JOURNAL OF ETHNOPHARMACOLOGY
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2020
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IF 3.69
Pengfei Li,Jingkang Wang,Chunguo Wang,Long Cheng,Quantao Ma,Yaqi Li,Yongcheng An,Hongyu Dai,Yuhui Duan,Tieshan Wang,Xuan Ma,Minghui Zhang,Ting Wang,Baosheng Zhao
Ethnopharmacological relevance Hanchuan Zupa Granule (HCZP), a traditional Chinese ethnodrug, has the functions of supressing a cough, resolving phlegm, warming the lungs, and relieving asthma. In clinical practice employing traditional Chinese medicine (TCM), HCZP is commonly used to treat acute colds, cough and abnormal mucous asthma caused by a cold, or “Nai-Zi-Lai” in the Uygur language. Studies have confirmed the use of HCZP to treat cough variant asthma (CVA) and other respiratory diseases . However, the pharmacological mechanisms of HCZP remain unrevealed. Aim of the study To investigate the anti-tussive and anti-asthmatic effects and the possible pharmacological mechanisms of HCZP in the treatment of CVA. Materials and methods A guinea pig CVA animal model was established by intraperitoneal injection of ovalbumin (OVA) combined with intraperitoneal injection of aluminium hydroxide adjuvant and atomized OVA. Meanwhile, guinea pigs with CVA received oral HCZP (at dosages of 0.571, 0.285 and 0.143 g/kg bodyweight). The number of coughs induced by aerosol capsaicin was recorded, and the airway hyperresponsiveness (AHR) of CVA guinea pigs was detected with the FinePointe series RC system. H&E staining of lung tissues was performed to observe pathological changes. ELISA was used to detect inflammatory cytokines. qRT-PCR and western blotting analyses were used to detect the expression of Th1-specific transcription factor (T-bet), Th2-specific transcription factor (GATA3), and Toll-like receptor 4 (TLR4) signal transduction elements. These methods were performed to assess the protective effects and the potential mechanisms of HCZP on CVA. Results Great changes were found in the CVA guinea pig model after HCZP treatment. The number of coughs induced by capsaicin in guinea pigs decreased, the body weights of guinea pigs increased, and inflammation of the eosinophilic airway and AHR were reduced simultaneously. These results indicate that HCZP has a significant protective effect on CVA. A pharmacological study of HCZP showed that the levels of interleukin-4 (IL-4) and IL-5 and tumour necrosis factor-α (TNF-α) in serum decreased. The amount of interferon-γ (IFN-γ) increased, mRNA and protein expression of TLR4 and GATA3 weakened, and mRNA and protein expression of T-bet increased. Conclusions HCZP ameliorated the symptoms of guinea pigs with CVA induced by OVA by regulating the Th1/Th2 imbalance and TLR4 receptors.
研究领域:
药理学
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传统中药
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呼吸系统疾病
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免疫学
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DOI
PubMed
高影响因子
JOURNAL OF NANOBIOTECHNOLOGY
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2025
·Vol. 23
·期 1
·1-17
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IF 12.6
Guo Xiaoping,Zuo Xu,Zheng Wenxue,Zhao Dan,Dong Chao,Zou Zheng,Shen Yuanyuan,Xu Caina,He Chaoliang,Wang Fang
Asthma is a chronic disease with typical pathological features such as airflow limitation, airway inflammation and remodeling. Of these, neutrophilic asthma is considered to be the more severe and corticosteroid-resistant subtype of asthma. Increasing evidence suggests that patients with neutrophilic asthma often accompany with dysbiosis of the internal microbiota, where the increased abundance of non-typeable Haemophilus influenzae (NTHi) is closely related to the neutrophilic asthma phenotype. Furthermore, emerging evidence suggests that reactive oxygen species (ROS) are pivotal in the pathogenesis of neutrophilic asthma. In this study, matrix metalloproteinase-9 (MMP-9)-responsive, catalase-loaded nanogels (M-CAT-NGs) were synthesized, which was composed of MMP-9-sensitive peptide (VPMS), arginine-grafted chitosan and maleimide (CS-Arg-Mal), catalase (CAT), sodium citrate (SC) and ε-poly(L-lysine) (ε-PLL). The M-CAT-NGs showed potent antimicrobial effects and exerted excellent therapeutic effects in the presence of MMP-9 by causing VPMS rupture and responsive release of CAT. In vitro experiments revealed that M-CAT-NGs effectively inhibited the proliferation of NTHi, Staphylococcus aureus ( S. aureus ), and Escherichia coli ( E. coli ), while also demonstrating the capacity to modulate the inflammatory response induced by lipopolysaccharide (LPS) and hydrogen peroxide (H 2 O 2 ) stimulation. In vivo experiments demonstrated that nebulized inhalation of M-CAT-NGs was effective in reducing airway hyperresponsiveness (AHR), alleviating inflammation, downregulating the expression level of ROS in the lung tissues, thus enabling the effective management of neutrophilic asthma. Thus, the development of M-CAT-NGs has shown strong potential for the clinical management of neutrophilic asthma by modulating the inflammatory response.
研究领域:
医学
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药学
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免疫学
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DOI
PubMed
高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
·
2025
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IF 4.7
Huan Chen,Jin Liu,Jia Zhang,Yuqian Chen,Yan Wang,Yuanjie Qiu,Huizhong Hu,Limin Chai,Qianqian Zhang,Qingting Wang,Manxiang Li
Bromodomain-containing protein 4 (BRD4) is recognized as a member of the bromodomain and extraterminal (BET) family that is involved in the airway inflammation and airway remodeling of asthma. However, the underlying mechanisms of BRD4 in airway smooth muscle cells (ASMCs) proliferation and airway remodeling remain unclear. Primary cultured rat ASMCs and ovalbumin (OVA)-induced rat asthma models were applied to address these issues in the present study. We showed that transforming growth factor β1 (TGF-β1) increased the protein expression of ubiquitin specific peptidase 22 (USP22), which deubiquitinated BRD4 therefore increased its expression, and then resulted in the upregulation of glioma-associated oncogene homolog 1 (GLI1) and osteopontin (OPN) leading to ASMCs proliferation. We further confirmed that induction of TGF-β1 sequentially upregulated USP22, BRD4, GLI1 and OPN leading to airway remodeling in OVA-induced rat asthma models, targeting TGF-β1/USP22/BRD4/GLI1/OPN pathway axis effectively attenuated airway remodeling and asthma development. Our study provides novel sights to understand the role of TGF-β1/USP22/BRD4/GLI1/OPN axis in airway remodeling, and targeting this pathway might have potential value for the prevention and treatment of asthma.
研究领域:
医学
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分子生物学
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免疫学
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DOI
PubMed
高影响因子
International Journal of Nanomedicine
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2024
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IF 6.6
Xu Zuo,Yinuo Gu,Xiaoping Guo,Wenxue Zheng,Haoyu Zheng,Yiming An,Caina Xu,Fang Wang
Purpose Inhaled corticosteroids, including budesonide (BUD), are widely employed for the treatment of asthma. However, the frequent use of corticosteroids is associated with numerous adverse effects and poses challenges to ongoing drug therapy and patient adherence. Budesonide liposomal nanoparticles (BUD-LNPs) were developed to improve the bioavailability of the drug and thereby improve the effectiveness of asthma treatment.Methods BUD-LNPs were prepared via thin-film hydration, and the characterizations, stability, and in vitro release of BUD-LNPs were studied. In vitro cellular uptake was observed by laser-scanning confocal microscope (LSCM) and flow cytometry. And the in vitro anti-inflammatory activity of BUD-LNPs was evaluated by measuring the expression of pro-inflammatory cytokines in activated macrophages. Besides, the accumulation time in the lung of drugs delivered via liposomal carriers and free drugs was compared in vivo. And the in vivo therapeutic efficacy of BUD-LNPs was assessed in OVA-induced asthmatic mice. Finally, in vivo biosafety assessment was performed.Results The particle size, PDI, and zeta potential of BUD-LNPs were 127.63±1.33 nm, 0.27±0.02, and 3.33±0.13 mV, respectively. BUD-LNPs exhibited excellent biosafety and anti-inflammatory activity in vitro. Furthermore, compared with the free drugs, the utilization of liposomal nano-vehicles for drugs delivery could effectively extend the duration of drugs accumulation in the pulmonary system. Additionally, treatment with BUD-LNPs alleviated airway hyperresponsiveness, reduced airway mucus secretion, and mitigated pulmonary inflammation in OVA-induced asthmatic mice. And the BUD-LNPs demonstrated superior therapeutic efficacy compared to free BUD.Conclusion BUD-LNPs was successfully prepared with excellent stability and sustained release for 24 h in vitro. The data of anti-inflammatory activity, asthma therapeutic effects and safety studies indicated that drug delivery mediated by liposomal nano-vehicles was a feasible and desirable strategy for medical strategy and showed great promise in the clinical therapy of asthma.
研究领域:
药剂学
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药理学
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纳米技术
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呼吸医学
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DOI
PubMed
高影响因子
Chinese Medicine
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2025
·Vol. 20
·期 1
·1-22
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IF 5.7
Li Xueyan,Ding Lu,Li Zirui,Cao Zhenghua,Li Min,Yin Kai,Song Siyu,Cao Liyuan,Xia Qinjing,Wang Zihan,Zhao Daqing,Tong Xiaolin,Li Xiangyan,Wang Zeyu
Background Asthma is a chronic inflammatory airway disease that remains inadequately controlled by existing conventional treatments. A traditional Chinese medicine (TCM) formula of Yangke powder (yǎng ké sǎn-YKS) has demonstrated potential in alleviating asthma symptoms and reducing its acute exacerbation. Despite clinical evidence supporting its benefit, there is still insufficient understanding of the active compounds in YKS and their underlying mechanisms, which limits its broader clinical application. Objective This study aims to identify the key active ingredients in YKS and explore their mechanisms, particularly through the PI3K/AKT/NF-κB pathways, to provide a scientific basis for its application in asthma treatment. Methods We employed UPLC-Q-Exactive Orbitrap-MS to analyze YKS constituents, identified key ingredients, and explored asthma treatment mechanisms through bioinformatics, network pharmacology, Mendelian randomization, and molecular docking. The asthma model was evaluated using ovalbumin (OVA) and pulmonary function tests, while pathological examination was conducted using hematoxylin and eosin (HE), periodic acid-Schiff (PAS), and Masson trichrome stains. Concentrations of IgE, IL-4, and IL-5 were measured by ELISA, and protein and mRNA expressions were confirmed via qPCR, immunohistochemistry, and Western blot analysis. Results A total of 174 compounds were identified in YKS by UPLC-MS, with 49 detected in the bloodstream, indicating their role as active ingredients. Bioinformatics analysis revealed 353 asthma-related targets and 972 potential targets for YKS. Key targets such as AKT1, TNF, and IL1B were validated by molecular docking. Our studies indicated that YKS modulates asthma primarily through the PI3K/Akt and NF-κB pathways, improving airway resistance, reducing inflammation, mucus production, and airway remodeling, and decreasing Th2 cytokines and IgE levels. Conclusion This investigation identifies Kaempferol, Norephedrine, Cynaroside, Genistein, and Rutin as critical active ingredients in YKS, impacting key biomarkers such as AKT1, TNF, and IL1B. These substances effectively modulate the PI3K/AKT/NF-κB pathway, enhancing the management of allergic asthma.
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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产品关联
DOI
PubMed
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
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2024
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IF 4.8
Yu Wang,Meihao Peng,Xin Yang,Liming Tu,Jiamin Liu,Yixi Yang,Rui Li,Xue Tang,Yuqing Hu,Guowu Zhang,Qi Zhao,Qiuxia Lu
ABSTRACT Ethnopharmacological relevance Fritillaria cirrhosa D. Don (FCD) is a traditional Chinese medicine used to treat respiratory disorders, known for its effects in clearing heat, moistening the lungs, resolving phlegm, and relieving cough. Additionally, the total alkaloids extracted from FCD can alleviate asthma symptoms and reduce airway inflammation. However, no studies have investigated the effects of total alkaloids on lung macrophages. Aim of the study This study explored whether the total alkaloids of FCD (TAs-FCD) reduce M2 macrophage polarization and, consequently, attenuate airway remodeling in asthmatic mice. This study further elucidated its mechanism of action in treating allergic asthma. Materials and methods The extracted TAs-FCD was analyzed for its composition using UPLC-Q-TOF/MS. Network pharmacology was employed to identify the active ingredients and potential mechanisms of TAs-FCD in the treatment of allergic asthma. A mouse model of ovalbumin-induced allergic asthma was established, adopted, and validated through in vivo experiments. Hematoxylin-eosin staining (H&E), immunohistochemistry (IHC), immunofluorescence staining (IF), enzyme-linked immunosorbent assay (ELISA), Western blotting (WB), and real-time fluorescence quantitative polymerase chain reaction (q-PCR) were used to investigate the role of TAs-FCD in inhibiting M2 macrophage polarization in the context of allergic asthma. Results A total of 66 active ingredients were screened from 116 compounds using SWISSADME. The targets of these 66 compounds were predicted by SwissTargetPrediction, resulting in 808 unique drug targets after excluding duplicates. Additionally, 1,756 targets related to allergic asthma were identified from the DisGeNET, Genecard, and OMIM databases. This led to 267 cross-targets between the active ingredient targets and allergic asthma targets, including interleukin (IL)-1β, tumor necrosis factor (TNF), and STAT3. Animal experiments demonstrated that TAs-FCD improved histopathological injury in mouse lungs, reduced peri-airway collagen fiber accumulation, airway mucus secretion, and airway smooth muscle proliferation. TAs-FCD also lowered IL-1β, TNF-α and IL-4 levels in lung tissues and alleviated airway inflammation. Furthermore, TAs-FCD significantly reduced levels of Arg1 and CD206, which are closely associated with M2 macrophages, and downregulated the expression of p-STAT3 and p-JAK2. Conclusion TAs-FCD may inhibit M2 macrophage polarization by regulating the JAK2/STAT3 pathway, thereby alleviating airway remodeling and inflammation in allergic asthmatic mice.
研究领域:
药理学
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免疫学
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呼吸医学
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中医药
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产品关联
DOI
PubMed
高影响因子
International Journal of Nanomedicine
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2020
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IF 5.115
Mingzhuo Cao,Mengling Zhan,Zheng Wang,Zeqian Wang,Xiu-Min Li,Mingsan Miao
Purpose Isoliquiritigenin (ILQ), an important component of Anti-Asthma Herbal Medicine Intervention (ASHMI), had shown potent anti-asthma effect in vitro in our previous study. However, poor solubility and low bioavailability hindered in vivo application to treat asthma. This study was to develop a novel ILQ loaded self-nanoemulsifying drug delivery system (ILQ-SMEDDS) with enhanced bioavailability. Methods The optimized SMEDDS formulation was composed of ethyl oleate (oil phase), Tween 80 (surfactant) and PEG400 (co-surfactant) at a mass ratio of 3:6:1. The physiochemical properties of ILQ-SMEDDS, including drug content, globule size, zeta potential, scanning electron microscopy (SEM), Fourier transform infrared (FTIR) spectroscopy, were characterized. And the in vitro release profile, in situ intestinal absorption, in vivo pharmacokinetic parameters and the anti-asthma effect of ILQ suspension and ILQ-SMEDDS were evaluated. Results The ILQ-SMEDDS had an average globule size of 20.63 ± 1.95 nm with a polydispersity index (PDI) of 0.11 ± 0.03, and its zeta potential was −12.64 ± 2.12 mV. The cumulative release rate of ILQ from ILQ-SMEDDS to the simulated gastrointestinal tract was significantly higher than that of free ILQ suspension. And area under curve with ILQ-SMEDDS was found to be 3.95 times higher than that of ILQ suspension indicating improved bioavailability by SMEDDS. Although ILQ-SMEDDS showed a slight less effective inhibitory effect on eotaxin-1 in human lung fibroblast (HFL-1) cells than free ILQ, in an ovalbumin-induced asthma model, ILQ-SMEDDS exhibited more efficacy than ILQ suspension in improving asthma-associated inflammation, including eosinophil production, ovalbumin-specific immunoglobulin E (OVA-sIgE), interleukin 4 (IL 4), interleukin 5 (IL 5) and interferon-γ (IFN-γ). Even the low dose of ILQ-SMEDDS group (10 mg/kg) showed better anti-asthma effect than that of the ILQ suspension group (20 mg/kg). Conclusion Compared with ILQ suspension, ILQ-SMEDDS showed significantly improved bioavailability and anti-asthma effect, revealing its potential as a favorable pharmaceutical agent for treating asthma.
研究领域:
药剂学
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药理学
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药物递送系统
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呼吸系统疾病
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产品关联
DOI
PubMed
高影响因子
JOURNAL OF PHOTOCHEMISTRY AND PHOTOBIOLOGY A-CHEMISTRY
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2020
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IF 3.306
Ping Li,Pu Ge,Senwen Ping,Wenting Lin,Xiaohan Zhang,Chaohai Wei,Yuan Ren
With serious air pollution, heavy use of asthma drugs caused the accumulation in environmental water, which might pose a potential risk on the organisms. In this study, the ultraviolet photodegradation of asthma drug salmeterol (SX) and influencing factors were studied, meanwhile, the possible photolysis pathway and toxicity trends during the photolysis process were further discussed. The results showed that the photolysis of SX conformed to the pseudo-first order kinetic reaction and 1 O 2 dominated the photolysis process with contribution of 41.7 %. As the temperature, pH value and HCO 3 − concentration increased, SX photolysis rate accelerated. The presence of NO 3 − could also promote the SX photolysis rate but with to Cl 2 − the increase of NO 3 − concentration, the promotion reduced via OH quenching and stronger optical shielding. When Cl − concentration increased to 0.1 mM, the promotion effect of Cl − turned to inhibition due to the transformation of Cl to Cl 2 − . Moreover, the photolysis of SX was inhibited by the Fulvic acid (FA) through optical screening effect and free radical scavenging. Based on the nine intermediates predicted by UPLC-Q-TOF, three possible transformation pathways were proposed. Luminous intensity test of photobacterium phoshoreum T3 spp indicated the toxicity of the final reaction system was reduced through the ultraviolet irradiation.
研究领域:
环境科学
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药理学
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毒理学
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DOI
高影响因子
CHEMICO-BIOLOGICAL INTERACTIONS
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2023
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IF 5.1
Huijuan Ma,Qi Shu,Peiyao Wang,Ruilin Qin,Sijia Li,Huan Xu
Exposure to formaldehyde (FA) has been indicated to be positively correlated with increased incidence of allergic asthma in many epidemiological and experimental studies. However, few studies have ever addressed the molecular basis of the correlation. In the present study, it was found that inhaling 2.0 mg/m 3 FA for 2 weeks could exacerbate the pulmonary inflammation and mucus over-accumulation in OVA-induced murine asthmatic model. The pro-inflammatory cytokines, such as IL-1β, TNF-α, IL-6 and IL-8, were increased in lung and serum of FA-exposed asthmatic mice. The contribution of HIF-1α signaling in FA-exacerbated allergic asthma was confirmed by bioinformatic analysis. HIF-1α and its downstream proteins, which are known as mediators of glycolysis, were found to be upregulated by 50 μM FA, and the FA-enhanced of glycolysis was reversed by inhibition of HIF-1α with PX-478 in vitro and YC-1 in vivo . Furthermore, it was confirmed that inhibition of HIF-1α signaling could restrain the macrophagic inflammatory responses and asthma exacerbation induced by FA. Collectively, these results revealed that FA could exacerbate asthma through the potentiation of HIF-1α-mediated inflammatory responses in macrophages, which also indicated the universal roles of FA-triggered macrophage metabolic and functional alterations in inflammatory or allergic diseases.
研究领域:
免疫学
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呼吸病学
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毒理学
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产品关联
DOI
PubMed
高影响因子
BMC Pulmonary Medicine
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2025
·Vol. 25
·期 1
·1-13
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IF 2.8
Huang Zhiheng,Li Liangxian,Zhang Bingxi,Yao Dong,Xiao Bo,Mo Biwen
Background Bronchial asthma, a chronic inflammatory airway disease, is characterized by airway remodeling, including thickening of the airway smooth muscle layer, primarily due to abnormal proliferation of airway smooth muscle cells (ASMCs). CBL0137 (Curaxin-137 hydrochloride), a histone chaperone facilitate chromatin transcription (FACT) inhibitor, has demonstrated anti-tumor properties, including inhibition of proliferation, promotion of apoptosis, and increased autophagy. However, its effects on ASMCs and airway remodeling remain unexplored. Methods Asthma models were established using ovalbumin (OVA) in female C57BL/6 J mice, with therapeutic interventions using CBL0137 and budesonide. Lung tissues were analyzed using Hematoxylin and eosin (H&E), PAS, Masson’s trichrome, and α-SMA immunofluorescence staining. ASMCs extracted from Sprague–Dawley rats were cultured in vitro experiments, with phenotypic changes assessed via flow cytometry. Gene and protein expressions were analyzed using RT-PCR and Western blotting. Results CBL0137 significantly reduced airway resistance, goblet cell proliferation, alveolar collagen deposition, and airway smooth muscle layer thickening in asthmatic mice. In vitro, CBL0137 inhibited ASMC proliferation and induced apoptosis, downregulating cyclin-B1, Cdc2, and Bcl-2 while upregulating caspase-3. Conclusions CBL0137 mitigates airway remodeling of asthmatic mice by modulating ASMC proliferation and apoptosis, presenting a potential therapeutic strategy for asthma treatment.
研究领域:
药理学
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呼吸病学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
MEDIATORS OF INFLAMMATION
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2025
·Vol. 2025
·期 1
·4955849
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IF 4.2
Zhengrong Chen,Dingwei Yan,Suyu Guo,Yiyi Song,Xinxing Zhang,Wenjing Gu,Heting Dong,Li Huang
Background: This study aimed to explore the mechanisms underlying T-cell differentiation in asthma. Methods and Results: Flow cytometry was performed to detect Th cells. LC-MS/MS was performed to assess lipid metabolism. HE staining was performed to assess the pathological changes of the lung tissues. ELISA was performed to detect cytokine levels. The results of quantitative real-time polymerase chain reaction (qRT-PCR) and western blot showed that miR-192-5p expression was decreased, while SCD1 expression was increased in CD4 + T cells isolated from the peripheral blood of children with asthma. The dual luciferase reporter assay determined the direct interaction between miR-192-5p and SCD1. MiR-192-5p inhibitor reduced ASCL3 and PPARα, increased FASN and SREBP1c mRNA expression and protein levels in mouse spleen CD4 + T cells, and elevated Th2 and Th17 cells, but these effects were reversed by the SCD1 inhibitor. Oleic acid (OA) reduced Th1 cells and increased Th2 and Th17 cells in mouse spleen CD4 + T cells treated with an SCD1 inhibitor. Additionally, pri-miR-192-5p expression was increased in CD4 + T cells isolated from the peripheral blood of asthmatic children, and the deletion of METTL3 upregulated pri-miR-192-5p expression in an m6A-dependent manner. MiR-192-5p mimic and inhibitor both reversed miR-192-5p and SCD1 expression affected by overexpression or deletion of METTL3, both in vivo and in vitro . Furthermore, METTL3 overexpression attenuated lung inflammation, elevated Th1 cells, and reduced Th2 and Th17 cells in CD4 + T cells isolated from the peripheral blood of asthmatic mice. These effects were reversed by the miR-192-5p inhibitor. Conclusion: These results suggest that METTL3/miR-192-5p/SCD1 axis regulates lipid metabolism and affects T cell differentiation, thus affecting asthma progression. This study may provide novel insights into the pathogenesis of asthma and a new treatment strategy.
研究领域:
免疫学
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分子生物学
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呼吸病学
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产品关联
DOI
PubMed
高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
·
2025
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IF 4.7
Longwei Yang,Wenhao Ge,Xi Lin,Ning Yu,Xiaodong Xu,Jianfa Zhang
Allergic asthma is an inflammatory airway disease in which mast cells play a key role in its pathogenesis. Riclinoctaose (Rios), an octasaccharide composed of glucose and galactose, has been reported to modulate macrophage polarization in renal ischemia-reperfusion injury. This study investigates the effects of nebulized Rios in an ovalbumin (OVA)-induced allergic asthma model. Nebulized Rios significantly reduced airway hyperresponsiveness (AHR), inflammatory cell infiltration, pulmonary fibrosis, and mucus production in OVA-treated mice. Additionally, Rios suppressed lung inflammatory cytokine production and protected against OVA-induced oxidative injury. In bronchoalveolar lavage fluid (BALF), Rios decreased the number of neutrophils and macrophages, as well as serum immunoglobulin E (IgE) and interleukin-4 (IL-4) levels. Metabolomics analysis using 1 H NMR showed significant changes in the lung metabolic profile of OVA-induced asthma mice, which were partially reversed by Rios treatment. Confocal laser microscopy (CLM) revealed that fluorescently labeled Rios specifically binds to mast cell membranes. In vitro, Rios reduced degranulation and inflammatory responses in mast cells RBL-2H3 following anti-Dinitrophenyl-Immunoglobulin E (anti-DNP-IgE) sensitization and anti-Dinitrophenyl-Bovine Serum Albumin (anti-DNP-BSA) stimulation. These results suggest that Rios has therapeutic potential for allergic asthma, likely through the modulation of mast cell degranulation and mediator release.
研究领域:
免疫学
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呼吸病学
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药理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
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