Jinwei Tang modulates HDAC2 expression in a rat model of COPD

Wu, Jianjun; Li, Xin; Yang, Qin; Cheng, Juan; Hao, Gaimei; Jin, Ran; Zhu, Chenjun

doi:10.3892/etm.2018.5707

Cited by 5 publications

(6 citation statements)

References 26 publications

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“…Jinwei decoction improved pulmonary function in a rat model of COPD; reduced the in ltration of macrophages, lymphocytes and neutrophils in lung tissue; reduced the formation of compensatory emphysema and delayed airway remodeling; decreased IL-8 and TNF-α levels in lung homogenate; and increased HDAC2 expression in lung tissue and HDAC2 content in lung homogenate. The mechanism is related to the recovery of HDAC2 activity, which enables GCs to activate Glucocorticoid Receptor, recruit HDAC2 to regions of transcriptional activation, increase histone deacetylation, and inhibit the expression of in ammatory factors [18] . However, the upstream mechanism of Jinwei decoction on HDAC2 expression is not clear.…”

Section: Introductionmentioning

confidence: 99%

WITHDRAWN: Network Pharmacology and Molecular Docking Study of Jinwei Decoction for Enhancement of Glucocorticoid Anti-Inflammatory Effect in COPD through miR-21

Zhang

Chen

et al. 2021

Preprint

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PurposeJinwei decoction can enhance the anti-inflammatory effect of glucocorticoid (GC) on chronic obstructive pulmonary disease (COPD) by restoring the activity of HDAC2. But the upstream mechanism of Jinwei decoction on HDAC2 expression is not clear. ObjectiveTo explore whether Jinwei decoction can enhance the anti-inflammatory effect of GC on COPD through microRNA21 (miR-21) by network pharmacology. MethodsThe TCMSP database was used to screen active ingredients and target genes of Jinwei decoction, and miRWalk2.0 was used to predict downstream target genes of miR-21. COPD-related genes were identified by searching GeneCards and OMIM databases; Venny 2.1 was used to screen intersection genes; Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways of intersection genes were analyzed by R software. Protein-protein interactions (PPIs) were analyzed by Cytoscape 3.7.2 software to identify core genes. Finally, interactions between main compounds and potential targets were verified by molecular docking. ResultsTwo hundred ninety-two active ingredients, 316 Jinwei drug targets, 10170 miR-21 target genes, 6617 COPD target genes, and 184 intersection gene were identified. Eleven core proteins of PPI networks may be involved. GO enrichment analysis showed that oxidative stress, regulation of inflammatory response, hormone transport, and histone modification were involved; KEGG pathway enrichment analysis concentrated in the PI3K-Akt, mitogen-activated protein kinase (MAPK), HIF-1, neutrophil extracellular bactericidal network, and other signaling pathways. ConclusionJinwei decoction can regulate histone deacetylase-2 activity and enhance the anti-inflammatory effect of GC on COPD by modulating miR-21. Its mechanism of action may be related to its effect on the PI3K Akt, MAPK, and TNF signaling pathways and neutrophil extracellular trap formation through miR-21.

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Section: Introductionmentioning

confidence: 99%

WITHDRAWN: Network Pharmacology and Molecular Docking Study of Jinwei Decoction for Enhancement of Glucocorticoid Anti-Inflammatory Effect in COPD through miR-21

Zhang

Chen

et al. 2021

Preprint

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“…Reduced HDAC2 expression was also observed even after 4 h in BEAS2B cell lines after induction with 5% cigarette smoke extract (CSE), and a similar trend also followed in rat COPD model of lipopolysaccharide (LPS) and cigarette smoke exposure model for 30 days. − HAT, on the other hand, did not show significant differences among all the stages of COPD and even in alveolar macrophages and bronchial biopsies samples from COPD patients . Thus, decreased HDAC2 expression is associated with increased expression of inflammatory genes via NF-kß pathway (Figure ).…”

Section: Inflammatory Markersmentioning

confidence: 62%

Molecular Mechanisms and the Interplay of Important Chronic Obstructive Pulmonary Disease Biomarkers Reveals Novel Therapeutic Targets

Sharma,

Banerjee,

Srivastava

2023

ACS Omega

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Chronic Obstructive Pulmonary Disease (COPD) is a progressive, age-dependent, and unmet chronic inflammatory disease of the peripheral airways, leading to difficulty in exhalation. Several biomarkers have been tested in general towards the resolution for a long time, but no apparent success was achieved. Ongoing therapies of COPD have only symptomatic relief but no cure. Reactive oxygen species (ROS) are highly reactive species which include oxygen radicals and nonradical derivatives, and are the prominent players in COPD. They are produced as natural byproducts of cellular metabolism, but their levels can vary due to exposure to indoor air pollution, occupational pollution, and environmental pollutants such as cigarette smoke. In COPD, the lungs are continuously exposed to high levels of ROS thus leading to oxidative stress. ROS can cause damage to cells, proteins, lipids, and DNA which further contributes to the chronic inflammation in COPD and exacerbates the disease condition. Excessive ROS production can overwhelm cellular antioxidant systems and act as signaling molecules that regulate cellular processes, including antioxidant defense mechanisms involving glutathione and sirtuins which further leads to cellular apoptosis, cellular senescence, inflammation, and sarcopenia. In this review paper, we focused on COPD from different perspectives including potential markers and different cellular processes such as apoptosis, cellular senescence, inflammation, sirtuins, and sarcopenia, and tried to connect the dots between them so that novel therapeutic strategies to evaluate and target the possible underlying mechanisms in COPD could be explored.

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“…TCM has been widely used in the treatment of chronic lung diseases ( 45 , 46 ). YQGB is composed of Dangshen [DS, Codonopsis pilosula (Franch.…”

Section: Discussionmentioning

confidence: 99%

Yiqigubiao pill treatment regulates Sirtuin 5 expression and mitochondrial function in chronic obstructive pulmonary disease

Meng,

Li,

et al. 2024

J Thorac Dis

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Background Chronic obstructive pulmonary disease (COPD) is a heterogeneous group of pathophysiological bases of airway inflammation and its anti-inflammatory response. Aberrant mitochondrial signaling and mitochondrial dysfunction underlie the pathomechanisms leading to COPD. This study aims to investigate the effects of the Yiqigubiao (YQGB) pill, a traditional Chinese medicine (TCM), on Sirtuin 5 (SIRT5) and mitochondrial function in patients with COPD. Methods Thirty-four patients with COPD were randomized into oral YQGB or placebo groups concurrent with a 24-week routine treatment. The pulmonary function was assessed by examining the levels of forced expiratory volume in one second (FEV 1 )/forced vital capacity (FVC), FEV 1 , and FVC. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot were used to detect SIRT5 expression in mitochondria isolated from peripheral blood. Flow cytometry was used to detect changes in mitochondrial membrane potential and reactive oxygen species (ROS) in peripheral blood lymphocytes. Human bronchial epithelial (HBE) cells stimulated by cigarette smoke extract (CSE) were treated with YQGB. After SIRT5 was knocked down in cells, the changes in mitochondrial membrane potential, levels of adenosine triphosphate (ATP), and ROS were detected. Results YQGB treatment significantly improved lung function in patients with COPD. The expression of SIRT5 and the mitochondrial membrane potential significantly increased and ROS decreased in patients with COPD after YQGB treatment. The CSE decreased cell proliferation and SIRT5 expression, which was alleviated after YQGB treatment. Furthermore, SIRT5 was knocked down in CSE-stimulated HBE cells, and its expression was elevated upon YQGB treatment. The knockdown of SIRT5 significantly altered the CSE-stimulation-induced dysregulation of mitochondrial membrane potential, ATP levels, and ROS. This was also restored after YQGB treatment. Conclusions YQGB treatment can elevate SIRT5 expression, restore mitochondrial function in COPD, and exert protective effects.

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Jinwei Tang modulates HDAC2 expression in a rat model of COPD

Cited by 5 publications

References 26 publications

WITHDRAWN: Network Pharmacology and Molecular Docking Study of Jinwei Decoction for Enhancement of Glucocorticoid Anti-Inflammatory Effect in COPD through miR-21

WITHDRAWN: Network Pharmacology and Molecular Docking Study of Jinwei Decoction for Enhancement of Glucocorticoid Anti-Inflammatory Effect in COPD through miR-21

Molecular Mechanisms and the Interplay of Important Chronic Obstructive Pulmonary Disease Biomarkers Reveals Novel Therapeutic Targets

Yiqigubiao pill treatment regulates Sirtuin 5 expression and mitochondrial function in chronic obstructive pulmonary disease

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