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
·
民族药理学
·
炎症研究
·
呼吸系统疾病
·
网络生物学
·
系统药理学
·
免疫学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
JOURNAL OF ANIMAL PHYSIOLOGY AND ANIMAL NUTRITION
·
2023
·
IF 2.7
Wenyue Qiu,Xinting Zhang,Xiaoyue Pang,Jianjia Huang,Shuilian Zhou,Ruixia Wu,Rongmei Wang,Zhaoxin Tang,Rongsheng Su
Inflammatory response induced by biological stress usually occurs in weaning piglets, it reduces the production performance of piglets and even causes death. Tert-butylhydroquinone (TBHQ) is a food additive that has the effect of anti-inflammation and anti-oxidation. However, there are few reports related to the protective mechanisms of TBHQ on lipopolysaccharide (LPS) induced injury in intestinal porcine epithelial (IPEC-J2) cells. Quantitative real-time polymerase chain reaction and western blot analysis, respectively, detected the mRNA levels and protein expressions related to pyroptosis, tight junction (TJ) protein and high-mobility group box 1/toll-like receptor 4/nuclear factor kappa-B (HMGB1/TLR4/NF-κB) axis. Localisation and expression of NOD-like receptor pyrin domain containing 3 (NLRP3), HMGB1 and P-NF-κB proteins detected by immunofluorescence. The results showed that TBHQ (12.5 and 25 μM) can increase cell activity and reduce intracellular lactate dehydrogenase (LDH) levels in a dose-dependent manner. LPS significantly decreases cell viability and increases the LDH level. However, pretreatment with TBHQ evidently increases cell viability and decreases the LDH level of IPEC-J2 cells. In addition, treatment with LPS decreased the mRNA level and protein expression of zonula occludens-1, occludin and claudin-1, and increased the mRNA level and protein expression of pyroptosis and HMGB1/TLR4/NF-κB axis. Interestingly, pretreatment with TBHQ increased the TJ protein expressions as well as decreased the mRNA level and protein expressions of pyroptosis and HMGB1/TLR4/NF-κB axis. Moreover, the results of immunofluorescence showed that TBHQ significantly reduced the expression of NLRP3, HMGB1 and P-NF-κB in LPS-induced injury of IPEC-J2 cells. Therefore, we come to the conclusion that TBHQ attenuates LPS-induced pyroptosis in IPEC-J2 cells through downregulation of the HMGB1/TLR4/NF-κB axis, TBHQ may become a potential feed additive for preventing inflammatory diarrhoea in piglets.
研究领域:
兽医学
·
细胞生物学
·
免疫学
·
动物营养学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
JOURNAL OF DRUG TARGETING
·
2024
·
IF 4.3
Can Wang,Yihang Yang,Ruming Liang,Shikui Wu,Chengrui Xuan,Wei Lv,Jian Li
We successfully prepared mercury sulphide nanoparticle hydrogels by physical encapsulation method. The successfully prepared mercuric sulphide nanoparticle hydrogel was a zinc folate hydrogel, which showed an obvious porous structure with interconnected and uniformly distributed pores and a pore size range of about 20 μm. The maximum drug loading of the hydrogels was 3%, and the in vitro cumulative release degree was in accordance with the first-order kinetic equation Mt = 149.529 (1 − e−0.026t). The particles in mercuric sulphide nanoparticle hydrogels significantly down-regulated the expression of the cell surface co-stimulatory molecule CD86 (p < .0001). Meanwhile, the inflammatory response was regulated through the NF-κB pathway in LPS-induced inflammatory cells. Later, it was observed that mercuric sulphide nanoparticle hydrogels could significantly counteract the inflammatory and immune models through a mouse ear swelling model, a rat foot-plantar swelling model and a rheumatoid arthritis model. This design targets the immunomodulatory, and anti-inflammatory effects through nanocomposite hydrogel technology. It reduces the drawbacks of low mercury utilisation and susceptibility to accumulation of toxicity. It aims to provide an experimental basis for the development of mercuric sulphide and the treatment of inflammatory and immune-related diseases.
HighlightsMercury sulphide nanoparticle hydrogel has an optimal mercury sulphide nanoparticle content of 2%, is structurally homogeneous and stable, and does not exhibit significant liver or kidney toxicity.Mercuric sulphide nanoparticle hydrogel exerts anti-inflammatory effects in cells and rats, and regulates the expression of macrophage surface molecules and factors related to the NF-κB pathway.Mercuric sulphide nanoparticle hydrogel improves the condition of ankle synovial joints in a rat model of rheumatoid arthritis.
研究领域:
纳米技术
·
药学
·
免疫学
·
炎症研究
✓ 已验证
产品关联
DOI
PubMed
高影响因子
CHEMISTRY & BIODIVERSITY
·
2025
·
IF 2.5
Zebin Huang,Wanying Zhang,Qi Shu,Xiao-Chun Guo,Xi Zheng,YuJing Lu
Inflammation is an important predisposing factor for many chronic diseases. The dietary flavonoid silibinin has excellent anti-inflammatory properties in cells, but its low bioavailability in the blood compromises its therapeutic potential. This study aims to investigate the potential of dibenzoylmethane (DBM) to synergistically enhance the anti-inflammatory benefits of silibinin (SB). The synergistic effects of DBM and SB in combination were evaluated in LPS-induced RAW264.7 cells and TPA-induced mice. In addition, a network pharmacology approach and molecular docking were used to explore the key targets and signaling pathways of DBM and SB in combination. The results showed that DBM and SB synergistically inhibited the production of NO, ROS, IL-1β, and TNF-α in a 1:1 concentration ratio. These two compounds may exert their synergistic effects by modulating the NF-κB and HIF-1 signaling pathways, among others. Molecular docking revealed that both compounds exhibited high binding affinities to iNOS and COX-2. Compared with single compound use, the two compounds in combination significantly reduced ear edema and inflammatory cell infiltration, and inhibited the protein expression of iNOS and COX-2 in TPA-induced mice. This research provides a rationale for the combination of DBM and SB as an effective anti-inflammatory agent.
研究领域:
药理学
·
免疫学
·
分子生物学
·
炎症研究
✓ 已验证
产品关联
DOI
PubMed
高影响因子
PHYTOMEDICINE
·
2021
·
IF 5.34
Xiaohui Wang,Lu Wang,Renchao Dong,Kai Huang,Changyuan Wang,Jiangning Gu,Haifeng Luo,Kexin Liu,Jingjing Wu,Huijun Sun,Qiang Meng
Background Chemical liver injury is one of the main causes of acute liver failure and death. To date, however, treatment strategies for acute liver injury have been limited. Therefore, there is an urgent need to find new therapeutic targets and effective drugs. NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome is a complex of multiple proteins that has been shown to induce cell death under inflammatory and stress pathologic conditions and is thought to provide new targets for the treatment of a variety of diseases. Purpose The purpose of this study was to investigate whether luteolin has a protective effect on the liver and further elucidate whether it is realized through the thioredoxin interacting protein (TXNIP)-NLRP3 axis. Study design Acute hepatic injury in mice caused by intraperitoneal injection of lipopolysaccharide (LPS) was treated with or without luteolin. Methods Male C57BL/6 mice and mouse primary hepatocytes were selected. TXNIP protein knockdown was achieved by siRNA , qPCR and Western blot were performed to explore the mechanism of luteolin in alleviating acute liver injury. Results The results indicated that luteolin had a markedly protective effect on acute liver injury induced by LPS in mice by inhibiting the TXNIP-NLRP3 axis. Luteolin inhibits NLRP3 inflammasome activation by suppressing TXNIP, apoptosis associated speck-like protein containing a CARD domain (ASC), caspase-1, interleukin-1β (IL-1β) and IL-18 to reduce liver injury. In addition, luteolin inhibits LPS-induced liver inflammation by inhibiting the production of inflammation-related gene tumor necrosis factor-α (TNF-α), IL-10, and IL-6. What's more, luteolin alleviated LPS-induced hepatocyte injury by inhibiting oxidative stress and regulating MDA , SOD , and GSH levels. However, the protective effect of luteolin on acute LPS-induced liver injury in mice was blocked by si-TXNIP in vitro . Conclusions These combined data showed that luteolin may alleviate LPS-induced liver injury through the TXNIP-NLPR3 axis, providing new therapeutic targets and therapeutic drugs for subsequent studies.
研究领域:
药理学
·
免疫学
·
肝病学
·
分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
·
2018
·
IF 3.118
Jing Xing,Zhenlong Yu,Xiangyu Zhang,Wenyang Li,Dongna Gao,Jian Wang,Xiaochi Ma,Xinshi Nie,Wei Wang
The p38 MAPK signaling pathway plays a key role in lung inflammation and the development of acute lung injury (ALI). We previously reported that the phenolic compound procyanidin B1 inhibits inflammation by suppressing the p38 MAPK signaling pathway. Here, we asked whether the monomer of procyanidin B1, epicatechin (EC), can alleviate LPS-induced ALI in mice, and if so, whether EC acts by inhibiting p38 MAPK. C57BL/6 mice were randomly divided into four groups ( n = 8) and received EC alone, vehicle (sham group), LPS alone, or LPS and EC. LPS was administered via intraperitoneal injection and EC via nasogastric feeding. Lung histopathology , alveolocapillary membrane permeability , inflammation, and p38 MAPK pathway activation were assessed by immunohistochemistry , tissue wet/dry weight analysis, quantitative PCR, protein assays, ELISA , and western blot analysis using lung tissue and/or bronchoalveolar fluid. We also performed molecular modeling and in vitro enzymatic assays to examine the potential interaction between EC and p38 MAPK at the molecular level. We found that LPS caused an increase in ALI-associated lung pathology accompanied by activation of p-p38 pathway components and the transcription factor AP1. All of these effects were substantially reduced by treatment with EC. Furthermore, molecular modeling suggested that EC suppressed p38 MAPK signaling by hydrogen bonding with Glu71, Ala 111, Asp112, and Leu171 in the active site of p38α. In vitro kinase assays confirmed the ability of EC to directly inhibit purified p38 MAPK. Collectively, our data suggest that the naturally occurring compound EC could be a new therapeutic option for ALI.
研究领域:
药理学
·
免疫学
·
分子生物学
·
病理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Advanced Healthcare Materials
·
2025
·
IF 9.6
Shuangfeng Ge,Xing-Huo Wang,Juntao Fan,Haofei Liu,Youtao Xin,Xiaohui Li,Yunjian Yu,Ying-Wei Yang,Hui Gao
Sepsis is an underappreciated yet severe threat to human life, marked by organ dysfunction and high mortality resulting from disordered inflammatory responses to blood infection. Unfortunately, no specific drugs are available for effective sepsis treatment. As a pivotal biomarker for sepsis, lactate levels are closely related to vascular permeability and sepsis-associated mortality. Herein, a dual-pipeline lactate removal strategy is reported from circulating blood to ameliorate vascular permeability and lipopolysaccharide (LPS)-induced sepsis. This is achieved by formulating lactate oxidase (LOX)-encapsulated hollow manganese dioxide (HMnO 2 ) nanohybrids (LOX@HMnO 2 -P[5]A) bearing pillar[5]arene (P[5]A) macrocycle with excellent host-guest properties. The highly biocompatible nanohybrids enable direct lactate consumption through LOX catalytic degradation and block lactate production by P[5]A-mediated LPS trapping, allowing for dual-pipeline lactate removal to maximize the reversal of lactate-mediated vascular hyperpermeability. Besides, HMnO 2 cores decompose hydrogen peroxide produced from lactate oxidation into oxygen, further contributing to lactate consumption and mitigating the hypoxic inflammatory environment. In vivo investigations demonstrate that intravenous administration of LOX@HMnO 2 -P[5]A nanohybrids with extended blood circulation can effectively ameliorate endothelial barrier dysfunction, inflammatory responses, and multiple organ injury, ultimately improving survival outcomes in LPS-induced sepsis. Taken together, this dual-pipeline lactate removal strategy offers a promising approach for efficient sepsis treatment.
研究领域:
医学
·
药理学
·
纳米技术
·
免疫学
·
重症监护
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Drug Design Development and Therapy
·
2022
·
IF 4.319
Yali Zhang,Chengguang Zhao,Wenfei He,Zhe Wang,Qilu Fang,Bing Xiao,Zhiguo Liu,Guang Liang,Shulin Yang
Sepsis is a systemic inflammatory response syndrome and is mainly caused by lipopolysaccharides (LPS) – a component of the cell walls of gram-negative bacteria, via toll-like receptor 4–mitogen-activated protein kinases/nuclear factor-kappa B-dependent proinflammatory signaling pathway. Here, we synthesized 26 asymmetric monocarbonyl analogs of curcumin and evaluated their anti-inflammatory activity by inhibiting the LPS-induced secretion of tumor necrosis factor-α and interleukin-6 in mouse RAW264.7 macrophages. Five active compounds (3a, 3c, 3d, 3j, and 3l) exhibited dose-dependent inhibition against the release of tumor necrosis factor-α and interleukin-6, and they also showed much higher chemical stability than curcumin in vitro. The anti-inflammatory activity of analogs 3a and 3c may be associated with their inhibition of the phosphorylation of extracellular signal-regulated kinase and the activation of nuclear factor-kappa B. In addition, 3c exhibited significant protection against LPS-induced septic death in vivo. These results indicate that asymmetrical monocarbonyl curcumin analogs may be utilized as candidates for the treatment of acute inflammatory diseases.
研究领域:
药理学
·
免疫学
·
药物化学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
FITOTERAPIA
·
2018
·
IF 2.642
Hong-Bo Xu,Tong-Hua Yang,Pei Xie,Zhi-Shu Tang,Xiao Song,Huai-Li Xu,Yan-Hong Li,Dong-Bo Zhang,Yan-Ru Liu,Yan-Ni Liang,Yu Zhang,Shi-Jun Liu,Si-Min Wei,Chen Sun,Hong-Bo Liu,Chong Deng,Wei Wang
Gracilistones A ( 1 ) and B ( 2 ), two new eudesmane-type sesquiterpenoids with an unusual tetrahydrofuran-fused 6/6/5 tricyclic ring system, were obtained from Acanthopanax gracilistylus under the guidance of LC-MS investigation. Their structures and absolute configurations were assigned by extensive spectroscopic analyses and quantum calculation methods. Compounds 1 and 2 showed potent inhibitory activity against LPS-induced nitric oxide production in RAW 264.7 macrophages, compared with the positive control L-NMMA. In addition, compounds 1 and 2 were also evaluated for their antioxidant (DPPH • and ABTS •+ ) and xanthine oxidase (XO) inhibitory activities, and they exhibited weak inhibitory effects at 100 μM.
研究领域:
药用植物学
·
药物化学
·
炎症研究
·
天然产物化学
✓ 已验证
DOI
PubMed
高影响因子
Frontiers in Microbiology
·
2024
·
IF 4
Qingfeng Guo,Shenyu Shen,Xinyang Wang,Lei Shi,Yuwei Ren,Dandan Li,Zhenhua Yin,Juanjuan Zhang,Baocheng Yang,Xuewei Wang,Gang Ding,Lin Chen
The chemical engineering of natural extracts has emerged as an effective strategy for the production of diverse libraries of chemicals, making it integral to drug discovery. A chemical engineering strategy based on the epoxidation and ring-opening reactions was used to prepare diversity-enhanced extracts of Chaetomium madrasense 375. Eleven unnatural cytochalasan derivatives ( 1–11 ) with unique functional groups, such as amine and isoxazole, were isolated and characterized from these chemically engineered extracts of C. madrasense 375. The identification of these new structures was accomplished through comprehensive spectroscopic analysis, supplemented by synthetic considerations. Notably, compounds 5 and 13 – 16 displayed potent phytotoxic effects on Arabidopsis thaliana , while compounds 1 , 2 , 5 , 10 , and 12 demonstrated inhibitory activities on LPS-induced NO production in RAW264.7 cells. Among them, compound 1 was found to be able to inhibit the upregulated expression of the inducible nitric oxide synthase (iNOS) protein induced by LPS, while also decreasing the production of pro-inflammatory cytokines (IL-6) and influencing the phosphorylation of p38, ERK1/2, and JNK at 100 μM. Our findings demonstrate that the chemical engineering of natural product extracts can be an efficient technique for the generation of novel bioactive molecules.
研究领域:
药理学
·
化学工程
·
天然产物化学
·
免疫学
·
植物科学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
PHYTOMEDICINE
·
2024
·
IF 6.7
Jia-Yi Dou,Mei-Jie Zhou,Mei-Yan Xuan,Jia Guo,Sai-Hu Liu,Li-Hua Lian,Zhen-Yu Cui,Ji-Xing Nan,Yan-Ling Wu
Background Astilbin (ATB), a natural dihydroflavonol compound, exists in many plants, processed and functional foods. ATB has multiple pharmacological effects, such as antioxidant, lipid-lowering, and hepatoprotective. However, its anti-hepatic fibrosis and mechanisms remain unclearly elucidated. Purpose This study explored the effect of ATB against the hepatic fibrosis and its regulation of hepatic microenvironment by regulating hepatic stellate cells-macrophage crosstalk. Method Thioacetamide (TAA) was intraperitoneal injected to establish hepatic fibrosis mice, and treated with ATB or curcumin by gavage, respectively. Hepatic stellate cells (HSCs) were stimulated with TGF-β or conditioned medium (CM) from LPS-induced THP-1, then cultured with ATB, PXR agonist or antagonist. Results In TAA-induced mice, ATB improved histopathological changes, serum transaminases increase; alleviated extracellular matrix (ECM) deposition, epithelial-mesenchymal transformation (EMT), inflammatory infiltration, PTEN induced kinase 1 (PINK1)/Parkin-mediated mitophagy and activated pregnane X receptor (PXR) expression. In vitro , ATB significantly reduced ECM, inflammatory cytokines release, mitophagy, EMT, and activated PXR expression. ATB could increase PXR and decrease PINK1/Parkin, functioning as a PXR agonist. PXR deficiency in LX-2 could degrade the regulation of ATB on ECM, inflammation, EMT, and mitophagy. CM from LPS-induced THP-1 activated LX-2 and resulted in PXR decreasing, while ATB could regulate the crosstalk between HSCs and macrophages. Deficiency of PXR, whether in LX-2 or in macrophages, all weakened the inhibitory effect of ATB on α-SMA, EMT, inflammatory cytokines, and PINK1/Parkin signaling. Conclusion ATB ameliorated hepatic fibrosis by inhibiting HSCs activation, inflammation and EMT through PXR-mediated PINK1/Parkin signaling. Especially, ATB targeted the hepatic microenvironment between hepatic stellate cells and macrophages, which might be a promising strategy for the treatment of hepatic fibrosis.
研究领域:
药理学
·
肝病学
·
细胞生物学
·
免疫学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
·
2024
·Vol. 25
·期 19
·10406
·
IF 4.9
Yan Zhang,Yaping Yang,Huicong Liang,Yuerun Liang,Guixin Xiong,Fang Lu,Kan Yang,Qi Zou,Xiaomin Zhang,Guanhua Du,Ximing Xu,Jiejie Hao
Asthma is a chronic airway inflammation that is considered a serious public health concern worldwide. Nobiletin (5,6,7,8,3′,4′-hexamethyl flavonoid), an important compound isolated from several traditional Chinese medicines, especially Citri Reticulatae Pericarpium, is widely used for a number of indications, including cancer, allergic diseases, and chronic inflammation. However, the mechanism by which nobiletin exerts its anti-asthmatic effect remains unclear. In this research, we comprehensively demonstrated the anti-asthmatic effects of nobiletin in an animal model of asthma. It was found that nobiletin significantly reduced the levels of inflammatory cells and cytokines in mice and alleviated airway hyperresponsiveness. To explore the target of nobiletin, we identified PDE4B as the target of nobiletin through pharmacophore modeling, molecular docking, molecular dynamics simulation, SPR, and enzyme activity assays. Subsequently, it was found that nobiletin could activate the cAMP-PKA-CREB signaling pathway downstream of PDE4B in mouse lung tissues. Additionally, we studied the anti-inflammatory and anti-airway remodeling effects of nobiletin in LPS-induced RAW264.7 cells and TGF-β1-induced ASM cells, confirming the activation of the cAMP-PKA-CREB signaling pathway by nobiletin. Further validation in PDE4B-deficient RAW264.7 cells confirmed that the increase in cAMP levels induced by nobiletin depended on the inhibition of PDE4B. In conclusion, nobiletin exerts anti-asthmatic activity by targeting PDE4B and activating the cAMP-PKA-CREB signaling pathway.
研究领域:
药理学
·
免疫学
·
分子生物学
·
呼吸医学
✓ 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）