Dexmedetomidine protected COPD-induced lung injury by regulating miRNA-146a

Abstract

OBJECTIVE: To study the mechanism of protection provided by dexmedetomidine against COPD-induced lung injury. METHODS: COPD rat model was determined by measuring lung function, and comparing HE staining between two different groups. We got the lung tissue and cells from the control and COPD groups. The cells were divided into three groups: control group, and blank and drug groups that were from the COPD rats. Cell apoptosis, relative gene expression and TNF-α and IL-1β from nutrient solution were measured. Chronic obstructive pulmonary disease (COPD) is a kind of main damage located in airways and lung tissue, causing systemic disease progressively affecting other tissues and organs The symptoms are not reversible. Clinical research shows that the incidence of hospitalized patients with chronic pulmonary disease gradually increases (1). In 2040, COPD will become the world's most endangering disease (2, 3). COPD pathogenesis is not yet entirely clear, but the current study showed that the main causes of COPD include protease/anti-protease imbalance, oxidant/antioxidant imbalance stress (4-7), infl ammatory/anti-infl ammatory response imbalance (8), mechanical stretch injury (9), etc. Clinical treatment is often used for the purpose of mechanical ventilation after induction of anesthesia. Dexmedetomidine is a highly selective α2-adrenergic receptor agonist (10); it not only can effectively calm, but also has some anti-infl ammatory effect (11). However, the mechanism of dexmedetomidine protection against COPD is unclear. The objective of the present study is to explain the latter mechanism. Material and method Animals and cigarette smoke exposureIn our study, we used 6-week-old SD rats at body weight 110±20 g from the animal center, Nanfang Hospital of Southern Medical University. Before the experiment, the rats were accommodated for seven days. All procedures were in compliance with the institutional and national guidelines for the care and use of laboratory animals. The Study Protocol was approved by The Institutional Animal Care and Use Committee, Hebei Medical University. Rats were randomized into two groups: Control Group (n = 8) and Smoking Group (n = 16). The rats in smoking group were exposed to cigarette smoke in a smoking device manufactured by Shijiazhuang Jinyang Science and Technology Inc. (model: JY-01, Shijiazhuang, Hebei, China). Briefl y, 20 cigarettes were burnt continuously and blown into a box together with oxygen, while the whole bodies of animals were exposed to the cigarette smoke in the box. Animals were exposed to cigarette smoke for one hour each time, twice a day, 5 days a week for 16 weeks. After 16 weeks, the rats were analyzed for relative index of COPD including tidal volume (TV), peak expiratory fl ow (PEF), 50 % exhaled tidal volume during expiratory fl ow rate (EF50), forced expiratory volume in 0.3 seconds (FEV0.3) and FEV0.3/ forced vital capacity (FVC). Tissues and cellThe rats were sacrifi ced by femoral artery bleeding. Lung tissue was extracted and a proportion was ...

Circulating miRNA Expression Profiling and Target Prediction in Patients Receiving Dexmedetomidine

“…Many reports have noted other possible applications including use as a protective agent against ischemia/ reperfusion (I/R) injury in various organs [10,11], including heart [12], kidney [13], brain [14], lung [15], liver [16], and even retina [17]. Only three studies have addressed the roles of miRNAs in mechanisms of organ protection [14,18,19]. Moreover, no clinical trials have focused on miRNA expression profiling after administration of dexmedetomidine, and there are no studies on the effects of dexmedetomidine on circulating miRNAs.…”

Protective Effect of Nalbuphine Combined With Dexmedetomidine on the Lungs of Children With Atelectasis and Foreign Body in the Bronchus During the Perioperative Period

“…It can activate the presynaptic α 2 receptors in peripheral sympathetic endings, inhibit the release of norepinephrine, and decrease the concentration of plasma catecholamine ( Giovannitti et al, 2015 ). Furthermore, it can stabilize hemodynamics, relieve oxidative stress caused by surgical trauma, ( He et al, 2021 ), reduce the synthesis and release of pro-inflammatory factors (e.g., TNF-α and IL-6) ( Xu et al, 2019 ), and protect the lung through multiple ways, including anti-sympathia and inhibition of apoptosis, oxidative stress, and inflammatory response ( Li et al, 2016 ).…”

“…Nalbuphine mainly activates κ opioid receptors and produces spinal analgesia ( He et al, 2021 ). Because of its long duration and few adverse reactions, it can be used before operations ( Xu et al, 2019 ) to effectively prevent anesthesia stimulation and central sensitization caused by operation trauma as well as reduce the intraoperative inflammatory response ( Li et al, 2016 ).…”

Geriatric Anesthesia-related Morbidity and Mortality in China

“…[ 19 ] The pain associated with thoracic surgery may release the inflammatory factors that might suppress the pulmonary function. [ 20 ] Thus, both laboratory and clinical studies suggested that dexmedetomidine may exert a protective effect on the pulmonary system,[ 21 22 ] leading to a reduced incidence of respiratory complications. The ischemic preconditioning combined with dexmedetomidine might decrease the incidence of postoperative pulmonary complications by alleviating the inflammatory response and oxidation reaction, which are corroborated by the prevention of the surge of interleukin-6 (IL-6) and enhancement of the activation of superoxide dismutase.…”