IN VITRO CELLULAR & DEVELOPMENTAL BIOLOGY-ANIMAL
·
2023
·Vol. 59
·期 3
·204-213
·
IF 2.1
Liu Xu-Ying,Li Qiu-Shi,Yang Wen-Hai,Qiu Yue,Zhang Fei-Fei,Mei Xiu-Hui,Yuan Qi-Wen,Sui Ru-Bo
Cerebral ischemia/reperfusion (CI/R) usually causes neuroinflammation within the central nervous system, further prompting irreversible cerebral dysfunction. Perilipin 2 (Plin2), a lipid droplet protein, has been reported to exacerbate the pathological process in different diseases, including inflammatory responses. However, the role and mechanism of Plin2 in CI/R injury are unclear. In this study, the rat models of transient middle cerebral artery occlusion followed by reperfusion (tMCAO/R) were established to mimic I/R injury, and we found that Plin2 was highly expressed in the ischemic penumbra of tMCAO/R rats. The siRNA-mediated knockdown of Plin2 significantly decreased neurological deficit scores and reduced infarct areas in rats induced by I/R. Detailed investigation showed that Plin2 deficiency alleviated inflammation of tMCAO/R rats as evidenced by reduced secretion of proinflammatory factors and the blockade of NLR family pyrin domain containing 3 (NLRP3) inflammasome activation. In vitro experiments showed that Plin2 expression was upregulated in mouse microglia subjected to oxygen–glucose deprivation/reoxygenation (OGD/R). Plin2 knockdown inhibited OGD/R-induced microglia activation and the accumulation of inflammation-related factors. Taken together, this study demonstrates that lipid droplet protein Plin2 contributes to the pathologic process of CI/R damage by impacting inflammatory response and NLRP3 inflammasome activation. Thus, Plin2 may provide a new therapeutic direction for CI/R injury.
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EUROPEAN JOURNAL OF PHARMACOLOGY
·
2023
·
IF 5
Shuang Zhou,Yuhua Li,Yi Hong,Zhitao Zhong,Min Zhao
Puerarin (Pue), an isoflavone compound extracted from Pueraria, has been shown to inhibit inflammation and reduce cerebral edema. The neuroprotective effect of puerarin has attracted much attention in recent years. Sepsis-associated encephalopathy (SAE) is a serious complication of sepsis that causes damage to the nervous system. This study aimed to investigate the effect of puerarin on SAE and elucidate the potential underlying mechanisms. A rat model of SAE was established by cecal ligation and puncture, and puerarin was injected intraperitoneally immediately after the operation. Puerarin was found to improve the survival rate and neurobehavioral score of SAE rats, alleviate symptoms, inhibit the level of brain injury markers NSE and S100β, and improve the pathological changes in rat brain tissue. Puerarin was also found to inhibit the level of factors related to the classical pathway of pyroptosis, such as NLRP3, Caspase-1, GSDMD, ASC, IL-1β, and IL-18. Puerarin also reduced the brain water content and penetration of Evan’s Blue dye in SAE rats, and reduced the expression of MMP-9. In the in vitro experiments, we further confirmed the inhibitory effect of puerarin on neuronal pyroptosis by establishing a pyroptosis model in HT22 cells. Our findings suggest that puerarin may improve SAE by inhibiting the classical pathway of NLRP3/Caspase-1/GSDMD-mediated pyroptosis and reducing blood-brain barrier damage, thus playing a role in brain protection. Our study may provide a novel therapeutic strategy for SAE.
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TOXICOLOGY AND APPLIED PHARMACOLOGY
·
2023
·
IF 3.8
Jiaxi Chen,Mengyue Pan,Jingjie Wang,Mengling Zhang,Mingmei Feng,Xiaoming Chai,Qi Zhang,Yang Sun
Hydroxysafflor yellow A (HSYA), a chalcone glycoside, is a component of Carthamus tinctorius L. and exerts anti-inflammatory and antioxidative effects. However, the therapeutic effect and the underlying mechanism of HSYA on ulcerative colitis is unclear. This study aimed to investigate the unexplored protective effects and underlying mechanisms of HSYA on UC. In vitro analyses showed that HSYA reduced the secretion of interleukin (IL)-1β, tumor necrosis factor (TNF)-α, and IL-6 and inhibited nucleotide-binding and oligomerization domain-like receptor protein 3 (NLRP3)/gasdermin D (GSDMD)-mediated pyroptosis in lipopolysaccharide/ adenosine-5′-triphosphate (LPS/ATP)-stimulated macrophages. Gas chromatography–mass spectrometry (GC–MS) profiling of intracellular metabolites showed that HSYA reduced the increased levels of glucose, glucose 6-phosphate, and lactic acid, and inhibited the increased hexokinase 1 (HK1) expression caused by LPS/ATP stimulation. HK1 shRNA transfection further confirmed that HSYA inhibited the NLRP3/GSDMD-mediated pyroptosis via HK1 downregulation. In vivo analyses showed that HSYA drastically attenuated UC symptoms by relieving body weight loss, a decline in colon length, and inflammatory infiltration in colonic tissues induced by dextran sulfate sodium (DSS). HSYA also reduced the secretion of pro-inflammatory cytokines including IL-1β, IL-6, TNF-α, and IL-18. Moreover, HSYA inhibited HK1/NLRP3/GSDMD-mediated pyroptosis in DSS-induced colitis mice. Finally, 16S rRNA sequencing analyses of gut microbiota revealed that HSYA reversed gut microbiota dysbiosis by reducing the abundance of Proteobacteria and increasing that of Bacteroidetes. This study demonstrated that HSYA not only exerted anti-inflammatory effects by inhibiting HK1/NLRP3/GSDMD and suppressing pyroptosis but also regulated gut microbiota in mice with DSS-induced colitis. Our findings provide new experimental evidence that HSYA might be a potential candidate for treating inflammatory bowel diseases.
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BMC Cardiovascular Disorders
·
2024
·Vol. 24
·期 1
·1-13
·
IF 2
Liu Hai-Hua,Wei Wei,Wu Fei-Fei,Cao Lu,Yang Bing-Jie,Fu Jia-Ning,Li Jing-Xia,Liang Xin-Yue,Dong Hao-Yu,Heng Yan-Yan,Zhang Peng-Fei
Background Hyperlipidemia damages vascular wall and serves as a foundation for diseases such as atherosclerosis, hypertension and stiffness. The NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome is implicated in vascular dysfunction associated with hyperlipidemia-induced vascular injury. Sodium tanshinone IIA sulfonate (STS), a well-established cardiovascular protective drug with recognized anti-inflammatory, antioxidant, and vasodilatory properties, is yet to be thoroughly investigated for its impact on vascular relaxant imbalance induced by hyperlipidemia. Methods In this study, we treated ApoE-knockout (ApoE-/-) mouse with STS and assessed the activation of the NLRP3 inflammasome, expression of MMP2/9, integrity of elastic fibers, and vascular constriction and relaxation. Results Our findings reveal that STS intervention effectively preserves elastic fibers, significantly restores aortic relaxation function in ApoE-/- mice, and reduces their excessive constriction. Furthermore, STS inhibits the phosphorylation of spleen tyrosine kinase (SYK), suppresses NLRP3 inflammasome activation, and reduces MMP2/9 expression. Conclusions These results demonstrate that STS protects vascular relaxation against hyperlipidemia-induced damage through modulation of the SYK-NLRP3 inflammasome-MMP2/9 pathway. This research provides novel insights into the mechanisms underlying vascular relaxation impairment in a hyperlipidemic environment and uncovers a unique mechanism by which STS preserves vascular relaxation, offering valuable foundational research evidence for its clinical application in promoting vascular health.
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Pharmaceuticals
·
2025
·Vol. 18
·期 8
·1109
·
IF 4.8
Lingxin Zhuo,Mingxuan Ma,Jiayi Zhang,Jiayu Zhou,Yuqi Zheng,Aiyin Liang,Qingqing Sun,Jia Liu,Wenting Liao
Background/Objectives: Sepsis-induced cardiomyopathy (SIC) is a serious clinical disorder with a high death rate. Qifu decoction (QFD) is a renowned traditional Chinese medicine with documented pharmacological actions, such as anti-inflammatory, anti-oxidant and anti-apoptosis activities, and it has good therapeutic effects on cardiovascular diseases. This study aimed to reveal the cardioprotective effects and underlying mechanisms of QFD against SIC.Methods: Electrocardiography, histopathological examination, and biochemical indicator determination were carried out to investigate the cardioprotective effects of QFD in the treatment of LPS-induced SIC mice. Metabolomics and network pharmacology strategies were employed to preliminarily analyze and predict the mechanisms of QFD against SIC. Molecular docking and Western blot were further applied to validate the core targets and potential pathways for the treatment of SIC in in vitro and in vivo models.Results: It was found that QFD considerably enhanced cardiac function; attenuated myocardial injury; and reduced the serum levels of LDH, CK-MB, IL-1β, and TNF-α by 28.7%, 32.3%, 38.6%, and 36.7%, respectively. Metabolomic analysis showed that QFD could regulate seven metabolic pathways, namely, glutathione metabolism; alanine, aspartate, and glutamate metabolism; arachidonic acid metabolism; glycerophospholipid metabolism; purine metabolism; sphingolipid metabolism; and fatty acid metabolism. Network pharmacology suggested that the anti-SIC effect of QFD may be mediated through the TNF, toll-like receptor, NOD-like receptor, NF-κB, and PPAR signaling pathways. Additionally, 26 core targets were obtained. Molecular docking revealed that active ingredients such as formononetin, kaempferol, quercetin, and (R)-norcoclaurine in QFD had a high affinity for binding to PPARα and TLR4. Further Western blot validation indicated that QFD could regulate the protein levels of NLRP3, TLR4, NF-κB, IL-6, TNF-α, COX2, sPLA2, PPARα, CPT1B, and CPT2.Conclusions: This study demonstrates that QFD can alleviate SIC by suppressing the TLR4/NF-κB/NLRP3 inflammatory pathway and modulating impaired FAO through the activation of the PPARα/CPT pathway, highlighting QFD as a promising candidate drug for SIC treatment.
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Molecular & Cellular Toxicology
·
2025
·
IF 1.4
He Chaojie,Fan Hongyan,Zhu Chunyan,Huang Yueqing
Background Ischemia–reperfusion (I/R) injury is a severe disorder during revascularization therapy against acute myocardial infarction. Objective Our study aims to investigate the role and regulation mechanism of Annexin A1 (ANXA1) against I/R injury. Results Western blotting analysis showed that ANXA1 expression in rat cardiomyocytes (H9C2 cells) was notably decreased by oxygen–glucose deprivation/reperfusion (OGD/R) treatment. Meanwhile, the NLRP3 inflammasome activation accompanied by pyroptosis and inflammation was observed in H9c2 cells under OGD/R induction. Besides, overexpression or knockdown of ANXA1 dramatically inhibited or aggravated NLRP3-mediated pyroptosis and inflammation. Further investigations found that the m 6 A level of ANXA1 was upregulated by OGD/R, thus leading to decreased mRNA stability in H9C2 cells. FTO, a N6-methyladenosine (m 6 A) “eraser”, was downregulated in H9C2 cells by OGD/R and shown to increase the ANXA1 protein expression by demethylating mRNA in H9c2 cells under OGD/R induction. Moreover, knockdown FTO reversed the protection of ANXA1 against NLRP3-mediated pyroptosis and inflammation in OGD/R-induced H9C2 cells. Conclusion ANXA1 protects cardiomyocytes against I/R injury by alleviating NLRP3-mediated pyroptosis and inflammation via FTO-mediate demethylation. These findings innovatively suggest the therapeutic potential of ANXA1 for myocardial I/R injury.
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JOURNAL OF ETHNOPHARMACOLOGY
·
2025
·
IF 5.4
HuiNa Yang,Qiao Peng,Ruonan Shuang,Zihang Guo,Hao Yang,Chang Chen,Weiwei Tao,Li Liu
Ethnopharmacological relevance Depression in traditional Chinese medicine is mechanistically linked to neuroinflammation–a key pathogenesis driving depressive disorders. Baixian Houpo Decoction (BXHPD), originating from the classical TCM text Jinkui Yaolue, is prescribed for depression attributable to “phlegm-qi stagnation”. While modern pharmacological studies confirm its potent anti-inflammatory properties, the molecular pathways underpinning BXHPD’s therapeutic effects against neuroinflammation remain undefined. Objective We aimed to evaluate the antidepressant effect of BXHPD in a cortical corticosterone (CORT)-induced mouse model of depression and its potential molecular mechanisms. Materials and Methods Male C57BL/6 wild-type and Aldh1l1-Cre/ERT2 mice received CORT injections to induce depression. Behavioral tests included sucrose preference (SPT), tail suspension (TST), forced swim (FST), and open field (OFT) tests. Hippocampal neuropathology was assessed via Nissl staining for neuronal damage and ELISA for pro-inflammatory (IL-1β, IL-6, TNF-α) and anti-inflammatory (IL-10, IL-4) cytokines. Molecular analyses involved CO-IP for O-linked N-acetylglucosamine (O-GlcNAc) transferase (OGT)-Cathepsin B (CTSB) interaction, O-GlcNAcylation, and NLRP3 inflammasome activation; western blotting for protein expression; immunofluorescence for OGT/GFAP and CTSB/LAMP1 colocalization; and DHE staining for ROS detection. Results BXHPD alleviated depressive-like behaviors, reduced neuronal damage, and inhibited pro-inflammatory cytokine release in depressed mice. Mechanistically, BXHPD downregulated OGT, thereby reducing CTSB O-GlcNAcylation to promote its maturation. This decrease in O-GlcNAcylation lowered ROS levels, attenuated lysosomal membrane permeabilization (LMP), limited cytoplasmic CTSB leakage, and ultimately suppressed NLRP3 inflammasome activation. Conclusion BXHPD targets astrocytes in the medial prefrontal cortex via the OGT /CTSB/NLRP3 pathway to alleviate neuroinflammation and improve depressive-like behaviors.
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INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
·
2025
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IF 8.5
Wen-Jing Xiao,Su Dong,Yue Xuan,Xiao-Jie Huang,Jing-Rui Feng,Hong-Jing You,Yang Chen
Existing studies lack systematic investigation of the polysaccharide components in Citri Reticulatae Pericarpium (CRP), despite established anti-inflammatory and cardioprotective effects of its bioactive constituents. This study isolated and characterized CRP-derived polysaccharides, focusing on CP-0's protective role against Lactobacillus casei cell wall extract (LCWE)-induced endothelial barrier dysfunction. Structural characterization identified CP-0 and CP-1 as novel triple-helical heteropolysaccharides (MW 81,404 and 83,540 Da; glucose, ribose, mannose). Following isolation and physicochemical screening, CP-0 exhibited low cytotoxicity and high anti-inflammatory activity. Mechanistic analyses revealed that CP-0 attenuated LCWE-induced endothelial injury by reducing inflammatory infiltration, IL-1β levels, and adhesion molecules (VCAM-1/ICAM-1) while upregulating tight junction proteins ZO-1/2 in mouse microvascular endothelial cells (MVECs). CP-0 suppressed NLRP3 inflammasome activation via decreased colocalization of NLRP3/Caspase-1/ASC, and competitive binding assays confirmed its interaction with TLR2, which blocked NF-κB nuclear translocation. By targeting TLR2-mediated signaling pathways, CP-0 effectively mitigated LCWE-induced coronary arteritis in vitro, demonstrating potential as a therapeutic candidate for cardiovascular diseases through early-stage anti-inflammatory intervention.
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Brain and Behavior
·
2026
·Vol. 16
·期 10
·e71773
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IF 2.8
Xin-ying Cai,Wen-jun Li,Cai-xia Chen,Lu Peng,Li-chao Yang,Xiao-ning Lin,Hong-tao Liu,Jian-bo Jia,Yan-chao Jiao,Ying Li
Background Glycyrrhizic acid (Gly-A) exhibits anti-inflammatory and antioxidant effects in various central nervous system disorders. Acute fatigue and chronic fatigue (CF) are associated with serious physical and psychological effects. However, the underlying pathophysiology and effective therapeutic strategies for these conditions remain poorly understood. Purpose This study aims to evaluate the therapeutic potential of Gly-A against fatigue, and to elucidate the underlying mechanisms of its action. Methods We established a mouse model of acute exercise-induced fatigue and evaluated fatigue-related indices. To identify specific pathways involved in Gly-A's therapeutic effects, we employed RNA sequencing, network pharmacology, and in vitro oxygen-deficit models, aiming to clarify the mechanisms. Additionally, we established a mouse model of CF to compare the therapeutic efficacy of Gly-A with positive control drugs by assessing identical parameters. Results Gly-A significantly improved fatigue-related indices without affecting body weight. RNA sequencing and network pharmacology analyses showed that Gly-A modulates oxidative stress responses and targets the NF-κB (nuclear factor-kappa B)/NLRP3 (NOD-like receptor thermal protein domain associated protein 3) signaling and apoptotic pathways. In the CF mouse model, oral administration of Gly-A significantly increased motor activity, alleviated anxiety and depression, and improved neurocognitive function compared to model mice, exhibiting superior efficacy to positive control drugs. These findings suggest that Gly-A exerts anti-inflammatory effects by targeting the NF-κB/NLRP3 signaling pathway, thereby reducing neuronal apoptosis in CF. Conclusions Gly-A exhibits therapeutic potential against acute exercise-fatigue and CF, primarily by attenuating apoptosis through the inhibition of the NF-κB/NLRP3 signaling pathway.
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EUROPEAN JOURNAL OF PHARMACOLOGY
·
2026
·
IF 5.7
Ting Yang,Min Feng,Hui Yin,Jian-Hua Wan,Yong-Hong Liang,Xiao Zhang,Chang Peng,Tao Yang,Ming Yang,Hai-Yan Zhang
The natural product-derived small-molecule ZY12 demonstrates potent therapeutic efficacy against ulcerative colitis (UC) in a preclinical model. • It alleviates colitis by specifically inhibiting the NLRP3 inflammasome, thereby ameliorating colonic inflammation, oxidative stress, and intestinal barrier damage. • ZY12 promotes intestinal homeostasis by remodeling gut microbiota, restoring beneficial SCFA levels, and correcting dysregulated host bile acid metabolism. • The study proposes that ZY12 exerts its effects through multi-target interactions spanning immune modulation, microbiome regulation, and metabolic reprogramming. Ulcerative colitis (UC) is a chronic inflammatory bowel disease (IBD) with limited treatment options. The natural compound 1,2,4-Trimethoxybenzene (ZY12) is a known NLRP3 inflammasome inhibitor, but its potential in UC remains unclear. This study evaluated the efficacy of ZY12 using a dextran sulfate sodium (DSS)-induced mouse model and integrated molecular, histological, 16S ribosomal RNA (16S rRNA) sequencing, short-chain fatty acids (SCFAs) and metabolomics analyses. Results showed that ZY12 significantly alleviated DSS-induced UC in mice, as evidenced by reduced weight loss, less colon shortening, and lower DAI scores. Mechanistically, ZY12 effectively inhibited NLRP3 inflammasome activation and downregulated the expression of pro-inflammatory cytokines, specifically interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α), and also reduced the level of calprotectin (S100A8/A9), a clinical marker of intestinal inflammation. Furthermore, ZY12 ameliorated colonic oxidative stress by enhancing the activities of the antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), while reducing the levels of the oxidative damage markers malondialdehyde (MDA) and myeloperoxidase (MPO). Concurrently, ZY12 upregulated the key intestinal barrier-related proteins, namely Claudin-1, Occludin, zonula occludens-1 (ZO-1), and mucin 2 (MUC2). Comprehensive analyses revealed that ZY12 reshapes the gut microbiota composition by enriching beneficial bacterial taxa, increases levels of SCFAs (i.e., acetic acid, propionic acid, and butyric acid), and restores dysregulated host-microbiota co-metabolism, particularly through targeted modulation of the primary bile acid biosynthesis pathway. In conclusion, ZY12 alleviates UC via a synergistic regulatory network involving “immune modulation-microbiota reshaping-metabolic restoration”. These findings highlight ZY12's potential as a promising multi-target therapeutic candidate for UC. Download: Download high-res image (329KB) Download: Download full-size image
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Small
·
2025
·
IF 12.1
Yushan Yang,Nana Chen,Jian Fan,Limin Fan,Yanni Cai,Liangyi Xue,Shiyu Chen,Zichen Yang,Lulu An,Jianwei Cheng,Tianbin Ren,Yongyong Li
Macrophage phenotypic dysregulation, spatially by biofilm and dynamically in time, impedes the healing of diabetic ulcers (DUs). Effective treatment requires enabling spatiotemporal regulation of macrophage polarization, balancing the M1 pro-inflammatory antimicrobial response with the M2 anti-inflammatory tissue-regeneration response. Here, a core-shell microneedle system (LM-MG@MN) is proposed with spatiotemporal immunomodulation features, designed to spatially disrupt biofilm barriers and sequentially induce macrophage polarization from M0 to M1 and subsequently to M2 by regulating the NLRP3/IL-1β pathway. Glucose oxidase (GOX)-loaded 2D MXene nanosheets (MG) are encapsulated in a hyaluronic acid-β-cyclodextrin (HA-β-CD) matrix as the MN shell layer. The rapid dissolution of this shell triggers MG to induce pro-inflammatory polarization of macrophages from M0 to M1, aiding in clearing biofilm infections. Liposomes (LM) carrying the NLRP3 inflammasome inhibitor MCC950 are embedded within a methacrylate hyaluronic acid (HAMA) matrix in the MN core. In the later stages of wound healing, LM is released gradually from the core, promoting the anti-inflammatory polarization of macrophages from M1 to M2 and accelerating tissue regeneration by enhancing crosstalk with fibroblasts and endothelial cells. Additionally, RNA sequencing indicates that LM-MG@MN regulates macrophage metabolic reprogramming to enhance DUs healing. This spatiotemporal immunomodulation strategy offers a promising approach for clinical DUs treatment.
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ACS Applied Materials & Interfaces
·
2026
·
IF 8.2
Mingjing Wang,Kang Liu,Peng She,Tianci Gao,Zhansen Shi,Yunlai Wang,Xiaoya Ding,Ye Yang,Dengke Yin,Wei Shen,Hanmeng Liu
Rheumatoid arthritis (RA) tissues exhibit high levels of reactive oxygen species (ROS) and free Ca2+, which contribute to a vicious cycle of sustained inflammatory responses. This study developed an in situ Ca2+-reinforced injectable full-active HPAP hydrogel. The full-active hydrogel is formed by cross-linking phenylboronic acid-functionalized hyaluronic acid (HA-PBA) with sodium alginate (ALG) and paeoniflorin (PF) through boronate ester bonds, all of which play significant roles in RA treatment. HPAP hydrogel exhibits relatively low strength in vitro, allowing for easy injection into the joint cavity. Then, ALG can trigger secondary cross-linking in the RA joint cavity using Ca2+, forming the HPAP/Ca2+ hydrogel in situ and enhancing drug retention (with significant signals detectable in vivo even 17 days postinjection). Furthermore, a decrease in the free Ca2+ concentration can inhibit the activation of the NLRP3 inflammasome pathway. HA-PBA participates in the formation of ROS-responsive boronate ester bonds in hydrogel, thereby reducing ROS levels in RA tissues. Additionally, the released PF inhibits the activation of the NF-κB pathway, mitigating the inflammatory response. In vitro and in vivo experiments demonstrate that the HPAP hydrogel can effectively scavenge ROS, inhibit the NF-κB and NLRP3 pathways, reprogram macrophages, and reduce osteoclast differentiation and cartilage matrix degradation. In the RA animal models, HPAP hydrogel significantly improved arthritis scores, bone erosion, and inflammation levels, showing better treatment efficacy compared to commercial dexamethasone. Given the simplicity of the components of this full-active hydrogel, all of which are natural and safe compounds, it exhibits promising clinical translation potential in RA treatment.
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