Advanced Healthcare Materials
·
2026
·
IF 9.6
Jingjing Yang,Jiawei Yang,Kunguo Liu,Shijie Wang,Ye Hu,Juanjuan Li,Hao Wang,Dan Jiang,Xin Han
Pyroptosis triggered by pore-forming Gasdermin proteins in cancer cells facilitates anti-tumor immune activation by releasing pro-inflammatory cytokines and immunogenic contents following cellular rupture. However, selectively triggering pyroptosis in tumors still remain limited in clinical applications. Here, it is reported a microfluidic-assisted bacterial delivery system using attenuated Salmonella typhimurium VNP20009 encapsulated with metal-phenolic networks composed of ferric ions (Fe 3 + ) and tannic acid (TA) to enhance intracellular gasdermin D (GSDMD) expression through targeted CRISPR/dCas9 delivery, thereby inducing robust tumor pyroptosis. Mechanistically, this system achieves cascade amplification of pyroptotic cell death through coordinated multi-modal mechanisms. Following systemic administration, VNP20009 specifically accumulates in hypoxic tumor regions while the coated Fe 3 + –TA nanofilm undergoes pH-responsive dissolution in the acidic tumor microenvironment (TME), simultaneously generating ROS through Fenton reaction and releasing CRISPR/dCas9 system to upregulate GSDMD expression. Concurrently, the abundant flagella of VNP activate caspase-1, which in turn cleaves the overexpressed GSDMD proteins into its active form, thereby triggering robust pyroptosis in tumor cells. Taken together, by coupling bacterial adjuvanticity with ROS-mediated stress and CRISPR-driven GSDMD upregulation, this strategy achieves efficient amplification of pyroptosis and promotes antitumor immune activation.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
CHEMICAL ENGINEERING JOURNAL
·
2026
·
IF 13.2
Linlin Xie,Xingye Ma,Zheng Wang,Caifang Wang,Zhongxin Xiao,Ling-Dong Sun,Chun-Hua Yan,Chen-Jie Fang
Pyroptosis resulted from photodynamic therapy (PDT) plays a crucial role in triggering photoimmunotherapy (PIT). However, visible light-triggered PDT may rise phototoxicity, with low penetration into biological tissues. Crucially, the efficacy of PDT in eliciting pyroptosis remains suboptimal. To address these formidable challenges, we developed a O 2 -supplementing photosensitizer AuNCs@TAT that could efficiently induce pyroptosis upon irradiation with second near-infrared (NIR-II) light in hypoxic tumor microenvironment (TME). Replacing GSH with TAT resulted in a gold nanocluster AuNCs@TAT. The ratio of Au (I) to Au (0) shifted from 1: 0.26 in pristine AuNCs to 1: 1.21 in AuNCs@TAT, which contributed to enhanced catalytic activity of AuNCs@TAT. The superior catalase-like activity of AuNCs@TAT produced 1.9-fold higher O 2 than AuNCs. This O 2 self-supplying capability of AuNCs@TAT not only relieved hypoxic condition in TME but also significantly enhanced the efficiency of AuNCs@TAT to induce pyroptosis upon 1064 nm light irradiation. Western blotting indicated both remarkable upregulation of cleft Caspase-3 and GSDME-N, suggesting GSDME mediated pyroptosis. Further, release of pro-inflammatory cytokines and damage-associated molecular patterns (DAMPs) triggered a strong systematic immune response and reprogrammed the immunosuppressive microenvironment into an immunostimulatory state, which led to a significant suppress of tumor metastasis in mice. Overall, this work sets the stage for future advancements in the design of NIR-II photosensitizer with O 2 -supplementing capability and therefore offers an innovative framework and solid foundation for tumor PIT.
✓ 已验证
产品关联
DOI
高影响因子
JOURNAL OF NUTRITIONAL BIOCHEMISTRY
·
2026
·
IF 4.9
Yuetong Sha,Yawen Xie,Xue Guan,Xinran Wang,Qianhui Zhang,Yonggang Cao,Pilong Shi,Hongli Sun
Cardiac microvascular damage exhibits a significant association with myocardial ischemia/reperfusion injury (MI/RI) development, which correlates with mitochondrial dysfunction. Lycopene has demonstrated pharmacological efficacy against cardiovascular diseases. Nevertheless, the potential roles and underlying mechanisms through which lycopene influences MI/RI remain incompletely understood. This study aimed to investigate the effect of lycopene on cardiac microvascular endothelial cell (CMEC) function in a rat model of MI/RI. This investigation sought to elucidate lycopene’s role in MI/RI and its mechanistic foundation. A rat MI/RI model was employed, and multiple experimental approaches were conducted, encompassing quantitative real-time polymerase chain reaction, Western blot analysis, immunofluorescence microscopy, enzyme-linked immunosorbent assay, molecular docking, and molecular dynamics simulations. In vitro studies involved the establishment of a hypoxia-reoxygenation model using CMECs to evaluate lycopene’s contribution to pyroptosis suppression and mitochondrial dysfunction prevention. Lycopene was found to enhance mitochondrial function through inhibition of the YTHDF1/E2F8/FABP3 axis in CMECs, suppress cGAS-STING signaling pathway activation, reduce cellular inflammatory responses, and inhibit cellular pyroptosis. These effects ultimately resulted in improved CMEC function, enhanced microvascular integrity, and increased perfusion and oxygen delivery to cardiomyocytes.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
·
2026
·
IF 6.8
Chuanqi Wan,Jiamin Lu,Lingyun Xu,Mei Jiang,Chen Zhu,Wen Zhang,Pingping Han,Jirong Zhang,Jing Wang,Weiwei Ren,Hui Chu,Bingzhi Zhou,Jiancheng Zhang,Guangjun Jin,Bangjiang Fang,Yuzhou He
Shenhuang Granules (SHG) attenuate sepsis-induced lung injury via the NLRP3/Caspase-1/GSDMD pathway. • (−)-Epicatechin gallate and gallic acid are the core bioactive monomers of SHG against PMVEC pyroptosis. • SHG inhibits pyroptosis by suppressing inflammasome assembly and pore formation. Ethnopharmacological relevance Shenhuang Granules (SHG) is a traditional Chinese medicine (TCM) formula composed of six medicinal materials: Panax ginseng C.A. Mey. (Ginseng Radix et Rhizoma), Rheum palmatum L. (Rhei Radix et Rhizoma), Sargentodoxa cuneata (Oliv.) Rehder & E.H. Wilson (Sargentodoxae Caulis), Taraxacum mongolicum Hand. -Mazz. (Taraxaci Herba), Aconitum carmichaelii Debeaux (Aconiti Lateralis Radix Praeparata), and Whitmania pigra Whitman (Hirudo). According to TCM theory, this formula is designed to replenish Qi and strengthen the body's resistance, clear heat and remove toxins, and promote blood circulation to eliminate blood stasis. In clinical practice, SHG has been used as an adjunctive therapy for sepsis, showing beneficial effects in ameliorating systemic inflammatory responses and microcirculatory disturbances. However, the underlying pharmacological mechanisms remain largely unclear. Aim of the study To validate that SHG and its active monomers alleviate sepsis-induced lung injury through targeted suppression of the NLRP3-driven PMVEC pyroptosis pathway. Materials and methods The chemical composition of SHG was analyzed by UHPLC-MS/MS. In vivo, SA-ARDS was induced in C57BL/6J mice by cecal ligation and puncture (CLP), with SHG (61.85 mg/mouse/d), its monomers, (−)-epicatechin gallate (ECG) and gallic acid (GA) (20 mg/kg/d), or the NLRP3 inhibitor MCC950 (10 mg/kg/d), were administered via intraperitoneal injection for 3 days prior to modeling. Lung injury severity and activation of the pyroptosis pathway were evaluated using histopathology, transmission electron microscopy, RT-qPCR, Western blotting, immunohistochemistry, immunofluorescence, and ELISA. In vitro, LPS-stimulated (1 μg/mL) PMVECs were used to screen 43 monomers, and the underlying mechanisms were subsequently verified. Results Compared with the Model group, SHG treatment significantly attenuated body weight loss in mice ( P < 0.001), reduced the lung wet-to-dry (W/D) weight ratio ( P < 0.05), and decreased Evans blue extravasation in lung tissues ( P < 0.01). SHG also significantly downregulated the mRNA expression levels of pyroptosis-related genes, including Twik2 , Nlrp3 , Asc , Caspase-1 , and Gsdmd , in lung tissues (all P < 0.01), and markedly reduced the protein expression of NLRP3, ASC, pro-Caspase-1, and Caspase-1 (all P < 0.05). ELISA results further demonstrated that SHG significantly decreased serum levels of the inflammatory cytokines TNF-α, IL-1β, IFN-γ, IL-18, pro-IL-1β, and pro-IL-18 in mice (all P < 0.05). In vitro, compared with the Model group, SHG significantly suppressed the transcriptional levels of Twik2 , Nlrp3 , Asc , Caspase-1 , and Gsdmd in PMVECs (all P < 0.05), and reduced the protein expression of NLRP3, ASC, GSDMD, GSDMD-NT, and IL-1β (all P < 0.05). Additionally, SHG markedly decreased lactate dehydrogenase (LDH) release ( P < 0.0001) and attenuated extracellular potassium ion (K + ) efflux ( P < 0.0001). Notably, ECG and GA individually exhibited potent inhibitory effects on PMVEC pyroptosis. Compared with the Model group, both ECG and GA significantly suppressed mRNA expression of Twik2, Nlrp3, Asc, Caspase-1, and Gsdmd (all P < 0.05) and reduced protein levels of NLRP3 , ASC , Caspase-1 , and GSDMD (all P < 0.05). Moreover, ECG significantly inhibited GSDMD-NT and IL-1β protein expression (all P < 0.05). Both ECG and GA markedly reduced TNF-α, IL-1β, and pro-IL-18 levels (all P < 0.05), and GA additionally suppressed IL-18 and pro-IL-1β expression (all P < 0.01). Furthermore, both ECG and GA significantly decreased LDH release ( P < 0.0001) and inhibited extracellular K + efflux ( P < 0.0001). However, this study has several limitations, including a small sample size, the absence of dose-gradient and time-course analyses, insufficient functional validation of the TWIK2 channel, and the lack of quantitative pharmacokinetic and synergy analyses, which should be addressed in future studies. Conclusion Shenhuang Granules attenuated PMVEC pyroptosis and ameliorated sepsis-induced lung injury by suppressing TWIK2 and the downstream NLRP3/Caspase-1/GSDMD pathway, with GA and ECG as the key active components. Download: Download high-res image (484KB) Download: Download full-size image
✓ 已验证
DOI
PubMed
高影响因子
Journal of Pharmaceutical Analysis
·
2026
·
IF 11.2
Yuejia Lan,Qingrui Zhong,Hongkai Huang,Xiao Deng,Lu Yang,Jiayi Sun,Mingyang Liu,Xianli Meng,Jiasi Wu
Evidence indicates that nuclear receptor subfamily 1 group H member 3 (NR1H3) activation mitigates sepsis-induced acute lung injury (SALI) by reducing inflammatory response. Nevertheless, the mechanisms underlying NR1H3-inflammation interactions in addressing SALI remain unclear. Moreover, limited phytochemicals have been documented to ameliorate SALI via this pathway. Here, we discovered that NR1H3 activation directly suppresses the clustering of toll-like receptor 4 (TLR4) to lipid rafts, which acts as a part of the priming of NLR family pyrin domain containing 3 (NLRP3) inflammasome. This process results in the suppression of NLRP3 inflammasome assembly and activation, consequently alleviating gasdermin-D (GSDMD)-mediated pyroptosis. Furthermore, through dual-luciferase reporter gene testing, drug binding assays, gene expression analysis, and biochemical evaluation, we determined lappaconitine hydrobromide (LAH) as a novel NR1H3 agonist that effectively suppresses TLR4-NLRP3 signaling pathway. Our results showed LAH attenuates inflammatory lung injury in both lipopolysaccharide and cecal slurry-induced SALI mouse models. In vivo and in vitro experiments revealed that LAH suppresses NLRP3 signaling activation and pyroptosis. Additionally, RNA-seq and bioinformatics analysis demonstrated that the differentially expressed genes (DEGs) linked to interleukin-1 beta (IL-1β) production, modulation of inflammatory response, and control of innate immune response were markedly enriched in LAH, and core genes amongst the DEGs included NR1H3. Mechanistically, LAH reduces inflammation and pyroptosis through modulation of NR1H3-NLRP3-GSDMD axis in mice. This finding was further substantiated by the suppression of NR1H3 in vitro . Our findings offer novel perspectives on the NR1H3-inflammation interaction in SALI regulation and indicate the therapeutic promise of LAH as an NR1H3 agonist for SALI management via NLRP3 suppression.
✓ 已验证
DOI
高影响因子
BIOCHEMICAL PHARMACOLOGY
·
2025
·
IF 5.6
Delong Meng,Qian Su,Kejuan Jia,Mengjie Jin,Wenting Liu,Shiqi Yang,Zhiqiang Su
Ischemic stroke is a kind of cerebrovascular disease with high mortality. The expression of ETS variant transcription factor 5 (ETV5) is down-regulated in ischemic stroke, but the specific role and mechanism remain unclear. In this study, the effects of ETV5 on ischemic stroke were investigated in vivo and in vitro by establishing the middle cerebral artery occlusion/reperfusion (MCAO/R) animal model and oxygen-glucose deprivation/reoxygenation (OGD/R) microglia model, respectively. We found that ETV5 reduced the infarct size, neurological deficit, microglia M1 polarization, and neuron pyroptosis level. Mechanistically, we further examined the expression of the HECT domain and ankyrin repeat-containing E3 ubiquitin protein ligase 1 (HACE1) and nuclear factor erythroid 2-related factor 2 (Nrf2) based on animal and cellular models to assess whether ETV5 affects ischemic stroke through the HACE1/Nrf2 signaling pathway. We found that ETV5 promoted the expression of HACE1 and Nrf2 in microglia and that HACE1 was transcriptionally activated by ETV5, which in turn competed with the E3 ligase KEAP1 for binding of Nrf2 and enhances the protein stability and nuclear expression of Nrf2. Our results suggest that ETV5 can ameliorate brain injury caused by ischemic stroke and this is closely related to inducing the HACE1/Nrf2 pathway to inhibit microglia M1 polarization.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
ACS Applied Nano Materials
·
2026
·
IF 5.8
Guanheng Wang,Lin Li,Biao Xue,Yu Li,Yaling Zhang,Jiapeng Wang,Yulei Cui,Chunlei Li,Xiuwen Zheng
In this study, a pH-responsive Cu-doped zeolitic imidazolate framework-8 nanoplatform was coloaded with paclitaxel and doxorubicin for synergistic tumor therapy. Hyaluronic acid modification on the outer surface of the nanomaterials enhances tumor targeting via CD44 receptor-mediated endocytosis. ZIF-8, derived from metal–organic frameworks, is an excellent nanocapsulator capable of specifically responding to the acidic tumor microenvironment. Upon reaching the tumor site, it rapidly degrades, releasing copper ions and chemotherapeutic drugs to exert antitumor effects. Copper ions consume endogenous hydrogen peroxide and glutathione through Fenton-like reactions, thereby generating cytotoxic reactive oxygen species, enhancing chemodynamic therapy efficiency, and inducing cuproptosis. The released PTX and DOX not only exert chemotherapeutic effects but also induce pyroptosis by activating the classical pathway mediated by caspase-3 and Gasdermin E. Due to excessive activation of the Wnt/β-catenin signaling pathway, PTX faces drug resistance in the treatment of triple-negative breast cancer, whereas DOX can inhibit this pathway by promoting β-catenin degradation. These therapies act synergistically to trigger immunogenic cell death, release damage-associated molecular patterns, promote dendritic cell maturation, activate T cells, and effectively reshape the immunosuppressive tumor microenvironment. This multimodal nanoplatform demonstrates remarkable potential as an antitumor treatment.
✓ 已验证
产品关联
DOI
高影响因子
Molecular Medicine Reports
·
2026
·Vol. 33
·期 4
·1-14
·
IF 5
Xiaoyu Zheng,Jinping Li,Tianyang Hu,Li Tan,Ding Lan,Ying Deng
Covers molecular medicine topics such as pharmacology, pathology, genetics, neuroscience, infectious diseases, molecular cardiology, and molecular surgery.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
·
2026
·
IF 5.6
Xizhi Li,Tingting Zhou,Yixi Wu,Jiayi Sun,Ziyu Wang,Yuhan Huang,Ke Xu,Hongwei Ling,Na Li,Tingting Yang,Tao Wang
Exenatide, the first glucagon-like peptide-1 receptor agonist (GLP-1RA), exerted multiple beneficial effects, including stimulating insulin secretion, slowing gastric emptying, and improving insulin resistance (IR). Our previous work demonstrated that the peroxisome proliferator-activated receptor delta (PPARδ) gene ( PPARD ) polymorphisms correlated with exenatide monotherapy efficacy, possibly due to the pivotal role of PPARδ in regulating IR. Specifically, PPARδ has been shown to modulate the nucleotide-binding domain and leucine-rich repeat pyrin domain-containing 3 (NLRP3) inflammasome, a key regulator of pyroptosis, thereby participating in the regulation of this inflammatory cell death pathway. However, the underlying mechanisms by which exenatide ameliorated hepatic IR in patients with type 2 Diabetes Mellitus (T2DM) remained incompletely understood. Herein, we found that exenatide suppressed pyroptosis and ameliorated hepatic IR; furthermore, it could bind to PPARδ and upregulate PPARδ protein expression both in vitro and in vivo. Notably, PPARδ knockdown abolished the protective effects of exenatide against pyroptosis and hepatic IR, whereas pharmacological activation of PPARδ enhanced these beneficial effects. Moreover, T2DM patients carrying the AA genotype at PPARD rs3777744 and exhibiting higher baseline homeostasis model assessment of insulin resistance (HOMA-IR) showed a superior response to exenatide. Collectively, our findings revealed that exenatide ameliorated hepatic IR by suppressing pyroptosis via PPARδ, underscoring the potential of PPARD rs3777744 as a biomarker for personalized exenatide therapy in T2DM.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
FREE RADICAL BIOLOGY AND MEDICINE
·
2026
·
IF 8
Hengchang Yao,Lichao Yang,Yawei Zhang,Qiang Wu,Kailing Xie,Hao Liu,Baojia Yao,Zhixian Jiang,Qi Sun,Zhuoxian Zeng,Lianwen Yuan
Inflammatory Bowel Disease (IBD) is a chronic inflammatory disorder where pyroptosis of intestinal epithelial cells, driven by the NEK7/NLRP3 axis, is a key pathological feature. This study aimed to identify a novel inhibitor of NIMA-related kinase 7 (NEK7) and develop a targeted delivery system to enhance its therapeutic efficacy for IBD. Through a virtual screening of FDA-approved drugs, nebivolol was identified as a potent NEK7 inhibitor. Subsequent biochemical and cellular assays confirmed that nebivolol directly binds to the LYS64 site of NEK7, inhibiting its kinase activity and disrupting its interaction with NLRP3. This inhibitory action was shown to protect intestinal epithelial cells from pyroptosis in vitro and to significantly ameliorate disease symptoms, histological damage, and molecular markers of pyroptosis in a chronic DSS mouse model of colitis, with a high safety profile. To enhance therapeutic efficacy and specificity, a quantitatively characterized targeted delivery system of lactoferrin-modified liposomes loaded with nebivolol (LF-Lipo@N) was developed. This system demonstrated superior uptake by intestinal cells via lactoferrin and lactoferrin receptors (LFRs)interaction and a more potent anti-pyroptotic effect in vitro . Crucially, the quantitative biodistribution analysis showed that the targeted LF-Lipo@N system significantly accumulated in the colon in vivo , leading to a significantly enhanced therapeutic effect compared to free nebivolol while eliminating systemic side effects on heart rate. In conclusion, the targeted delivery of nebivolol via lactoferrin-modified liposomes represents a promising and effective strategy for treating IBD by specifically inhibiting NEK7-mediated intestinal pyroptosis.
✓ 已验证
DOI
PubMed
高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
·
2026
·
IF 5.6
Qiang Yuan,Yaoke Li,Kaiwen Shen,Ruibo Zhang,Qiang Wang,Shasha Xia,Jun Shen
Background Renal ischemia-reperfusion injury (RIRI) contributes significantly to acute kidney injury (AKI), which is associated with high morbidity and mortality rates. Currently, therapeutic options for RIRI remain limited. Sarsasapogenin (Sar), a steroidal saponin from Anemarrhena asphodeloides, exhibits strong anti-inflammatory properties. However, its renoprotective effects, dose-response characteristics, and tissue-specific benefits in acute RIRI have not been thoroughly explored. This study aimed to determine whether Sar provides protection against RIRI-induced AKI and to investigate the potential signaling pathways involved. Methods Rats underwent 45 min of renal ischemia followed by reperfusion. Sar (20 or 60 mg/kg) was administered daily via gavage for one week prior to surgery. As a positive control, INF39 (7.5 mg/kg), an NLRP3 inhibitor, was injected intraperitoneally 2 h before surgery. Renal function was assessed through serum creatinine and BUN levels, while histopathology was evaluated using H&E and TEM. Tubular injury markers, such as KIM-1, were also assessed. Total cell death was determined using the TUNEL assay, which detects DNA fragmentation but does not specifically identify pyroptosis. The expression of inflammatory factors (IL-1β, IL-6, TNF-α) and key proteins of the NF-κB pathway (p-p65/p65) and NLRP3 inflammasome (NLRP3, Caspase-1, GSDMD) were measured using ELISA, immunohistochemistry, immunofluorescence, and Western blotting. Results RIRI led to severe renal dysfunction, structural damage, and increased KIM-1 expression. These pathological changes were linked to significant activation of the NF-κB pathway, upregulation of NLRP3 inflammasome components, and increased pyroptosis, indicated by elevated levels of cleaved Caspase-1, GSDMD-N, and mature IL-1β. Pretreatment with Sar dose-dependently improved renal function and reduced histopathological injury. Sar provided tissue-specific protection by maintaining mitochondrial integrity in renal tubular epithelial cells. These beneficial effects were accompanied by decreased phosphorylation of p65, reduced expression of NLRP3, cleaved Caspase-1, and GSDMD-N, as well as lower IL-1β production. High-dose Sar exhibited renoprotective effects comparable to INF39, acting as a multi-stage regulator that inhibits both NF-κB priming and NLRP3 inflammasome activation, suggesting advantages over single-target inhibitors. Conclusion Sar effectively attenuated RIRI-induced AKI, demonstrating favorable dose-dependent and tissue-specific renoprotective effects. This protective effect was associated with suppression of the NF-κB/NLRP3 inflammasome axis and reduced pyroptosis, highlighting its potential as a safe, multi-stage, natural candidate for treating ischemia-related renal injury.
✓ 已验证
DOI
PubMed
高影响因子
Frontiers in Immunology
·
2022
·
IF 8.786
Gu Lingui,Sun Mingjiang,Li Ruihao,Zhang Xingyu,Tao Yihao,Yuan Ye,Luo Xu,Xie Zongyi
Neuroinflammation has been proven to exert an important effect on brain injury after intracerebral hemorrhage (ICH). Previous studies reported that Didymin possessed anti-inflammatory properties after acute hepatic injury, hyperglycemia-induced endothelial dysfunction, and death. However, the role of Didymin in microglial pyroptosis and neuroinflammation after ICH is unclear. The current study aimed to investigate the effect of Didymin on neuroinflammation mediated by microglial pyroptosis in mouse models of ICH and shed some light on the underlying mechanisms. In this study, we observed that Didymin treatment remarkably improved neurobehavioral performance and decreased BBB disruption and brain water content. Microglial activation and neutrophil infiltration in the peri-hematoma tissue after ICH were strikingly mitigated by Didymin as well. At the molecular level, administration of Didymin significantly unregulated the expression of Rkip and downregulated the expression of pyroptotic molecules and inflammatory cytokines such as Nlrp3 inflammasome, GSDMD, caspase-1, and mature IL-1β, TNF-α, and MPO after ICH. Besides, Didymin treatment decreased the number of Caspase-1-positive microglia and GSDMD-positive microglia after ICH. Inversely, Locostatin, an Rkip-specific inhibitor, significantly abolished the anti-pyroptosis and anti-neuroinflammation effects of Didymin. Moreover, Rkip binding with Asc could interrupt the activation and assembly of the inflammasome. Mechanistically, inhibition of Caspase-1 by VX-765 attenuated brain injury and suppressed microglial pyroptosis and neuroinflammation by downregulation of GSDMD, mature IL-1β, TNF-α, and MPO based on Locostatin-treated ICH. Taken together, Didymin alleviated microglial pyroptosis and neuroinflammation, at least in part through the Asc/Caspase-1/GSDMD pathway via upregulating Rkip expression after ICH. Therefore, Didymin may be a potential agent to attenuate neuroinflammation via its anti-pyroptosis effect after ICH.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）