Frontiers in Pharmacology
·
2024
·
IF 4.4
Changfeng Yin,Yushan Tian,An Yan,Hongjuan Wang,Fengjun Lu,Xianmei Li,Xiao Li,Shulei Han,Ruijuan Miao,Huan Chen,Di Li,Hongwei Hou,Qingyuan Hu
Introduction Chronic obstructive pulmonary disease (COPD) is a disease with severe therapeutic obstacles and high worldwide death rate. COPD progresses predominantly through inflammatory response followed by fibrotic destruction. Quercetin (Que), recognized for its anti-inflammatory effects, presents significant promise as a therapeutic candidate for COPD therapy. However, poor water solubility and low bioavailability of Que hinder its further clinical application. Liposomes are renowned for their unique structure and function, which provided an efficient approach for the delivery of Que in various drug delivery systems. This study was aim to prepare a novel Que liposome (Que-lipo) and administrated via intratracheal (i.t.) with cigarette smoke induced COPD mice. The underlying therapeutic mechanisms against lung damage of Que-lipo were explored. Methods Que-lipo were prepared based on thin film dispersion method and administrated via intratracheal administration. The cigarette smoke induced COPD mice were established and a comprehensive approach was employed to explore the inflammation, pulmonary function and histopathology of lung after i.t. administration of Que-lipo, including enzyme-linked immunosorbent assay, histopathology and immunohistochemistry, reverse transcription-quantitative polymerase chain reaction. Results and discussion Que-lipo not only improved the solubility and biocompatibility of Que but also demonstrated effective cellular uptake in vitro . The inflammation, pulmonary function and pathological condition of lung were improved after i.t. administration of Que-lipo. Que-lipo also regulated the expression of key apoptosis-associated proteins such as Bcl-2 and caspase-3/7, leading to significant inhibition of apoptotic activity in COPD. Furthermore, Que-lipo markedly enhanced its ability to alleviate lung inflammation and fibrosis symptoms by modulating inflammation-related factors and fibrosis signaling molecules. The potential mechanisms of Que-lipo in treating COPD were elucidated, including the suppression of the NLRP3/IL-1β inflammasome pathway and the TGF-β1-related fibrosis signaling pathway.
研究领域:
药理学
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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 CELLULAR AND MOLECULAR MEDICINE
·
2018
·Vol. 22
·期 7
·3514-3525
·
IF 4.302
Wenhui Cui,Zhihui Zhang,Panpan Zhang,Jiao Qu,Cheng Zheng,Xiaoting Mo,Wencheng Zhou,Liang Xu,Hongwei Yao,Jian Gao
Chronic obstructive pulmonary disease (COPD) is characterized by persistent airflow limitation and abnormal inflammatory response. Wnt/β-catenin and AMP-activated protein kinase (AMPK) have been shown to modulate lung inflammatory responses and injury. However, it remains elusive whether Wnt/β-catenin and AMPK modulate nuclear factor erythroid-2 related factor-2 (Nrf2)-mediated protective responses during the development of emphysema. Here we showed that treatment with a Wnt pathway activator (LiCl) reduced elastase-induced airspace enlargement and cigarette smoke extract (CSE)-induced lung inflammatory responses in WT mice, which was associated with increased activation of Nrf2 pathway. Interestingly, these effects of LiCl were not observed in Nrf2 −/− mice exposed to elastase. In normal human bronchial epithelial (NHBE) cells, Wnt3a overexpression up-regulated, whereas Wnt3a knockdown further down-regulated the levels of Nrf2 and its target proteins heme oxygenase-1 (HO-1) and NAD(P)H: quinone oxidoreductase 1 (NQO1) by CSE treatment. In contrast, Nrf2 deficiency did not have any effects on Wnt/β-catenin pathway in mouse lungs and NHBE cells. Both elastase and CSE exposures reduced AMPK phosphorylation. A specific AMPK activator metformin increased Wnt3a, β-catenin, Nrf2 phosphorylation and activation but reduced the levels of IL-6 and IL-8 in NHBE cells and mouse lungs exposed to CSE. Furthermore, Nrf2 deficiency abolished the protection of metformin against CSE-induced increase in IL-6 and IL-8 in NHBE cells. In conclusion, Nrf2 mediates the protective effects of both Wnt3a/β-catenin and AMPK on lung inflammatory responses during the development of COPD/emphysema. These findings provide potential therapeutic targets for the intervention of COPD/emphysema.
研究领域:
医学
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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 MEDICAL RESEARCH
·
2025
·Vol. 30
·期 1
·1-14
·
IF 3.4
Guan Pin,Cai Wentao,Zhong Chunrong,Wu Chunmei
Background Nuclear factor erythroid-2-related factor 2 ( Nrf2 ) could alleviate chronic obstructive pulmonary disease (COPD)-induced muscle dysfunction, and this study aimed to explore the specific mechanisms involved. Methods We successfully established a 12-week cigarette smoke-induced mouse model to replicate COPD-related sarcopenia. The Nrf2 agonist sulforaphane (SFN) and inhibitor ML385 were used to comprehensively assess the regulatory function of Nrf2 in COPD-related sarcopenia. Lung function tests, muscle tension measurements, flow cytometry, H&E staining, qRT-PCR, Western blotting, and biochemical assays were performed to evaluate changes in inflammation, oxidative stress, autophagy, and the Nrf2 /Keap1 axis, so as to verify the pivotal role of Nrf2 signaling in modulating immune responses and skeletal muscle injury from multiple perspectives. Results In the COPD model group, FEV 0.1 /FVC was significantly decreased ( p < 0.05), along with markedly reduced quadriceps muscle mass and grip strength ( p < 0.05). Additionally, the numbers of neutrophils, monocytes, and macrophages in the lung tissues were notably increased ( p < 0.05), accompanied by elevated levels of inflammatory cytokines IL-1b, IL-6, and IL-18 ( p < 0.05). The level of Malondialdehyde (MDA) was increased ( p < 0.05), while that of heme oxygenase 1 (HO-1), glutathione-S-transferase (GST), and total superoxide dismutase (T-SOD) was decreased ( p < 0.05). SFN treatment significantly upregulated Nrf2 and downregulated Keap1 expression ( p < 0.05), reversed the changes in inflammatory and oxidative stress markers ( p < 0.05), and inhibited the protein levels of ATG7 and LC3 ( p < 0.05). In contrast, the ML385-treated group showed opposite trends. Conclusion The present study demonstrated that the Nrf2 pathway played a key role in the regulation of inflammatory response, oxidative stress and autophagy in COPD-associated sarcopenia.
研究领域:
分子生物学
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药理学
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呼吸医学
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免疫学
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病理学
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产品关联
DOI
PubMed
高影响因子
Frontiers in Medicine
·
2025
·
IF 3
Jianing Sun,Di Zhang,Panpan Wang,Junhan Shi,Tan Xue,Panpan Zhang,Qi Wang,Xinjing Gui,Suyun Li,Jiansheng Li,Xuelin Li,Ruixin Liu
Purpose: This study aims to identify the transdermal penetration components of Shufeitie ointment (SFTOT) and investigate the potential active components and mechanisms through which SFTOT exerts its effects on Chronic Obstructive Pulmonary Disease (COPD).Methods: An in vitro permeation test (IVPT) of SFTOT was conducted using a modified Franz diffusion cell method. Ultra-high-performance liquid chromatography-quadrupole/electrostatic field orbitrap high-resolution mass spectrometry (UHPLC-Q-Orbitrap/MS) was employed to analyze data from the transdermal receiving solution, enabling comprehensive identification of the components that permeate through the skin. To predict the potential mechanisms by which SFTOT may treat COPD, network pharmacology was used to construct a component-target-collaterals network. Additionally, molecular docking was applied to verify the interactions between the potential transdermal active components of SFTOT and the core targets.Results: Using UHPLC-Q-Orbitrap/MS, we identified 129 transdermal permeation components in SFTOT. Network pharmacology analysis revealed 222 common targets between SFTOT and COPD. The primary active components were predicted to be luteolin, kaempferol, quercetin, 7-O-methylluteolin, apigenin, ferulic acid, palmitic acid, inapinic acid, 6-shogaol, and myristic acid. These components were primarily enriched in the AGE-RAGE, TNF, PI3K-Akt, and MAPK signaling pathways. Protein–protein interaction (PPI) analysis identified TNF, ALB, AKT1, EGFR, and CASP3 as core targets. Molecular docking results showed that 72% of component-target interactions had a binding energy of < −5.0 kcal/mol, indicating strong binding activity. Among these, apigenin exhibited the lowest binding energy with EGFR and consistently lower binding energies with other core targets compared to the other components. This suggests that apigenin may play a key role in treatment.Conclusion: High-resolution liquid chromatography-mass spectrometry effectively identified the transdermal penetration components of SFTOT, providing a foundation for further screening of key active compounds. Our findings suggest that SFTOT may alleviate COPD by downregulating TNF, ALB, AKT1, EGFR, and CASP3 while inhibiting inflammatory mediator release through the AGE-RAGE, TNF, PI3K-Akt, and MAPK signaling pathways. These effects may help reduce COPD-related symptom clusters. Notably, apigenin appears to be a crucial bioactive component in the prevention and treatment of COPD.
研究领域:
药理学
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呼吸系统疾病
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药物分析
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生物信息学
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产品关联
DOI
PubMed
高影响因子
PHARMACEUTICAL CHEMISTRY JOURNAL
·
2018
·Vol. 52
·期 2
·95-102
·
IF 0.679
Xu Xiaoya,Chen Yajun,Zhang Min,Wang Dianlei,Wu Jie,Yao Zhaomin,Wu Qingqing,Fang Wei
The therapy of Huatanjiangqi capsule (HTJQ) has been used in the treatment of chronic obstructive pulmonary disease (COPD) clinically, with remarkable benefits. A lower functional activity of MRP1 is related to COPD development. However, the mechanism that contributes to MRP1 up-regulation by HTJQ was unclear. This study aimed to investigate the effects of HTJQ on the expression of Nrf2 and MRP1 in COPD rats. Rats were exposed to cigarette smoke plus lipopolysaccharide tracheal instillation to induce a COPD model. Then, Nrf2, HO-1, and MRP1 mRNA expression and their protein production in lung tissues were examined. The model group showed significant changes in the above assessments as compared to those of the control group ( p < 0.05). The lung function of model group treated with low/high dose of HTJQ was significantly strengthened (both p < 0.05), and the inflammatory cells and goblet cells were decreased in lung tissues. Treatment with low/high dose of HTJQ resulted in obvious increase in Nrf2, HO-1, and MRP1 mRNA and protein expression levels ( p < 0.05). HTJQ could up-regulate Nrf2 and MRP1 expression in lung tissues of COPD model rats. The mechanism by which HTJQ up-regulates MRP1 expression may be associated with Nrf2.
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
高影响因子
International Journal of Chronic Obstructive Pulmonary Disease
·
2024
·
IF 2.7
Liguo Lu,Chengdong Zhu,Jian Xu,Yulan Hu,Juxiang Dai,Sheng Wang,Tao Wei
Introduction The Lifei Decoction (LD) is a commonly utilized Chinese medicine for the treatment of sepsis and bronchial inflammation. However, its therapeutic potential in chronic obstructive pulmonary disease (COPD) remains unknown. Therefore, the objective of this study was to investigate the therapeutic efficacy and underlying mechanism of LD in a mouse model of COPD induced by cigarette smoke (CS) combined with lipopolysaccharide (LPS).Methods Hematoxylin-eosin (H&E) staining was employed to observe the pathological alterations in lung tissue, while ELISA was utilized for the detection of levels of inflammatory factors in both lung tissue and bronchoalveolar lavage fluid (BALF). Additionally, Western blot analysis was conducted to assess the expression of p-NF-κB, GDF11, ZO-1, and Occludin-1 proteins. The changes in intestinal flora were evaluated using the viable bacteria count method.Results The administration of LD demonstrates significant efficacy in mitigating pulmonary tissue damage in a murine model, while concurrently inhibiting the activation of the inflammatory pathway NF-κB to attenuate the levels of pro-inflammatory factors. Moreover, LD exhibits the capacity to enhance the expression of intestinal functional proteins ZO-1 and Occludin-1, thereby rectifying dysbiosis within the gut microbiota.Conclusion The LD shows great promise as a potential treatment for COPD.
研究领域:
药理学
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呼吸病学
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免疫学
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微生物学
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产品关联
DOI
PubMed
高影响因子
Journal of Advanced Research
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2025
·
IF 13
Lin-Tao Xu,Qing-Tong Han,Zhen-Peng Xu,Xiao-Ning Wang,Hua Zhang,Tao Shen
Introduction Chronic obstructive pulmonary disease (COPD) represents a significant global health challenge, characterized by substantial morbidity and mortality rates. In traditional Chinese medicine (TCM), Farfarae Flos (FF) has been widely utilized as a therapeutic agent for COPD. However, its specific bioactive compounds and the underlying mechanisms are unclear. Objectives This study aims to identify bioactive constituent of FF against COPD and illustrate its therapeutic target and mechanism. Methods and Results In this research, a high-throughput screening on constituents of FF was conducted, leading to the identification of a potent anti-COPD lead, tussilagone (TUS). Utilizing biotin-labeling approach, Kelch-like ECH-associated protein 1 (KEAP1), the ubiquitin E3 ligase of nuclear factor erythroid 2-related factor 2 (Nrf2), was identified to be the direct target of TUS. Mechanistically, TUS activated KEAP1-Nrf2 axis by covalent modification of cysteine 434 (Cys434), a novel high-reactivity cysteine of KEAP1. TUS-mediated Nrf2 activation further suppressed the activation of nuclear factor kappa-B (NF-κB) and NOD-like receptor thermal protein domain associated protein 3 (NLRP3) inflammasome, consequently attenuating lung inflammation in COPD. Conclusion TUS was identified as the bioactive constituent of FF against COPD, which directly targeted Cys434 of KEAP1. KEAP1 was proven to be a pharmacological target for the treatment of COPD, and Cys434 was identified to be the first highly reactive cysteine in Kelch domain of KEAP1. TUS inhibits lung inflammation by regulating Nrf2 and NF-κB/NLRP3, which is the mechanism of FF against COPD
研究领域:
药理学
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分子生物学
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呼吸医学
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民族药理学
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生物化学
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免疫学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
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2025
·
IF 5.4
Qinfeng Lu,Zhu Chen,Bai-Xiang Mu,Bo-Han Wang,Fanchao Feng,Jun Zhao,Hailang He,Yu Wei
Ethnopharmacological relevance COPD, marked by coughing, sputum production, and wheezing, is categorized as "Lung Distension" in Traditional Chinese Medicine (TCM). The combined use of Suzi Jiangqi Decoction and Sanzi Yangqin Decoction, known as Jia Wei Su Zi Jiang Qi Formula (JWSZJQF), is a common treatment for Lung Distension with phlegm accumulation in the lungs. It is particularly effective for symptoms like excessive phlegm and chest tightness. However, the specific active components of JWSZJQF and their molecular mechanisms in addressing mucus hypersecretion in COPD remain unclear, requiring further investigation and validation. Aim of the study This study aims to identify the potential targets and signaling pathways of JWSZJQF in treating COPD-associated mucus hypersecretion using UHPLC-Q-Orbitrap MS/MS, network pharmacology, and in vitro experimental verification. Materials and methods All plant names were verified through WorldFloraOnline ( www.worldFloraonline.org ) and MPNs ( http://mpns.kew.org ). First, the effective components of JWSZJQF were identified and analyzed using UHPLC-Q-Orbitrap MS/MS, supplemented by data from TCMSP. Network pharmacology analysis was used to determine the potential targets and pathways of JWSZJQF in COPD treatment. A mucus hypersecretion cell model was created using IL-17 cytokine, and the effectiveness of JWSZJQF in reducing mucus hypersecretion was assessed through immunofluorescence assay, Western blotting, and quantitative real-time polymerase chain reaction (qPCR). Lastly, a prospective study was conducted to collect data from 30 inpatients with AECOPD between September 2023 and July 2024. Serum samples before and after treatment were analyzed to validate the findings. Results A total of 864 active components were identified, with 79 potential COPD therapeutic targets confirmed based on the top 30 active components, including TNF, IL-6, and AKT1. The involved KEGG pathways included the IL-17 and NF-κB signaling pathways. In vitro experiments showed that JWSZJQF inhibited mucin (MUC5AC) secretion at both mRNA and protein levels. Additionally, JWSZJQF modulated i-κBα and p65 expression in the NF-κB pathway. Compared to the control group, patients treated with JWSZJQF exhibited lower levels of IL-17 and MUC5AC in their serum. Conclusion This study preliminarily explored the mechanisms of JWSZJQF in treating COPD-associated mucus hypersecretion through UHPLC-Q-Orbitrap MS/MS, network pharmacology, in vitro experiments, and clinical observation. The main active components and potential targets were identified, laying a scientific foundation for further research.
研究领域:
药理学
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民族药理学
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呼吸病学
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分子生物学
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网络药理学
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临床研究
✓ 已验证
产品关联
DOI
PubMed
高影响因子
COPD-Journal of Chronic Obstructive Pulmonary Disease
·
2023
·
IF 2.2
Chuanxin Yang,Libing Deng,Fang Bao,Hui Jiang,Long Zhang
Chronic obstructive pulmonary disease (COPD) is a difficult-to-cure disease that mainly affects the respiratory system. Inhaled anesthetic drug such as sevoflurane plays a controversial role in COPD by different concentration, but the underlying epigenetic mechanism remains unclear. Here, we prepared lipopolysaccharide (LPS)-induced COPD rat model, and isolated Alveolar type II (ATII) cells. We mainly focused DNA methylation on the promoter of COPD-related genes including Sftpa1, Napsa, Ca2, Sfta2, Lamp3, Wif1, Pgc, and Etv5. We observed COPD rat treated by sevoflurane with low (0.5%) and high (2%) concentrations displayed an opposite DNA methylation pattern. These six genes' promoter were all hypomethylated by 0.5% sevoflurane whereas hypermethylated by 2% sevoflurane, accompanied with the opposite transcriptional activity. We further verified that the DNMT1 binding ability contributed to DNA methylation these six genes' promoter. Moreover, we also captured DNMT1 and identified REC8 meiotic recombination protein (REC8) as the specific binding protein only existed in ATII cells treated with 0.5% sevoflurane rather than 2% and control. The binding ability of REC8 on these target genes' promoter showed highly positive correlation with DNMT1. In summary, we uncovered a potential epigenetic role of sevoflurane with low concentration in ATII cells of COPD that may help us deeply understand the pathogenesis and treatment mechanism of inhaled anesthesia drugs in COPD via a dose-dependent manner.
研究领域:
肺病学
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分子生物学
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表观遗传学
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药理学
✓ 已验证
DOI
高影响因子
PHYTOCHEMICAL ANALYSIS
·
2025
·
IF 2.6
Peng Yang,Hu-Dong Lv,Jie Wu,Fang Long,Jing Zhou,Cheng-Ying Wu,Jin-Di Xu,Shan-Shan Zhou,Qing-Ling Xiao,Song-Lin Li,Hong Shen
Introduction The role of macromolecular components in traditional Chinese medicines (TCMs) decoction remains poorly understood, primarily because of their structural complexity and limited systemic bioavailability. In the modernization of TCMs' decoctions, macromolecular components are often removed as “poor bioavailable impurities” by ethanol precipitation that might attenuate the efficacy thereof. Purpose A novel strategy integrating LC–MS-based serum pharmacochemistry, network pharmacology, and pharmacodynamics was developed to reveal the role of macromolecular components in TCMs' decoction, using Qi-Huo-Yi-Fei decoction (QH) treating chronic obstructive pulmonary disease (COPD) as a case study. Materials and Methods QH was separated into macromolecular components (QH-M) and small molecular components (QH-S) by ethanol precipitation. The absorbed components of QH and QH-S in serum were qualitatively and semiquantitatively analyzed by UPLC-QTOF-MS/MS. The differences in targets and pathways of the absorbed components were predicted by network pharmacology analysis. The therapeutic effects on pulmonary function, histopathology, and inflammation of QH, QH-S, and QH-M were comparatively investigated on a COPD rat model. Result A total of 103 components were identified in QH and QH-S, whereas 86 and 72 were detectable in QH- or QH-S-treated serum, respectively. The highest levels of absorbed components appeared from 15 to 60 min for QH-S and at 15 min for QH. The concentrations of most absorbed components of QH were twofold higher than those of QH-S. Their protein–protein interaction (PPI), herb–component–target networks, and GO/KEGG enrichment pathways were quite different, mainly in inflammatory, immunity, and cell apoptosis processes. QH-M improved pulmonary function, histopathology, and inflammatory infiltration, mainly on FVC ( p < 0.05), thickness/external diameter ( p < 0.01), Wac/Pbm ( p < 0.01), TNF-α ( p < 0.01), and IL-17 ( p < 0.05). Meanwhile, QH was more effective than QH-S, mainly on FEV0.3/FVC, MAN, GC/CC, TNF-α, and IL-17. Conclusion QH-M was not only effective independently on COPD but also showed integrative effects with the coexisting QH-S in improving their absorption, thus strengthening the component–target interactions, and consequently contributing to the COPD therapeutic effects of QH. Therefore, it was confirmed that QH-M was essential for QH's COPD therapy and should not be removed during the modern preparation development.
研究领域:
药理学
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分析化学
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系统生物学
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中医药学
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呼吸医学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
MICROCHEMICAL JOURNAL
·
2025
·
IF 5.1
Guobin Huang,Weiting Xu,Jinxin Chi,Chenchen Lin,Jiabin Wang,Xucong Lin
Environmental smog pollution induces chronic obstructive pulmonary disease (COPD), and causes the urgent need of timely, safe and quantitative testing for risk assessment. The miRNA-based bioanalysis offers a non-invasive access to rapid COPD screening, while challenges remain in accurately identifying miRNAs from complex matrices. Herein, a novel bionic aptasensor has been pioneered for meeting the specific and sensitive detection of the miR-155 in serum for COPD diagnosis, integrating tetrahedral framework nucleic acid (tFNA) confined affinity recognition and enzyme-free hybridization chain reaction (HCR) amplification strategy. Precision-designed tFNAs were fabricated and hybridized with FAM-labeled cDNAs, enabling dual-mode recognition mechanism including spatially confined aptamer recognition and bionic molecular sieve size-selective action. Proteins and pre-miRNAs were excluded, and the target microRNA-155 was specifically captured. This triggered a structural switch of tFNAs and activated cDNA-mediated HCR, assembling double-stranded DNA and achieving exponential fluorescence enhancement synergistically produced by SYBR Green I (SGI) and FAM. The optimal limit of detection as 53 fM for miRNA-155 was achieved with laser-induced fluorescence (LIF). Applied to COPD diagnosis, the detections of trace miRNA-155 were satisfactory and the recovery yields were ranged in 96.4 ± 5.2 % ∼106.2 ± 2.1 % ( n = 3) in the serum of COPD patients. Smoke-exposed model rats were also analyzed, and the miRNA-155 was achieved with a significant concentration up-regulation to light the COPD. It offers a high-performance protocol for meeting the non-invasive rapid screening of COPD, further providing promising technologies for evaluating safety issues of environmentally induced diseases.
研究领域:
生物传感器
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分子诊断学
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环境健康
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RNA生物学
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肺部疾病研究
✓ 已验证
产品关联
DOI
高影响因子
MOLECULAR MEDICINE
·
2024
·Vol. 30
·期 1
·1-16
·
IF 6
Xie Bin,Chen Qiong,Dai Ziyu,Jiang Chen,Chen Xi
Background Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory lung disease associated with high morbidity and mortality worldwide. Oxidative injury and mitochondrial dysfunction in the airway epithelium are major events in COPD progression.Methods and resultsThe therapeutic effects of Progesterone (P4) were investigated in vivo and in vitro in this study. In vivo, in a cigarette smoke (CS) exposure-induced COPD mouse model, P4 treatment significantly ameliorated CS exposure-induced physiological and pathological characteristics, including inflammatory cell infiltration and oxidative injury, in a dose-dependent manner. The c-MYC/SIRT1/PGC-1α pathway is involved in the protective function of P4 against CS-induced COPD. In vitro, P4 co-treatment significantly ameliorated H2O2-induced oxidative injury and mitochondrial dysfunctions by promoting cell proliferation, increasing mitochondrial membrane potential, decreasing ROS levels and apoptosis, and increasing ATP content. Moreover, P4 co-treatment partially attenuated H2O2-caused inhibition in Nrf1, Tfam, Mfn1, PGR-B, c-MYC, SIRT1, and PGC-1α levels. In BEAS-2B and ASM cells, the c-MYC/SIRT1 axis regulated P4’s protective effects against H2O2-induced oxidative injury and mitochondrial dysfunctions.Conclusion P4 activates the c-MYC/SIRT1 axis, ameliorating CS-induced COPD and protecting both airway epithelial cells and smooth muscle cells against H2O2-induced oxidative damage. PGC-1α and downstream mitochondrial signaling pathways might be involved.
研究领域:
呼吸病学
·
药理学
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细胞生物学
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分子生物学
✓ 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）