Department of Respiratory and Critical Care Medicine, Cangzhou Central Hospital, Cangzhou 061001, Hebei, China.
Hemodialysis Room, Cangzhou Central Hospital, Cangzhou 061001, Hebei, China.
J Healthc Eng. 2022 Apr 21;2022:6556208. doi: 10.1155/2022/6556208. eCollection 2022.
Chronic obstructive pulmonary disease (COPD) is one of the most common chronic respiratory diseases in the world. COPD is a general term for a class of lung diseases, including emphysema, chronic bronchitis, and refractory asthma. It is characterized by irreversible airflow obstruction and chronic tracheal inflammation.
This study aimed to investigate the expression and related mechanisms of miR-100 and TRIB2 in patients with COPD.
We collected the serum of patients admitted to our hospital and healthy volunteers undergoing physical examination at the same time, pulmonary fibroblasts were purchased for the experiments, miR-100 was overexpressed, and TRIB2 expression was inhibited in cells. The miR-100 and TRIB2 expression levels in serum and cells were detected by qRT-PCR and Western blot, cell proliferation and apoptosis were detected by CCK-8 and flow cytometry, and the relationship between miR-100 and TRIB2 was explored by the dual-luciferase report.
The miR-100 expression in the serum of the COPD group was expressed normally, while the TRIB2 expression was expressed abnormally ( < 0.05). The AUC of serum miR-146a and TRIB2 for COPD diagnosis were 0.965 and 0.954, respectively. Overexpressing miR-100 and inhibiting the TRIB2 expression could decrease cell proliferation and increase apoptosis rate. According to the dual-luciferase report, miR-100 and TRIB2 had a targeted regulatory relationship. Rescue experiments showed that overexpressing TRIB2 could reverse the changes of cell proliferation and apoptosis caused by overexpression of miR-100.
miR-100 and TRIB2 were expressed abnormally in serum of COPD patients, and miR-100 could inhibit proliferation of pulmonary fibroblasts and promote their apoptosis.
慢性阻塞性肺疾病（COPD）是世界上最常见的慢性呼吸道疾病之一。COPD 是一类肺部疾病的统称，包括肺气肿、慢性支气管炎和难治性哮喘。其特征为气流受限不可逆转且慢性气管炎症。
本研究旨在探讨 COPD 患者中 miR-100 和 TRIB2 的表达及相关机制。
收集我院收治的患者血清和同期健康体检志愿者血清，购买肺成纤维细胞进行实验，细胞中转染 miR-100 过表达载体，抑制 TRIB2 表达。采用 qRT-PCR 和 Western blot 检测血清和细胞中 miR-100 和 TRIB2 的表达水平，采用 CCK-8 和流式细胞术检测细胞增殖和凋亡情况，通过双荧光素酶报告探究 miR-100 和 TRIB2 的关系。
COPD 组患者血清中 miR-100 表达正常，而 TRIB2 表达异常（<0.05）。血清 miR-146a 和 TRIB2 对 COPD 诊断的 AUC 分别为 0.965 和 0.954。过表达 miR-100 并抑制 TRIB2 表达可降低细胞增殖并增加细胞凋亡率。根据双荧光素酶报告，miR-100 和 TRIB2 具有靶向调控关系。挽救实验表明，过表达 TRIB2 可逆转 miR-100 过表达引起的细胞增殖和凋亡变化。
COPD 患者血清中 miR-100 和 TRIB2 表达异常，miR-100 可抑制肺成纤维细胞增殖并促进其凋亡。
