM cell proliferation and metastasis in both in vitro and in vivo experiments. Inhibition of MALT1 reversed the promotive effects of miR-181d-5p knock down on GBM cell proliferation and metastasis. Mechanistic studies revealed that MIR4435-2HG upregulates MALT1 expression and activates the NF-κB signaling pathway by sponging miR-181d-5p. In conclusion, MIR4435-2HG overexpression facilitates the malignant progression of GBM through the miR-181d-5p/MALT1/NF-κB pathway.
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Frontiers in Microbiology
·
2026
·
IF 5.8
Yidong Xu,Xinyi Li,Yaodong Miao,Xiaoxi Liu,Xiya Zang,Qinghao Meng,Ying Li,Fengwen Yang,Zhiguang Yuchi,Yiwen Wang
Objective Xuanfei Baidu decoction (XFBD), one of China’s recommended prescriptions for COVID-19, has demonstrated clinical efficacy in mitigating gastrointestinal inflammation associated with SARS-CoV-2 infection, yet its exact therapeutic mechanism remains incompletely understood, necessitating further in vivo investigation. In this study, we utilized a fruit fly ( Drosophila melanogaster ) model of intestinal inflammation to assess the therapeutic potential and underlying mechanisms of XFBD in ameliorating intestinal inflammation. Methods We induced intestinal inflammation in D. melanogaster by dextran sulfate sodium (DSS) administration. We examined XFBD’s protective effects on D. melanogaster ’s intestine and explored changes in the IMD and JNK-JAK/STAT signaling pathways. Furthermore, we analyzed the intestinal microbiota through 16S rRNA gene sequencing. Results XFBD effectively mitigated DSS-induced intestinal inflammation, leading to a significant extension of the flies’ lifespan. It enhanced the integrity of intestinal barrier while reducing reactive oxygen species (ROS) levels in intestine. Additionally, XFBD restored the disrupted intestinal microbiota by regulating immune homeostasis, notably inhibiting the IMD, Toll, and JNKJAK/STAT pathways. Furthermore, the reintroduction of symbiotic microbiota partially alleviated the DSS-induced dysregulation. Conclusion In conclusion, our study underscores the therapeutic potential of XFBD for intestinal inflammation, providing valuable insights into its key mechanisms and highlighting the pivotal role of symbiotic microbiota in anti-inflammatory responses and immune pathway regulation.
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NEUROSCIENCE LETTERS
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2026
·
IF 2.2
Wuwei Xu,Yanxin Xu,Chunyan Yao,Xianmei Fu,Xiaoling Liu,Jinping Fan,Kexue Wang,Yumeng Zhou,Yuefei Li,Ting Hu,Yan Sai,Peng Luo,Tongjian Cai
T-2 toxin is a widely distributed environmental mycotoxin that poses severe neurotoxic risks to humans and animals. Neuroinflammatory responses constitute a key mechanism underlying the neurotoxicity of T-2 toxin. However, its molecular mechanisms for inducing inflammatory responses in the nervous system remain incompletely understood. This study investigated the role of B-cell translocation gene 2 (BTG2) in T-2 toxin-induced microglial activation and evaluated the neuroprotective potential of resveratrol (Res). In vivo experiments demonstrated that exposure to T-2 toxin resulted in spatial learning, memory impairments and locomotor deficits in mice. These behavioral phenotypes were accompanied by neuroinflammation in the hippocampus and cerebral cortex, characterized by microglial activation and the upregulation of BTG2. Res pre-treatment effectively reversed these neurobehavioral deficits and suppressed the neuroinflammatory response. Mechanistic analyses revealed that Res considerably alleviated T-2 toxin-induced TLR4/MyD88/NF-κB pathway activation. In vitro studies using BV-2 microglial cells confirmed these findings. Notably, siRNA-mediated knockdown of BTG2 also abolished TLR4 pathway activation and subsequent cytokine expression induced by T-2 toxin, establishing BTG2 as a critical upstream regulator. Furthermore, RNA sequencing systematically verified that BTG2 regulates the immune response network, specifically targeting the TLR4 cascades. Collectively, these findings provide novel evidence that Res may target the BTG2-regulated TLR4/MyD88/NF-κB signal pathway to exert neuroprotection, providing a promising intervention option for reducing the environmental and health hazards associated with exposure to T-2 toxin
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BMEMat
·
2026
·
IF 17.2
Hui Xing,Yuhui Yang,Ziyi Zhao,Kai Lv,Yiran Shao,Zhi Zhang,Dong Ma
Psoriasis, an immune-mediated skin disorder, affects over 125 million people worldwide. Its primary manifestations include abnormal keratinocyte proliferation, epidermal inflammatory cell infiltration, and excessive neovascularization, and no fundamental intervention is currently available. Although siRNA therapy based on the RNA interference mechanism has opened a new avenue for the definitive treatment of psoriasis, its clinical application is limited by rapid degradation and low transfection efficiency, compounded by the skin's dense structure that hinders noninvasive transdermal delivery. To address these issues, we developed a transdermal siRNA delivery system using polyethylenimine (PEI) and Tween 80-modified transfersomes (TCPL) as carriers for NF-κB p65 siRNA (TCPL@siNF-κB). By embedding Tween 80 and PEI into the TCPL, the system achieves excellent proton buffering capacity, enabling multilayer encapsulation of siNF-κB at both the core and surface levels, effectively preventing its degradation in serum and enzymatic environments. This strategy resolves the molecular weight-dependent conflict between the transfection efficiency and toxicity of PEI, achieving a balanced performance. Moreover, TCPL exhibits ultradeformability, and this study demonstrates the advantages of Tween 80 in promoting transdermal gene transfection. TCPL@siNF-κB demonstrated efficient lysosomal escape and intracellular delivery via clathrin-mediated endocytosis and macropinocytosis, achieving high transfection efficiency. In vitro inflammatory models and a psoriasis-like mouse model confirmed that TCPL@siNF-κB enables efficient gene delivery through simple topical application, effectively silences NF-κB signaling, modulates the immune microenvironment, inhibits aberrant angiogenesis, and significantly alleviates psoriatic symptoms, while exhibiting excellent biocompatibility. Therefore, this study offers a promising non-invasive gene therapy strategy for psoriasis and other potential inflammatory skin disorders.
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CHEMICAL ENGINEERING JOURNAL
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2026
·
IF 12.5
Yana Ma,Wen Luo,Weijia Zhu,Zhichao Deng,Shijun Xu,Hang Yuan,Wei-jun Fan,Quanjun Yao,Wei Yao,Ho-Young Song,Mingzhen Zhang,Jizhao Wang,Hongtao Hu
Oxidative stress, resulting from excessive reactive oxygen species (ROS), is critically involved in the development and progression of inflammatory diseases such as inflammatory bowel disease. Therefore, targeting ROS for the treatment of inflammation holds great potential, and the underlying mechanism is of great significance for clinical medication. In this work, carbon dots (C-dots) based on chrysanthemum as carbon source were obtained through a hydrothermal method. The as-prepared C-dots exhibited favorable ROS scavenging capacity and biocompatibility. The ROS level and the oxidative damage were reversed, the expression of proinflammatory factors was reduced, and the disrupted barrier was recovered by chrysanthemum-derived C-dots in the cellular inflammatory model. The anti-inflammatory effects were also validated in mice colitis model. Mechanistically, the chrysanthemum-derived C-dots regulated the Keap1/Nrf2 antioxidant signaling and inhibited the NF-κB/NLRP3 inflammasome-mediated inflammatory signaling, thereby restoring redox homeostasis and modulating the inflammatory microenvironment. Collectively, the C-dots from chrysanthemum with preferable biocompatibility hold a bright prospect in inflammation resolution through remodeling redox and inflammatory microenvironment.
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BIOCHEMICAL PHARMACOLOGY
·
2026
·
IF 6.5
Xia Wu,Chun-Feng Liu
Septic cardiomyopathy (SCM) is a prevalent complication among septic patients, accompanied by high mortality. Estrogen‐related receptor alpha (ERRα), a transcription factor, is implicated in various cardiovascular diseases. Nonetheless, its role in SCM remains unclear. Here, the cecum ligation and puncture (CLP) procedure was used to construct a mouse sepsis model. We found that the ERRα expression was downregulated in septic hearts. Adeno-associated virus-9 (AAV-9)-mediated cardiomyocyte-specific ERRα overexpression improved the survival rate of septic mice. Additionally, ERRα overexpression ameliorated CLP-induced cardiac dysfunction and myocardial pathological damage. In vitro , HL-1 mouse cardiomyocytes were transduced with an ERRα overexpression adenovirus before LPS stimulation. The results demonstrated that ERRα overexpression mitigated LPS-induced inflammatory cytokines (IL-6, IL-1β, TNF-α, IL-18) and apoptosis (Bax, cleaved caspase-3/9) in HL-1 cells. Mechanistically, ERRα inhibited the NF-κB/NLRP3 inflammasome activation in septic hearts and LPS-stimulated HL-1 cells. Furthermore, we overlapped the differentially expressed genes of septic hearts (GSE125042) and ERRα KO hearts (GSE7196) to identify the downstream target genes. Meteorin like, glial cell differentiation regulator (METRNL) was identified as the target gene of ERRα. Notably, ERRα bound to the METRNL promoter and upregulated its activity, which was confirmed via dual-luciferase reporter assay, ChIP-qPCR, and oligonucleotide pull-down assay. Knockdown of METRNL prevented the effects of ERRα overexpression on the apoptosis and inflammatory response of cardiomyocytes induced by LPS. Our findings underscore the role of ERRα in mitigating myocardial injury in SCM, indicating its potential as a new therapeutic approach.
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International Journal of Nanomedicine
·
2026
·
IF 8.7
Pongsigeraxi Borjigin,Caixia Deng,Rilaga Su,Juan Li,Ying Ying,Yingsong Chen,Tegexibaiyin Wang
Purpose This study aimed to enzymatically synthesize pearl powder fluorescent carbon dots (PFCDs) and investigate their neuroprotective potential against cerebral ischemia/reperfusion injury (CIRI) by modulating the Anxa2/NF-κB signaling pathway.Methods PFCDs were synthesized through enzymatic digestion and characterized. Neuroprotective effects were assessed using an in vitro oxygen–glucose deprivation/reoxygenation (OGD/R) model in PC12 cells and a middle cerebral artery occlusion/reperfusion (MCAO/R) rat model. Cell viability, neurological function, cerebral infarct volume, and neuronal injury were evaluated. Expression of Anxa2/NF-κB signaling pathway proteins and inflammatory cytokines (TNF-α, IL-6, IL-1β) was analyzed by Western blot, immunofluorescence, and ELISA.Results The synthesized PFCDs exhibited an organic–inorganic hybrid structure, uniform particle size below 10 nm, and distinctive optical properties. In vitro, PFCDs enhanced cell viability under OGD/R conditions, inhibited phosphorylation of Anxa2 and NF-κB p65, and reduced secretion of pro-inflammatory cytokines (TNF-α, IL-6, IL-1β). In vivo, treatment with PFCDs in MCAO/R rats improved neurological function, reduced cerebral infarct volume, and alleviated neuronal injury. These protective effects were linked to downregulation of the Anxa2/NF-κB signaling pathway and reduced serum levels of inflammatory cytokines.Conclusion We successfully achieved the enzymatic synthesis of carbon dots from pearl powder, characterized by a unique organic–inorganic hybrid structure. PFCDs effectively alleviated CIRI-induced neuroinflammation by suppressing the Anxa2/NF-κB signaling pathway, highlighting their therapeutic potential as a nanomedicine derived from natural products.
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JOURNAL OF FOOD BIOCHEMISTRY
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2026
·Vol. 2026
·期 1
·8438287
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IF 2.3
Shiying Mai,Liyan Li,Yinfeng Tan,Minghai Fu,Junqing Zhang,Fang Zhang,Yonghui Li,Qi Wang,Yuhuang Wu
Background Lihuabidouyan Tablet is a compound Chinese herb preparation used for the treatment of respiratory diseases. As the main active ingredient in it, Ficus pumila ( F . pumila ) contains polysaccharides that exert unique biological activity. In this study, polysaccharides in F . pumila were extracted and purified, and the protective effect and mechanism of action of F . pumila polysaccharide 1-1 (FPP1-1) in lipopolysaccharide (LPS)-induced acute lung injury (ALI) mice were discussed. Methods BALB/c mice were randomly divided into control, model, dexamethasone (DEX), and FPP-1-1 groups (50, 100, and 200 mg/kg), and the drug was administered by gavage for one week. Hematoxylin–eosin staining (H&E) and wet/dry ratio were used to evaluate lung injury and pulmonary edema. The ELISA was used to detect inflammatory factors. qRT-PCR was used to examine mRNA expression in tissues. Proteins related to inflammation were evaluated by western blotting. 16S rDNA sequencing was used to analyze the gut microbiota. Results FPP-1-1 significantly reduced lung injury in the ALI mice and significantly reduced levels of the proinflammatory factors interleukin (IL)-6 and tumor necrosis (TNF)- α and promoted the anti-inflammatory factor IL-10 in bronchoalveolar lavage fluid. FPP-1-1 inhibited the expression of phospho-ERK1/2, phospho-P38, and phospho-NF- κ B p65 proteins. FPP-1-1 also increased the diversity of the gut microbiota and increased the abundance of Lachnospiraceae in the ALI mice. Correlation analysis results showed that there was a significant correlation between the MAPK/NF- κ B pathway and inflammatory cytokines and gut microbiota in ALI mice. Conclusion The present study characterized the structure and molecular weight of a novel homogeneous polysaccharide, FPP-1-1, isolated from F. pumila . In addition, FPP-1-1 affected the expression of inflammatory factors by inhibiting the MAPK/NF- κ B pathway. FPP-1-1 also restored the diversity of gut microbiota and changed the relative abundance of key bacterial genera such as Lachnospiraceae and Alloprevotella , suggesting that the “gut–lung” axis may serve as a crucial pathway through which FPP-1-1 exerts its effect.
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MOLECULES
·
2026
·Vol. 31
·期 11
·1933
·
IF 5.1
Yanlong Li,Anning Zhan,Xiaobing Zhang,Yu Duan,Jiawen Tang,Hua Bai,Qi Wang
Objective: The present study investigates the effect of 1,8-cineole on improving lipid metabolism disorder by regulating oxidative stress and inflammation via the TLR4/MyD88/NF-κB pathway. 1,8-Cineole is a monoterpene compound widely found in the essential oils of many plants and has been reported to possess anti-inflammatory and antioxidant activities. However, its role in regulating lipid metabolism disorders remains unclear. This study aimed to investigate the effects of 1,8-cineole on lipid metabolism and explore the potential mechanisms related to oxidative stress and inflammation. Methods: Cell viability was assessed by MTT assay to determine the optimal PA concentration for inducing lipid accumulation and the non-cytotoxic range of 1,8-cineole in HepG2 and AML-12 cells. Lipid droplets were visualized by Oil Red O staining, while triglyceride (TG) and total cholesterol (TC) levels were quantified using enzymatic kits. Oxidative stress markers (ROS by DCFH-DA fluorescence; MDA by TBA method; CAT activity by ammonium molybdate method) and inflammatory cytokines (TNF-α, IL-6, IL-1β, IL-18 by ELISA) were measured. Western blotting analyzed key proteins in the TLR4/MyD88/NF-κB pathway (TLR4, MyD88, p-P65, p-IκBα). Pathway-specific inhibitors were employed for mechanistic validation. Results: 1,8-Cineole (up to 1000 μg/mL) showed no cytotoxicity. It significantly attenuated PA-induced lipid droplet accumulation, reduced TG and TC levels (p< 0.05), and ameliorated oxidative stress by decreasing ROS and MDA while enhancing CAT activity in AML-12 cells (p< 0.01). Furthermore, 1,8-cineole suppressed pro-inflammatory cytokine release (TNF-α, IL-6, and IL-1β;p< 0.01), whereas no significant effect was observed on IL-18 levels. Downregulated TLR4/MyD88/NF-κB pathway activation. Inhibition of TLR4 or NF-κB mirrored these protective effects. Conclusions: 1,8-Cineole alleviates PA-induced lipid metabolism disorders, oxidative stress, and inflammation in hepatocytes, likely through suppression of the TLR4/MyD88/NF-κB signaling pathway.
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Journal of Translational Medicine
·
2025
·Vol. 23
·期 1
·1385
·
IF 7.5
Gong Jiaxin,Wei Feng,Wu Tianyu,Zhang Ningzhi,Zhang Yongqiao,Cui Zhaoqiang,Ge Junbo
Background Obesity-related cardiac injury is a serious global condition associated with excessive fat intake, which is strongly linked to chronic low-degrade inflammation. Pyroptosis, a pro-inflammatory form of cell death, has been implicated in obesity recently. L-Fucose (Fuc), a sulfated polysaccharide with anti-inflammatory and antioxidant properties, remains unexplored in the area of pyroptosis and obesity-related cardiac injury. Methods Six-week-old wide type C57BL/6 mice were subjected to high-fat diet (HFD) feeding for 20 weeks to induce obesity with or without Fuc gavaging, followed by assessment of metabolic related indicators. Echocardiography, histopathological analysis and enzymatic assays were used to assess cardiac function. The level of pro-inflammatory cytokines was detected by ELISA, qRT-PCR and CD68 staining. Pyroptosis-related protein including NLRP3, GSDMD, pro-caspase-1, cleaved-caspase-1, IL-1β, and ASC were evaluated by western blot. Oxidative stress was detected by ROS level. Cardiac mitochondrial structure was assessed by electron microscopy and mitotracker staining. Mitochondrial function was measured by mitochondrial membrane potential (MMP) and oxygen consumption rate (OCR) assay. Molecular docking and molecular dynamics (MD) simulations were conducted to look for the potential target of Fuc. Cellular thermal shift assay (CETSA) and western blot were used to investigate the interaction between Fuc and its target. Palmitic acid (PA) induced lipotoxicity model in AC16 cells was used to further confirm the protective effects of Fuc and its downstream signaling pathway against inflammation, pyroptosis and mitochondrial injury in vitro. Results In vivo, Fuc treatment alleviated obesity-related weight gain, hyperlipidemia, elevated systolic blood pressure and cardiac diastolic dysfunction. It also reduced the expression of pro-inflammatory cytokines and pyroptosis-related proteins, the level of oxidative stress, and mitochondrial abnormalities in the myocardium. Moreover, the vitro lipotoxicity model further confirmed the protective effect of Fuc. The molecular docking analysis identified TLR4 as the key target of Fuc. Fuc reduced the level of TLR4 and its downstream proteins MyD88 and p-NF-κB, while activating TLR4/MyD88/NF-κB pathway by TLR4 agonist Neoseptin3 reversed the protective function of Fuc in vitro. Conclusions These findings demonstrated that Fuc mitigated cardiac inflammation, pyroptosis and mitochondrial injury by inhibiting the TLR4/MyD88/NF-κB pathway, highlighting its potential as a therapeutic agent for obesity-associated cardiac injury.
研究领域:
心脏病学
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分子生物学
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免疫学
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代谢性疾病
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药理学
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Frontiers in Immunology
·
2025
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IF 5.9
You Zhou,Kai Yang,Jian Wang,Ruijuan Guan,Wei Liu,Chaowei Wen,Liang Yuan,Tiange Zhang,Wei Feng,Yuanyuan Li,Jingyi Xu,Wenju Lu
Backgrounds: Exposure to fine particulate matter (PM2.5) triggers airway inflammation through the activation of the Toll-like receptor 4 (TLR4)/nuclear factor-κB (NF-κB) signaling pathway, contributing to the pathogenesis of various acute and chronic respiratory diseases. Mucin 1 (MUC1), a transmembrane glycoprotein highly expressed on airway epithelial cells, is known to modulate TLR-mediated inflammatory responses. However, the specific role and molecular mechanism by which MUC1 regulates PM2.5-induced airway inflammation remain inadequately understood.Methods: Lung injury models were established using Muc1+/+ and Muc1-/- rats via intranasal instillation of PM2.5. Histopathological changes and inflammatory responses were evaluated following treatment. In parallel, human bronchial epithelial cells (16HBE) were transfected with MUC1 overexpression and knockdown plasmids, along with corresponding controls. An IRAK4-specific inhibitor was employed to explore the mechanistic role of MUC1 in regulating the TLR4/IRAK4/NF-κB signaling cascade and associated pyroptosis.Results: PM2.5 exposure caused notable epithelial disruption, inflammatory infiltration, and submucosal fibrosis in Muc1-/- rats compared to Muc1+/+ controls. While TLR4 expression was not significantly altered, NF-κB and NLRP3 inflammasome activity were markedly elevated in Muc1-deficient rats. In 16HBE cells, MUC1 overexpression attenuated, whereas MUC1 knockdown exacerbated, PM2.5-induced activation of the IRAK4/NF-κB signaling axis and pyroptosis-related markers (IL-1β, IL-18, NLRP3, GSDMD). Furthermore, pharmacological inhibition of IRAK4 mitigated these effects, confirming the involvement of the IRAK4 pathway in MUC1-mediated protection.Conclusions: MUC1 is upregulated in airway epithelial cells upon PM2.5 exposure and serves as a key endogenous inhibitor of airway inflammation. It exerts its anti-inflammatory and anti-pyroptotic effects by suppressing IRAK4 phosphorylation, thereby modulating downstream NF-κB/NLRP3/GSDMD signaling. These findings highlight MUC1 as a potential therapeutic target for PM2.5-induced airway inflammatory diseases.
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