Newborn department, Yancheng Maternity and Child Health Care Hospital, Yancheng, Jiangsu Province, 224000, China.
Nursing department, Yancheng Maternity and Child Health Care Hospital, Yancheng, Jiangsu Province, 224000, China.
Inflammation. 2017 Aug;40(4):1375-1381. doi: 10.1007/s10753-017-0580-y.
The present study was designed to evaluate the anti-inflammatory effect of fluoxetine (Flu) against cigarette smoke (CS)-induced chronic obstructive pulmonary disease (COPD) in rats. Forty male Sprague-Dawley (SD) rats were randomly assigned to five groups: control group, CS group, dexamethasone (2 mg/kg) group, and flu (2 mg/kg). H&E staining demonstrated that Flu inhibited CS-induced pathological injury. In addition, Flu could restore the levels of superoxide dismutase (SOD) and malondialdehyde (MDA) in serum. Flu also inhibited the levels of cytokines including tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β). Furthermore, flu significantly inhibited the protein levels of TLR/NF-κB and apoptosis pathway in CS-induced rats. Our findings suggested that flu might effectively ameliorate the progression of COPD via inflammation and apoptosis pathway in rats.
本研究旨在评估氟西汀（Flu）对香烟烟雾（CS）诱导的大鼠慢性阻塞性肺疾病（COPD）的抗炎作用。40 只雄性 Sprague-Dawley（SD）大鼠随机分为五组：对照组、CS 组、地塞米松（2mg/kg）组和氟（2mg/kg）组。H&E 染色表明氟西汀抑制 CS 诱导的病理损伤。此外，氟西汀还可恢复血清中超氧化物歧化酶（SOD）和丙二醛（MDA）水平。氟西汀还抑制了肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）和白细胞介素-1β（IL-1β）等细胞因子的水平。此外，氟西汀显著抑制了 CS 诱导的大鼠 TLR/NF-κB 和凋亡通路的蛋白水平。我们的研究结果表明，氟西汀可能通过炎症和凋亡通路有效改善大鼠 COPD 的进展。
