scholarly journals The Mechanism of Penehyclidine Hydrochloride and Its Effect on the Inflammatory Response of Lung Tissue in Rats with Chronic Obstructive Pulmonary Disease During Mechanical Ventilation

2021 ◽  
Vol Volume 16 ◽  
pp. 877-885
Author(s):  
Zhi-yuan Chen ◽  
Yi Zhang ◽  
Jian-hua Wu ◽  
Xiao-hua Gao ◽  
Chun-ling Huang ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Mechanical Ventilation ◽  
Inflammatory Response ◽  
Pulmonary Disease ◽  
Lung Tissue ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Penehyclidine Hydrochloride

Health Informatics of Doxofylline Combined with Penehyclidine Hydrochloride on Pulmonary Inflammation in Chronic Obstructive Pulmonary Disease Based on ANOVA Statistical Analysis

2021 ◽  
Vol 11 (7) ◽  
pp. 1999-2005
Author(s):  
Zhiyuan Chen ◽  
Yi Zhang ◽  
Jianhua Wu ◽  
Xiaohua Gao ◽  
Yumei Lin ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Statistical Analysis ◽  
Inflammatory Response ◽  
Drug Treatment ◽  
Pulmonary Disease ◽  
Signaling Pathway ◽  
Health Informatics ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Penehyclidine Hydrochloride

Objective: This study evaluated the effect of doxofylline combined with penehyclidine hydrochloride on the pulmonary inflammatory response during mechanical ventilation in chronic obstructive pulmonary disease (COPD), as well as to identify the effects of JNK/SAPK signaling pathway in this inflammatory response. Methods: The COPD model can be constructed by exposing it to cigarette smoke and injections of lipopolysaccharide into the airway. Rats were selected randomly for treatment with doxofylline, penehyclidine hydrochloride, a combination of these two drugs. The control Group received no drug treatment. The date were processed using ANOVA statistical analysis. Results: In all rats, the lung tissue was pathologically characteristic of COPD. Peak airway pressure, the wet/dry weight of lungs, and degrees of TNF-α, IL-10, malondialdehyde, JNK, and p-JNK decreased; while IL-10 and superoxide dismutase levels increased (p < 0.05) in all Groups having received drug treatment (p < 0.05) when compared to control. The combination of penehyclidine hydrochloride with doxofylline had a stronger effect on all of these metrics than either drug alone (p < 0.05). Conclusion: Based on health informatics, This study suggests that the combination of penehyclidine hydrochloride with doxofylline can promote the recovery and maintenance of immune homeostasis in mechanically ventilated COPD rats, and that the underlying mechanism may be is influenced by downregulation of the JNK/SAPK signaling pathway.

The role of gene polymorphisms in the pathogenesis of chronic obstructive pulmonary disease

Biologia ◽  
2008 ◽  
Vol 63 (1) ◽  
Author(s):  
Eva Slabá ◽  
Pavol Joppa ◽  
Ján Šalagovič ◽  
Ružena Tkáčová
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Inflammatory Response ◽  
Candidate Genes ◽  
Pulmonary Disease ◽  
Gene Polymorphisms ◽  
Association Studies ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Positional Candidate ◽  
Linkage Analyses

AbstractChronic obstructive pulmonary disease (COPD) is a major cause of morbidity and mortality worldwide. Irreversible airflow limitation, both progressive and associated with an inflammatory response of the lungs to noxious particles or gases, is a hallmark of the disease. Cigarette smoking is the most important environmental risk factor for COPD, nevertheless, only approximately 20–30% of smokers develop symptomatic disease. Epidemiological studies, case-control studies in relatives of patients with COPD, and twin studies suggest that COPD is a genetically complex disease with environmental factors and many involved genes interacting together. Two major strategies have been employed to identify the genes and the polymorphisms that likely contribute to the development of complex diseases: association studies and linkage analyses. Biologically plausible pathogenetic mechanisms are prerequisites to focus the search for genes of known function in association studies. Protease-antiprotease imbalance, generation of oxidative stress, and chronic inflammation are recognized as the principal mechanisms leading to irreversible airflow obstruction and parenchymal destruction in the lung. Therefore, genes which have been implicated in the pathogenesis of COPD are involved in antiproteolysis, antioxidant barrier and metabolism of xenobiotic substances, inflammatory response to cigarette smoke, airway hyperresponsiveness, and pulmonary vascular remodelling. Significant associations with COPD-related phenotypes have been reported for polymorphisms in genes coding for matrix metalloproteinases, microsomal epoxide hydrolase, glutathione-S-transferases, heme oxygenase, tumor necrosis factor, interleukines 1, 8, and 13, vitamin D-binding protein and β-2-adrenergic receptor (ADRB2), whereas adequately powered replication studies failed to confirm most of the previously observed associations. Genome-wide linkage analyses provide us with a novel tool to identify the general locations of COPD susceptibility genes, and should be followed by association analyses of positional candidate genes from COPD pathophysiology, positional candidate genes selected from gene expression studies, or dense single nucleotide polymorphism panels across regions of linkage. Haplotype analyses of genes with multiple polymorphic sites in linkage disequilibrium, such as the ADRB2 gene, provide another promising field that has yet to be explored in patients with COPD. In the present article we review the current knowledge about gene polymorphisms that have been recently linked to the risk of developing COPD and/or may account for variations in the disease course.

scholarly journals Lights and shadows of non-invasive mechanical ventilation for chronic obstructive pulmonary disease (COPD) exacerbations

2015 ◽  
Vol 10 (2) ◽  
pp. 87 ◽  
Author(s):  
JoseLuis Lopez-Campos ◽  
Luis Jara-Palomares ◽  
Xavier Muñoz ◽  
Víctor Bustamante ◽  
Esther Barreiro
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Mechanical Ventilation ◽  
Pulmonary Disease ◽  
Invasive Mechanical Ventilation ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Copd Exacerbations ◽  
Non Invasive
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