JOURNAL OF NEUROCHEMISTRY
·
2015
·Vol. 134
·期 5
·904-914
·
IF 4.281
Zhuang Wu,Linlang Li,Long-Tai Zheng,Zhihong Xu,Lin Guo,Xuechu Zhen
Recent studies have shown that sigma-1 receptor orthodox agonists can inhibit neuroinflammation. SKF83959 (3-methyl-6-chloro-7,8-hydroxy-1-[3-methylphenyl]-2,3,4,5-tetrahydro-1H-3-benzazepine), an atypical dopamine receptor-1 agonist, has been recently identified as a potent allosteric modulator of sigma-1 receptor. Here, we investigated the anti-inflammatory effects of SKF83959 in lipopolysaccharide (LPS)-stimulated BV2 microglia. Our results indicated that SKF83959 significantly suppressed the expression/release of the pro-inflammatory mediators, such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), inducible nitric oxide synthase (iNOS), and inhibited the generation of reactive oxygen species. All of these responses were blocked by selective sigma-1 receptor antagonists (BD1047 or BD1063) and by ketoconazole (an inhibitor of enzyme cytochrome c 17 to inhibit the synthesis of endogenous dehydroepiandrosterone, DHEA). Additionally, we found that SKF83959 promoted the binding activity of DHEA with sigma-1 receptors, and enhanced the inhibitory effects of DHEA on LPS-induced microglia activation in a synergic manner. Furthermore, in a microglia-conditioned media system, SKF83959 inhibited the cytotoxicity of conditioned medium generated by LPS-activated microglia toward HT-22 neuroblastoma cells. Taken together, our study provides the first evidence that allosteric modulation of sigma-1 receptors by SKF83959 inhibits microglia-mediated inflammation. SKF83959 is a potent allosteric modulator of sigma-1 receptor. Our results indicated that SKF83959 enhanced the activity of endogenous dehydroepiandrosterone (DHEA) in a synergic manner, and inhibited the activation of BV2 microglia and the expression/release of the pro-inflammatory mediators, such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), inducible nitric oxide synthase (iNOS).
研究领域:
神经科学
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免疫学
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药理学
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DOI
PubMed
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
INTERNATIONAL IMMUNOPHARMACOLOGY
·
2024
·
IF 4.8
Qiang Zhou,Meiyu Chang,Shuhan Guo,Yiming Zhang,Qiufang Qu,Qingnan Zhou,Zhiheng Li,Sanqiao Yao
Silicosis is a life-threatening occupational disease because of inhaling silica dust, leading to chronic inflammation, pyroptosis, and fibrosis. Unfortunately, it is still lacking effective pharmacological intervention currently. Honokiol ( HKL ), a natural extract with biological activity from Magnolia bark, is known for its antioxidant and anti-inflammatory biological effects. The current work aimed to investigate the therapeutic potential of HKL in mitigating silica-induced lung fibrosis and pyroptosis, particularly focusing on the cGAS/STING signaling pathway. The pulmonary pathological results shown in H&E and Masson’s trichrome staining images confirmed the protective effects of HKL on lung tissue structure. In addition, HKL significantly reduced lung inflammation, collagen deposition, and oxidative stress compared to mice in the silicosis group. HKL treatment also alleviated silica-induced pyroptosis by suppressing the activation of the cGAS/STING signaling pathway in lung tissues. Moreover, the in vitro experiments using J774A.1 macrophages demonstrated that HKL reduced pyroptosis and improved cell viability under exposure to silica combined lipopolysaccharide (LPS). These were attributed to HKL downregulating the activation of the cGAS/STING signaling pathway in pyroptotic J774A.1 cells induced by silica combined with LPS. Meanwhile, inhibition of STING signaling induced by DNase I significantly enhanced the protective effects of HKL on the inflammatory and pyroptotic processes induced by silica. Overall, HKL could attenuate silica-induced pyroptosis by modulating the cGAS/STING signaling pathway against pulmonary fibrosis. The current study offers a promising approach for treating silicosis and related inflammatory responses.
研究领域:
药理学
·
肺病学
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免疫学
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分子生物学
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DOI
PubMed
高影响因子
Materials Science & Engineering C-Materials for Biological Applications
·
2019
·
IF 4.959
Yangyang Duan,Nan Wang,Zixu Huang,Hongxiu Dai,Ling Xu,Shengjun Sun,Houyi Ma,Meng Lin
An electrochemical aptasensor for the lipopolysaccharide (LPS) detection was constructed by using copper-based metal-organic framework (Cu-MOF) as a label and the LPS aptamer of specific single-stranded DNA as a probe. The carboxyl-functionalized polypyrrole nanowires (PPy NWs) were synthesized by electrochemical polymerization method, and the amino-terminated aptamer covalently coupling with the carboxyl group of the PPy NWs was immobilized onto the modified electrode. The aptamer can specifically combine with the target LPS molecules, and Cu-MOF was labeled by adsorption based on specific interactions of LPS carbohydrate portions with anionic groups. The fabrication processes of the aptasensor were characterized by scanning electron microscopy (SEM), X-ray photoelectron spectroscopy (XPS) and electrochemical impedance spectroscopy (EIS). Differential pulse voltammetry (DPV) was used to measure electrochemical performance of the aptasensor, and the electrochemical signal can be directly measured by the electrochemical redox reaction of Cu(II)/Cu(I) existed in the Cu-MOF. The electrochemical aptasensor exhibited a high sensitivity toward LPS ranging from 1.0 pg/mL to 1.0 ng/mL with a detection limit of 0.29 pg/mL. Moreover, the developed sensor was found to have good selectivity, stability and regeneration properties, and the sensor also successfully detected LPS in real tap water samples.
研究领域:
分析化学
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电化学
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生物传感器
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环境监测
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DOI
PubMed
高影响因子
Foods
·
2024
·Vol. 13
·期 10
·1523
·
IF 4.7
Mengyao Zhang,Huiqian Liu,Linlin Xu,Xizi Zhang,Wei Chen,Chengtao Wang
Histamine, a bioactive component in certain foods such as Huangjiu has been associated with liver injury and disrupted intestinal balance. This study explored the potential therapeutic effects of fucoidan (FCD) in mitigating histamine-induced imbalances in mice. We found that FCD mitigated liver injury, reducing transaminases, oxidative stress, and inflammation. Histological improvements included decreased cell infiltration and necrosis. FCD restored tight junction proteins and suppressed inflammation-related genes. Western blot analysis revealed FCD’s impact on TGF-β1,p-AKT, AKT, CYP2E1, Grp78, NLRP3, Cas-1, and GSDMD. Gut LPS levels decreased with FCD. Gut microbiota analysis showed FCD’s modulation effect, reducing Firmicutes and increasing Bacteroides. FCD demonstrates potential in alleviating histamine-induced liver injury, regulating inflammation, and influencing gut microbiota. Further research exploring higher dosages and additional parameters is warranted.
研究领域:
药理学
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肝病学
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免疫学
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微生物学
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DOI
PubMed
高影响因子
Journal of Translational Medicine
·
2024
·Vol. 22
·期 1
·1-19
·
IF 6.1
Qin Qian,Shan Zhiyan,Xing Lei,Jiang Yutong,Li Mengyue,Fan Linlin,Zeng Xin,Ma Xinrui,Zheng Danyang,Wang Han,Wang Hui,Liu Hao,Liang Shengjun,Wu Lijie,Liang Shuang
Autism spectrum disorder (ASD) is a multifaceted neurodevelopmental disorder predominant in childhood. Despite existing treatments, the benefits are still limited. This study explored the effectiveness of mesenchymal stem cell-derived extracellular vesicles (MSC-EVs) loaded with miR-137 in enhancing autism-like behaviors and mitigating neuroinflammation. Utilizing BTBR mice as an autism model, the study demonstrated that intranasal administration of MSC-miR137-EVs ameliorates autism-like behaviors and inhibits pro-inflammatory factors via the TLR4/NF-κB pathway. In vitro evaluation of LPS-activated BV2 cells revealed that MSC-miR137-EVs target the TLR4/NF-κB pathway through miR-137 inhibits proinflammatory M1 microglia. Moreover, bioinformatics analysis identified that MSC-EVs are rich in miR-146a-5p, which targets the TRAF6/NF-κB signaling pathway. In summary, the findings suggest that the integration of MSC-EVs with miR-137 may be a promising therapeutic strategy for ASD, which is worthy of clinical adoption.
研究领域:
神经科学
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干细胞生物学
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分子生物学
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药理学
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DOI
PubMed
高影响因子
Nano Today
·
2024
·
IF 13.2
Hongbing Liu,Muse Ji,Yi Qin,Yin Sun,Hanxun Wang,Peifu Xiao,Jiansong Zhao,Yaxin Deng,Zhen Zhang,Jingxin Gou,Tian Yin,Haibing He,Guoliang Chen,Xing Tang,Yu Zhang
Cytokine storm and pulmonary fibrosis caused by Coronavirus Disease 2019 (COVID-19) are the two major culprits threatening human life and health. Herein, we engineered a novel disulfide-bridged carrier-free prodrug self-assembled nanoparticles (DSSL NPs) composed of Dexamethasone (Dex) and α-linolenic acid (LNA) for synergistic inhibition of cytokine storm and pulmonary fibrosis. DSSL NPs possess the capability to selectively target injured lung tissue and precisely release drugs after intravenous administration. Consequently, a single administration of DSSL NPs effectively mitigated pro-inflammatory cytokines and tissue damage in mice with lipopolysaccharide (LPS)-induced cytokine storm by blocking the TNF, NF-κB, and Toll-like receptor signaling pathways. Moreover, long-term administration of DSSL NPs alleviated the abnormal fibroblast activation and collagen deposition in mice with LPS-induced pulmonary fibrosis by inhibiting the Wnt-PCP signaling pathway without obvious Dex-related side effects. Together, DSSL NPs achieved the effect of ‘killing two birds with one stone’, presenting a safe and reliable strategy for comprehensive treatment for COVID-19-related diseases.
研究领域:
药学
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纳米技术
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免疫学
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肺科学
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病毒学
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DOI
高影响因子
INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE
·
2025
·Vol. 66
·期 5
·21-21
·
IF 4.7
Xianyang Liu,Hangjia Zuo,Chao Wu,Na Li,Qian Zhou,Fan Cao,Baorui Chu,Shuhao Zeng,Hui Feng,Yakun Wang,Fengyang Lei,Ke Hu,Shengping Hou
Purpose:Uveitis is an immune-mediated ocular disorder that poses a significant threat to vision, particularly among young and middle-aged adults. The treatment of uveitis is complicated by the presence of the blood-retinal barrier (BRB), which restricts the passage of large molecular drugs into the eye, thus limiting effective therapeutic options. The primary objective of this study is to identify a novel therapeutic agent capable of treating uveitis and explore its underlying mechanism.Methods:In this study, we used a mouse model of experimental autoimmune uveitis (EAU) induced by interphotoreceptor retinoid-binding protein (IRBP) and lipopolysaccharide (LPS) and interferon-gamma (IFN-γ)-induced inflammatory BV2 cells. Evans blue and fundus fluorescein angiography (FFA) experiments were performed to evaluate the destruction of BRB. Silt lamp and hematoxylin and eosin (H&E) staining were conducted to evaluate the inflammatory response. In vivo proteomics and Western blot were carried to investigate the underlying mechanisms.Results:Our study reveals that Muscone significantly alleviates EAU and restores the integrity of BRB. Moreover, Muscone treatment markedly downregulated inflammatory factors within the retinas and BV2 cells. In vivo proteomic combined with liquid chromatography-mass spectrometry (LC-MS) has elucidated that Muscone exerts its anti-inflammatory effects by modulating the PI3K-AKT signaling pathway. Moreover, by using LY294002 to specifically inhibit PI3K, we observed a marked decrease in inflammatory phenotype and BRB destruction of EAU.Conclusions:In summary, this study establishes the protective efficacy of Muscone against the progression of EAU and provides insights into the molecular mechanisms responsible for its therapeutic action.
研究领域:
免疫学
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眼科学
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药理学
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分子生物学
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神经炎症
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产品关联
DOI
PubMed
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
·
2025
·
IF 5.4
Xia Liu,Nannan Wang,Tingting Cai,Hua Chen,Chunhui Dai,Wanping Zhu
Ethnopharmacological relevance Acute lung injury (ALI), a critical complication of severe pneumonia, lacks targeted therapies. Astilbe chinensis (Maxim.) Franch. & Sav. possesses documented anti-inflammatory and respiratory-protective properties, yet its efficacy against ALI, bioactive constituents, and mechanisms remain unexplored. Aim of the study This study sought to evaluate the therapeutic efficacy and elucidate the mechanisms of action of Astilbe chinensis in the treatment of ALI through the application of network pharmacology and experimental methodologies. Materials and methods UHPLC-MS was used to analyze plasma components absorbed after Astilbe chinensis administration in rats. Inflammation-related targets and pathway enrichment analyses were conducted via network pharmacology technique. Pulmonary function was assessed using forced lung function measurements in a LPS-induced ALI mouse model. ELISA quantified inflammatory mediators, including pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, IFN-γ), chemokines (CCL5, CXCL2), and the anti-inflammatory cytokine IL-10 in mouse lung tissue. Flow cytometry evaluated macrophage polarization, and HE staining examined histopathological changes. qRT-PCR determined the mRNA expression levels of genes like CCR1, IKBKB, CXCL8, STAT3, CXCR4, AKT1, CCL3, CCL5, iNOS, Arg1, YM1 and CCR5, while simple western analysis evaluated the protein expression of t-AKT, p-AKT, t-STAT3, p-STAT3, CCR1 and CCR5 in mouse lung tissues affected by Astilbe chinensis . Results In this study, 20 blood-borne components of Astilbe chinensis were identified, predicted to interact with 369 potential molecular targets, with 331 related to ALI treatment. GO and KEGG pathway analyses showed that 36 targets participate in inflammatory processes, mainly via chemokine signaling pathways. Key targets identified include CCR1, IKBKB, CXCL8, STAT3, CXCR4, AKT1, and CCR5. The principal active constituents of Astilbe chinensis with potential efficacy against ALI were identified as cyclo(phenylalanyl-prolyl), 5-(6-hydroxy-6-methyloctyl)- -2,5-dihydrofuran-2-one, nicotinamide, 3-phenyllactic acid, and phloretin. In vivo studies demonstrated that Astilbe chinensis administration significantly increased M2 macrophage populations in lung tissue while improving forced pulmonary function parameters. Furthermore Astilbe chinensis reduces the levels of inflammatory factors TNF-α, IL-6, IFN-γ, CCL5 (the ligand for CCR5 and CCR1), and the neutrophil chemokine CXCL2 in the lung tissues of ALI mice, while significantly increasing the content of the anti-inflammatory cytokine IL-10. Additionally, Astilbe chinensis significantly downregulated gene expression of chemokine receptors CCR1, CCR5 and their ligands CCL3, CCL5 in ALI mouse lung tissues, while upregulating anti-inflammatory markers Arg1 and Ym1 (M2 macrophage biomarkers). Meanwhile, it exerts a notable inhibitory effect on the protein expression of CCR1, CCR5, p-AKT, and p-STAT3. Conclusion This study demonstrates that Astilbe chinensis significantly improves lung function and pulmonary inflammation in mice with ALI. Component identification combined with network pharmacology analysis reveals that its major anti-inflammatory components are cyclo(phenylalanyl-prolyl), 5-(6-hydroxy-6- -methyloctyl)-2,5-dihydrofuran-2-one, nicotinamide, 3-phenyllactic acid, and phloretin. The anti-inflammatory mechanism may involve inhibiting the gene and protein expression of inflammatory chemokines CCR1 and CCR5, suppressing the activity of the AKT/STAT3 signaling pathway, reducing the expression of inflammatory factors, promoting M2 macrophage polarization, and thereby increasing the release of anti-inflammatory genes and cytokines, ultimately exerting anti-inflammatory effects.
研究领域:
药理学
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民族药理学
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炎症研究
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呼吸系统疾病
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网络生物学
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系统药理学
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免疫学
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产品关联
DOI
PubMed
高影响因子
Chinese Medicine
·
2025
·Vol. 20
·期 1
·1-18
·
IF 5.7
Wang Xu,Peng Hui-Ming,Zhang Meng-Ru,Li Jing-Jing,Zhao Chuan-Peng,Zhang Ya-Li,Wang Si-Yu,Zhu Si-Ying,Lu Jian-Kang,Yin Hai-Long,Yin Qiang,Fang Jin-Bo
Background Steroid-resistant asthma (SRA) is a form of asthma resistant to corticosteroid therapy, which is characterized by the presence of neutrophil-predominant inflammatory response and neutrophil extracellular traps (NETs) formation. Hyssopus cuspidatus Boriss., a traditional Uyghur medicine, is known for its efficacy in treating inflammatory lung conditions such as asthma. However, the therapeutic impact and underlying mechanisms of Hyssopus cuspidatus Boriss.’s volatile oil (HVO) in SRA have not been fully elucidated. Methods This study established an ovalbumin/lipopolysaccharide (OVA/LPS)-induced SRA mice model to evaluate the therapeutic effect of HVO on SRA. UPLC-QE-Orbitrap-MS was applied to analyze the serum compositions of HVO. Network pharmacology and molecular docking were employed to uncover the complex mechanisms of HVO in treating SRA and predict potential effective compounds in HVO. Furthermore, in vivo studies in SRA mice and in vitro studies using HL-60 cells and bone marrow neutrophils were conducted to validate the mechanism. Results HVO could significantly ameliorate OVA/LPS-induced SRA symptoms, including airway hyperresponsiveness, airway inflammation, mucus overproduction and airway remodeling. 41 prototype compounds, 65 Phase I metabolites and 50 Phase II metabolites were identified in serum-containing HVO. The integration of network pharmacology with experimental validation revealed that HVO can inhibit the formation of NETs by targeting neutrophil elastase, thereby exerting a therapeutic influence on SRA. Meanwhile, molecular docking results showed that 3-methoxy-4-hydroxy mandelonitrile, 1,2,3,4-tetrahydro-1,5,7-trimethyl-naphthalene, cis-calamenene and aristol-1(10)-en-9-yl isovalerate may be the therapeutic compounds of HVO in treating SRA. Conclusion These findings suggest that HVO is a promising therapeutic candidate for neutrophil-dominant SRA by targeting NETs formation.
研究领域:
药理学
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免疫学
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呼吸病学
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传统医学
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产品关联
DOI
PubMed
高影响因子
SusMat
·
2024
·
IF 18.7
Anxiong Liu,Lu Chen,Luhe Qi,Jing Huang,Yongkang Zou,Zhiwen Hu,Le Yu,Zibiao Zhong,Qifa Ye,Chaoji Chen
Sepsis is responsible for approximately 5.3 million deaths globally each year. Here, we constructed hierarchical chitin microspheres loaded with MOF-919 (Ch/metal–organic frameworks [MOFs]) for the rapid and efficient removal of lipopolysaccharide (LPS) in complex blood environments. Furthermore, abundant active sites on MOF-919(Sc) also enable a record-high adsorption capacity of 9.56 mg/g in biomass-based adsorbents due to the coordination interactions between endotoxin and MOF-919(Sc). The LPS level of sepsis rabbits was less than 2 EU/mL (clearance rate >95%) after 90-min hemoperfusion, showing no adverse effect on the rabbit organs. Additionally, compared to the commonly used LPS scrubber Toraymyxin (polymethyl methacrylate), the chitin adsorbent is significantly more cost-effective and environmentally friendly. The preparation strategy for hierarchical porous microspheres offers notable advantages in designability, recyclability, and renewability, providing a new approach to sepsis treatment and promising prospects for the biomedical application of sustainable biomass materials.
研究领域:
生物医学工程
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材料科学
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败血症治疗
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生物材料
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环境科学
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DOI
高影响因子
MOLECULES
·
2024
·Vol. 29
·期 7
·1534
·
IF 4.2
Zhizhi Chen,Lei Wang,Dongxia He,Qi Liu,Qinqin Han,Jinyang Zhang,A-Mei Zhang,Yuzhu Song
Antibiotic resistance has emerged as a grave threat to global public health, leading to an increasing number of treatment failures. Antimicrobial peptides (AMPs) are widely regarded as potential substitutes for traditional antibiotics since they are less likely to induce resistance when used. A novel AMP named Brevinin-1BW (FLPLLAGLAASFLPTIFCKISRKC) was obtained by the Research Center of Molecular Medicine of Yunnan Province from the skin of thePelophylax nigromaculatus. Brevinia-1BW had effective inhibitory effects on Gram-positive bacteria, with a minimum inhibitory concentration (MIC) of 3.125 μg/mL againstEnterococcus faecalis(ATCC 29212) and 6.25 μg/mL against bothStaphylococcus aureus(ATCC 25923) and multidrug-resistantStaphylococcus aureus(ATCC 29213) but had weaker inhibitory effects on Gram-negative bacteria, with a MIC of ≥100 μg/mL. Studies using scanning electron microscopy (SEM) and flow cytometry have revealed that it exerts its antibacterial activity by disrupting bacterial membranes. Additionally, it possesses strong biofilm inhibitory and eradication activities as well as significant lipopolysaccharide (LPS)-binding activity. Furthermore, Brevinin-1BW has shown a significant anti-inflammatory effect in LPS-treated RAW264.7 cells. In conclusion, Brevinin-1BW is anticipated to be a promising clinical agent with potent anti-Gram-positive bacterial and anti-inflammatory properties.
研究领域:
微生物学
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药理学
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传染病学
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分子生物学
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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）