BRITISH JOURNAL OF PHARMACOLOGY
·
2022
·Vol. 180
·期 3
·287-307
·
IF 9.473
Li Li,Xulin Xu,Keyu Lv,Guijuan Zheng,Hao Wang,Shuai Chen,Lang Huang,Yi Liu,Yadong Zhang,Zhaoming Tang,Lili Zhang,Jinyu Wang,Jianlin Qiao,Hongliang Li,Xuanbin Wang,Guangmin Yao,Chao Fang
Background and Purpose Thrombosis is a major cause of morbidity and mortality worldwide. Platelet activation by exposed collagen through glycoprotein VI (GPVI) and formation of neutrophil extracellular traps (NETs) are critical pathogenic factors for arterial and venous thrombosis. Both events are regulated by spleen tyrosine kinase (Syk)-mediated signalling events. Asebogenin is a dihydrochalcone whose pharmacological effects remain largely unknown. This study aims to investigate the antithrombotic effects of asebogenin and the underlying molecular mechanisms. Experimental Approach Platelet aggregation was assessed using an aggregometer. Platelet P-selectin exposure, integrin activation and calcium mobilization were determined by flow cytometry. NETs formation was assessed by SYTOX Green staining and immunohistochemistry. Quantitative phosphoproteomics, microscale thermophoresis, in vitro kinase assay and molecular docking combined with dynamics simulation were performed to characterize the targets of asebogenin. The in vivo effects of asebogenin on arterial thrombosis were investigated using FeCl 3 -induced and laser-induced injury models, whereas those of venous thrombosis were induced by stenosis of the inferior vena cava. Key Results Asebogenin inhibited a series of GPVI-induced platelet responses and suppressed NETs formation induced by proinflammatory stimuli. Mechanistically, asebogenin directly interfered with the phosphorylation of Syk at Tyr525/526, which is important for its activation. Further, asebogenin suppressed arterial thrombosis demonstrated by decreased platelet accumulation and fibrin generation and attenuated venous thrombosis determined by reduced neutrophil accumulation and NETs formation, without increasing bleeding risk. Conclusion and Implications Asebogenin exhibits potent antithrombotic effects by targeting Syk and is a potential lead compound for the development of efficient and safe antithrombotic agents. Graphical
研究领域:
药理学
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血液学
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分子生物学
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PubMed
高影响因子
ACTA BIOCHIMICA ET BIOPHYSICA SINICA
·
2024
·
IF 3.3
Yanyan Heng,Wei Wei,Linzhong Cheng,Feifei Wu,Haoyu Dong,Jingxia Li,Jianing Fu,Bingjie Yang,Xinyue Liang,Chunyan Liu,Haiju Li,Haihua Liu,Pengfei Zhang
Diabetes accelerates vascular senescence, which is the basis for atherosclerosis and stiffness. The activation of the NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome and oxidative stress are closely associated with progressive senescence in vascular smooth muscle cells (VSMCs). The vascular protective effect of FGF21 has gradually gained increasing attention, but its role in diabetes-induced vascular senescence needs further investigation. In this study, diabetic mice and primary VSMCs are transfected with an FGF21 activation plasmid and treated with a peroxisome proliferator-activated receptor γ (PPARγ) agonist (rosiglitazone), an NLRP3 inhibitor (MCC950), and a spleen tyrosine kinase (SYK)-specific inhibitor, R406, to detect senescence-associated markers. We find that FGF21 overexpression significantly restores the level of catalase (CAT), vascular relaxation, inhibits the intensity of ROSgreen fluorescence and p21 immunofluorescence, and reduces the area of SA-β-gal staining and collagen deposition in the aortas of diabetic mice. FGF21 overexpression restores CAT, inhibits the expression of p21, and limits the area of SA-β-gal staining in VSMCs under high glucose conditions. Mechanistically, FGF21 inhibits SYK phosphorylation, the production of the NLRP3 dimer, the expression of NLRP3, and the colocalization of NLRP3 with PYCARD (ASC), as well as NLRP3 with caspase-1, to reverse the cleavage of PPARγ, preserve CAT levels, suppress ROSgreen density, and reduce the expression of p21 in VSMCs under high glucose conditions. Our results suggest that FGF21 alleviates vascular senescence by regulating the SYK-NLRP3 inflammasome-PPARγ-catalase pathway in diabetic mice.
研究领域:
内分泌学
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心血管生物学
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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
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
·
2023
·
IF 6.2
Jiajia Zhang,Yu Tu,Jiajia Wei,Ruyi Zheng,Ji Shao,Qinhua Chen,Guang Liang,Huazhong Ying,Xue Han,Qiaojuan Shi
Vascular injury is an early manifestation leading to end-organ damage in hypertension pathogenesis, which involves a macrophage-associated immune response. Dendritic cell-associated C-type lectin-1 (Dectin1) is a pivotal player in regulating inflammation-mediated cardiovascular disease. However, its role in hypertension-induced vascular damage and the underlying mechanisms remain unclear. We hypothesized that Dectin1 might accelerate angiotensin II (Ang II)- or deoxycorticosterone acetate–salt (DOCA-salt)-induced vascular injury through proinflammatory actions in macrophages. Macrophage Dectin1 was upregulated in mouse aortic tissues stimulated with Ang II. In the peripheral blood, Ang II also increased CD11b + F4/80 + macrophages in mice. In our constructed Dectin1 knockout mice, Dectin1 deletion protected against Ang II-induced EB extravasation and aortic wall thickness. Deficiency of Dectin1 or its pharmacological inhibition considerably improved fibrosis and inflammation responses, accompanied by a reduction in M1 macrophage polarization as well as proinflammatory cytokines and chemokines induced by Ang II or DOCA-salt. Through the bone marrow (BM) transplantation assay, these effects were verified in the wild type mice reconstituted with Dectin1-deficient BM cells. Mechanistically, Ang II promoted Dectin1 homodimerization, thereby triggering the spleen tyrosine kinase/nuclear factor kappa B pro-inflammatory cascade to induce the expression of inflammatory factors and chemokines in vivo and in vitro . In conclusion, Dectin1 has an essential role in the pathogenic procedure of Ang II-stimulated or DOCA-salt-induced vascular damage in mice and represents a promising therapeutic target for cardiovascular diseases.
研究领域:
心血管疾病
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免疫学
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分子生物学
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病理生理学
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DOI
PubMed
高影响因子
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.
研究领域:
心血管药理学
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炎症
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血管生物学
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分子生物学
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DOI
PubMed
高影响因子
PHYTOMEDICINE
·
2025
·
IF 8.3
Junsong Jing,Yi Sun,Yiyang Shui,Junyi Wang,Wenjing Ye,Ranran Chen,Lianhao Wu,Lijuan Xing,Rongrong Huang,Ting Zhou,Wenwen Zhu,Yueguo Wu,Sheng Zhang,Jing Shi,Yuanyuan Li,Yan Liu,Zhenqiang You
Background Viral pneumonia is an infection of the lungs caused by numerous different viruses, which can lead to severe respiratory distress and even life-threatening conditions. In the absence of specific treatments for viral pneumonia, natural traditional medicines offer an alternative in terms of innovative drug therapies. Morus alba L. (common name mulberry leaf) is a Chinese medicine that has been used clinically as an antiviral. Purpose The therapeutic effect of M. alba on viral pneumonia was investigated along with its mechanism of action. Methods Network pharmacology and molecular docking were used to analyze the mechanism of action of M. alba in the treatment of viral pneumonia. Histology, immunofluorescence, Western blotting, qPCR, and flow cytometry were used to evaluate the protective effect of MLE (the ethanol extract of Morus alba L. ) on PR8 (A/Puerto Rico/8/1934 H1N1, a murine lung-adapted influenza A virus strain)-induced viral pneumonia. SiRNA was used to validate the relationship between the therapeutic effects of MLE on viral pneumonia and the target Syk (a crucial non-receptor tyrosine kinase). Results MLE alleviated PR8-induced viral pneumonia by reducing inflammatory factor expression in the lungs, decreasing NF-κB pathway activation, slowing oxidative damage in the lungs, and inhibiting lung tissue cell apoptosis. Meanwhile, MLE for viral pneumonia was significantly associated with Syk targets. Notably, knockdown of the Syk gene not only reduced the therapeutic effect of MLE, but also suppressed PR8-induced viral pneumonia. Conclusion MLE can alleviate PR8-induced viral pneumonia through inhibiting the Dectin-1/Syk pathway.
研究领域:
药理学
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分子生物学
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病毒学
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PubMed
高影响因子
International Journal of Oral Science
·
2026
·Vol. 18
·期 1
·6
·
IF 17.6
Guo Jiajie,Qiu Qiujing,Yan Xiaoyuan,Zhang Zeying,Zhang Xiyue,An Na,Yin Chengcheng,Yang Di,Okamura Hirohiko,Yoshida Kaya,Sun Hongchen,Qiu Lihong
Rheumatoid arthritis (RA) is an autoimmune disorder that triggers progressive joint destruction by inducing excessive osteoclastogenesis. Porphyromonas gingivalis ( Pg ), the main pathogenic bacterium involved in periodontitis (PD), is closely related to RA. Pg can secrete extracellular vesicles (EVs), which carry numerous virulence factors. The aim of this study was to investigate whether Pg- derived EVs can be transported and exacerbate bone destruction in RA by promoting osteoclastogenesis and to elucidate the underlying mechanisms involved. EVs derived from Porphyromonas endodontalis ( Pe ), which is weakly associated with PD or RA, were used as controls. Pg and Pe EVs interact with osteoclasts after translocating into the marrow and metacarpal joints of mice. In vitro, Pg EVs induce osteoclastogenesis via various components, such as lipopolysaccharide, proteins, lipoproteins, and proteases. TNF-α, IL-1β, and IL-6 promote but cannot independently control Pg EV-induced osteoclastogenesis. RNA sequencing and verification experiments further demonstrated that Pg EVs induced osteoclastogenesis by promoting the phosphorylation of spleen tyrosine kinase (Syk). In vivo, Pg EVs exacerbated RA-induced bone destruction by activating Syk-dependent osteoclastogenesis. R406, a Syk inhibitor, significantly attenuated Pg EV-induced RA osteoclastogenesis and bone destruction. However, Pe- derived EVs presented an extremely weak ability to promote osteoclastogenesis and RA. Our findings reveal a new mechanism by which Pg EVs can exacerbate RA via transport through the circulation and the promote Syk-dependent osteoclastogenesis. This study deepens our understanding of the significant pathogenic role of EVs derived from oral bacterial in RA and explores targeted therapeutic strategies by inhibiting the activation of Syk.
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高影响因子
BIOSCIENCE BIOTECHNOLOGY AND BIOCHEMISTRY
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2024
·
IF 1.4
Chen Xue,Kang Yulai,Tang Chunhua,Zhang Lili,Guo Lu
Foam cells are primarily formed through scavenger receptors that mediate the uptake of various modified low-density lipoproteins (LDL) into cells. In addition to the receptor-dependent pathway, macropinocytosis is an essential non-receptor endocytic pathway for vascular smooth muscle cells (VSMCs) to take up lipids. However, the molecular mechanisms underlying this process remain unclear. Primary cultured VSMCs were stimulated with 200 ng/ml lipopolysaccharide (LPS) and 200 μg/ml native LDL (nLDL). We observed a significant increase in TLR4 protein expression and a significant activation of macropinocytosis, which correlated with the highest uptake of nLDL and intracellular lipid deposition in WT VSMCs. However, macropinocytosis was inhibited and lipid accumulation decreased after treatment with macropinocytosis inhibitors and Syk inhibitors in WT VSMCs. Consistently, TLR4 knockout significantly suppressed macropinocytosis and lipid droplets accumulation in VSMCs. Taken together, our findings suggest a critical role of TLR4/Syk signaling in promoting receptor-independent macropinocytosis leading to VSMC-derived foam cells formation.
研究领域:
心血管生物学
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细胞生物学
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免疫学
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PubMed
高影响因子
Cellular & Molecular Immunology
·
2022
·Vol. 19
·期 5
·602-618
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IF 22.096
Ma Xiaojian,Tan Xi,Yu Bingbing,Sun Wanwei,Wang Heping,Hu Huijun,Du Yanyun,He Ruirui,Gao Ru,Peng Qianwen,Cui Zhihui,Pan Ting,Feng Xiong,Wang Junhan,Xu Chengqi,Zhu Bin,Liu Wei,Wang Chenhui
Fungal infections cause ~1.5 million deaths each year worldwide, and the mortality rate of disseminated candidiasis currently exceeds that of breast cancer and malaria. The major reasons for the high mortality of candidiasis are the limited number of antifungal drugs and the emergence of drug-resistant species. Therefore, a better understanding of antifungal host defense mechanisms is crucial for the development of effective preventive and therapeutic strategies. Here, we report that DOCK2 (dedicator of cytokinesis 2) promotes indispensable antifungal innate immune signaling and proinflammatory gene expression in macrophages. DOCK2-deficient macrophages exhibit decreased RAC GTPase (Rac family small GTPase) activation and ROS (reactive oxygen species) production, which in turn attenuates the killing of intracellular fungi and the activation of downstream signaling pathways. Mechanistically, after fungal stimulation, activated SYK (spleen-associated tyrosine kinase) phosphorylates DOCK2 at tyrosine 985 and 1405, which promotes the recruitment and activation of RAC GTPases and then increases ROS production and downstream signaling activation. Importantly, nanoparticle-mediated delivery of in vitro transcribed (IVT) Rac1 mRNA promotes the activity of Rac1 and helps to eliminate fungal infection in vivo. Taken together, this study not only identifies a critical role of DOCK2 in antifungal immunity via regulation of RAC GTPase activity but also provides proof of concept for the treatment of invasive fungal infections by using IVT mRNA.
研究领域:
免疫学
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微生物学
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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
EUROPEAN JOURNAL OF PHARMACOLOGY
·
2026
·
IF 5.7
Hui Zhang,Qimei Yun,Zezhou Xu,Yifan Wang,Xianzhi Zhou,Ling Deng,Binsheng He
Neuroinflammation plays an essential role in neurological dysfunction in cerebral ischemia and reperfusion injury. Understanding the molecular network associated with neuroinflammation will provide potential targets for the neuroprotective treatment of ischemic stroke. An ischemia/reperfusion (I/R) rat model was established by middle cerebral artery occlusion (MCAO) and verified by laser speckle imaging and neurological function scoring. The ipsilateral cortex was analyzed using transcriptomic sequencing. The resulting transcriptomic dataset was combined with the ischemic stroke-associated C0948008 dataset from DisGeNet to screen differentially expressed genes (DEGs). Protein‒protein interaction (PPI) analysis was performed on DEGs associated with the inflammatory response. The candidate genes were verified using Western blotting or ELISA. I/R rats were subsequently treated with the TLR4 inhibitor TAK-242 to investigate the role of the TLR4/SYK/NF-κB pathway in neuroinflammation during ischemic stroke. A total of 264 genes were identified, most of which were enriched in inflammatory response pathways. PPI analysis of the DEGs associated with the inflammatory response revealed a total of three mutually interacting gene clusters, with TLR4, SYK, and NF-κB serving as the hub genes. The expression of proteins in the TLR4/SYK/NF-κB pathway and inflammatory cytokines significantly upregulated the I/R rats, whereas the trends were dramatically reversed by TAK-242. In addition, TAK-242 efficiently decreased the infarct area, improved neurological function, alleviated poststroke cognitive impairment (PSCI), recovered neuronal viability, and inhibited the overactivation of microglia and astrocytes. These data suggest that the TLR4/SYK/NF-κB pathway plays an important role in neuroinflammation and provide potential targets for neuroprotective therapy for ischemic stroke.
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高影响因子
Chinese Medicine
·
2025
·Vol. 20
·期 1
·1-18
·
IF 5.7
Li Dong-Dong,Li Zi-Xuan,Zhou Yang-Fan,Jin Ling,Liang Wan-Li,Xu Wen-Dong,Luo Xiang,Xiao Guan-Di,Chen Qi-Jun,Xie Ting,Xu Hui,Liu Yang,Cai Hong-Fei,Cao Yun-Feng,Sun Wan-Yang,Li Yi-Fang,Liang Lei,Liu Ju-Yan,Wu Yan-Ping,He Rong-Rong
Background Ganoderma lucidum ( G. lucidum ), has been documented as a medicinal herb in classical texts and officially recognized in both Eastern and Western pharmacopeias. G. lucidum spore oil (GLSO), a lipid substance extracted from sporoderm-broken spores, has shown potential in enhancing immune function and prolonging the survival of tumor patients. However, the mechanisms underlying GLSO’s immunomodulatory effects remain poorly unknown. Methods The effect of psychological stress on tumor progression and macrophage phagocytosis was analyzed by an in vivo small animal imaging system and flow cytometry. The effect of psychological stress on phospholipid composition in mice was investigated by LC–MS/MS based lipidomic analysis. The effectiveness of GLSO in tumor-bearing mice subjected to restraint stress was observed by tumor burden and phagocytosis of macrophages. Finally, the underlying mechanism of GLSO on macrophage phagocytosis in mice subjected to psychological stress was explored by RNA-seq, and the FcγR/SYK-mediated macrophage phagocytosis pathway was confirmed by qPCR, Western blotting, and confocal laser technology. Results Our study discovered that psychological stress-triggered tumor progression is contributed to by liposoluble components-impaired macrophage phagocytosis. Lipidomics analysis further identified lysophosphatidylinositol [LPI (18:0)] as a key factor suppressing macrophage phagocytic capacity under psychological stress. GLSO was shown to mitigate psychological stress-evoked tumor progression by enhancing macrophage-mediated phagocytosis of tumor cells in vivo . Mechanistically, transcriptomics analysis revealed that the LPI-mediated FcγR phagocytosis pathway is a crucial axis driving the therapeutic effect of GLSO under psychological stress. Conclusion Our findings illustrate that psychological stress-promoted cancer progression is contributed by the critical liposoluble components LPI (18:0)-mediated FcγR phagocytosis signaling inhibition. GLSO alleviates the dampened phagocytosis of macrophages caused by stress through regulating LPI/FcγR-mediated phagocytosis-related pathways, underscoring its potential as a therapeutic intervention for stress-related tumor progression. Graphical
研究领域:
免疫学
·
肿瘤学
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药理学
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脂质组学
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分子生物学
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植物学
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DOI
PubMed
高影响因子
Pharmaceuticals
·
2025
·Vol. 18
·期 7
·1059
·
IF 4.8
Yujin Shen,Xi Ma,Zhenzhen Du,Yang Li,Zhinan Mei,Ling Zhao
Background:Allergic rhinitis (AR) is a prevalent allergic disorder characterized by a complex pathogenesis. Drawing on traditional Chinese medicine theory and contemporary pharmacological principles, this study developed an inhalation-based herbal formulation, ZHW, to explore a novel non-invasive therapeutic approach.Objective:To investigate the therapeutic effects of ZHW on AR and elucidate its underlying mechanisms and potential targets through an integrated analysis of network pharmacology and proteomics.Materials and Methods:The volatile components of ZHW were analyzed by gas chromatography–mass spectrometry (GC-MS). The mouse model of AR was induced by OVA sensitization. The therapeutic efficacy of ZHW was assessed based on nasal symptom scores, histopathological examination, and inflammatory cytokine levels. Furthermore, the underlying mechanisms and potential targets of ZHW were investigated through integrated network pharmacology and proteomics analyses.Results:GC-MS analysis identified 39 bioactive compounds in ZHW. Inhalation treatment with ZHW demonstrated significant anti-allergic effects in OVA-sensitized mice, as evidenced by (1) reduced sneezing frequency and nasal rubbing behaviors; (2) decreased serum levels of IL-4, histamine, and OVA-specific IgE; (3) attenuated IL-4 concentrations in both nasal lavage fluid and lung tissue; (4) diminished nasal mucosal thickening; and (5) suppression of inflammatory cell infiltration. Integrated network pharmacology and proteomics analyses indicated that ZHW’s therapeutic effects were mediated through the modulation of multiple pathways, including the PI3K-Akt signaling pathway, the B cell receptor signaling pathway, oxidative phosphorylation, and the FcεRI signaling pathway. Key molecular targets involved Rac1, MAPK1, and SYK. Molecular docking simulations revealed strong binding affinities between ZHW’s primary bioactive constituents (linalool, levomenthol, linoleic acid, Linoelaidic acid, and n-Valeric acid cis-3-hexenyl ester) and these target proteins.Conclusions:The herbal formulation ZHW demonstrates significant efficacy in alleviating allergic rhinitis symptoms through multi-target modulation of key signaling pathways, including PI3K-Akt- and FcεRI-mediated inflammatory responses. These findings substantiate ZHW’s therapeutic potential as a novel, non-invasive treatment for AR and provide a strong basis for the development of new AR therapies. Future clinical development will require systematic safety evaluation to ensure optimal therapeutic outcomes.
研究领域:
药理学
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免疫学
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药物化学
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呼吸系统疾病
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系统生物学
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药物研发
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产品关联
DOI
PubMed
高影响因子
Journal of Translational Medicine
·
2025
·Vol. 23
·期 1
·1-15
·
IF 7.5
Li Xingyu,Tang Zhaoxia,Kuang Liangjian,Wu Yongjian,Huang Xi
Background Platelets play a critical role in the pathophysiology of acute lung injury (ALI) by activating neutrophils and promoting the formation of neutrophil extracellular traps (NETs). Excessive NETs formation exacerbates lung injury by triggering inflammation, impairing essential alveolar macrophage functions and activating the coagulation cascade. Consequently, inhibiting NETs formation represents a promising strategy for treating ALI. Methods In this study, we developed platelet membrane-coated nanoparticles (PNPs) by encapsulating poly(lactic-co-glycolic acid, PLGA) nanoparticles within platelet membranes, and we characterized their physicochemical and functional properties. We investigated the effects of PNPs on platelet activation, NETs formation, mitochondrial ROS (mtROS) production and Syk phosphorylation in vitro. Furthermore, we evaluated the therapeutic effects of PNPs on acute lung inflammatory responses in a murine model. Results Compared with red blood cell membrane-coated nanoparticles (RBC-NPs), PNPs significantly inhibited both platelet activation and NETs formation. Mechanistic studies demonstrated that NETs generation was markedly attenuated via CD62P signaling inhibition in platelets and mitochondrial ROS scavenging in neutrophils (using mito-TEMPO), and these treatments exhibited a suppression efficiency that was comparable to that of PNPs treatment. In vivo experiments revealed that PNPs preferentially accumulated in the lungs of mice with ALI, reducing neutrophil infiltration and NETs formation. Furthermore, PNP treatment attenuated lung injury, as evidenced by reduced collagen deposition, decreased total protein levels and cell numbers in BALF, and decreased levels of proinflammatory cytokines in the lungs. Conclusions Our findings demonstrate that PNPs have potential for use in treating ALI by simultaneously attenuating platelet activation and NETs formation.
研究领域:
纳米医学
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肺病学
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免疫学
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血液学
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药理学
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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）