Department of Anesthesiology, The First Affiliated Hospital of Anhui Medical University, Hefei 230022, Anhui, China.
Department of Geriatric Respiratory and Critical Care, Anhui Geriatric Institute, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China.
Biosci Rep. 2019 Nov 29;39(11). doi: 10.1042/BSR20193282.
Sevoflurane was found to show protective roles in mice with asthma, however, the mechanism of which needs further exploring. Aquaporins (AQPs) have been demonstrated to be involved in the pathogenesis of asthma, while endoplasmic reticulum stress has been reported to be related to many inflammatory diseases and involved in protein processing, including AQPs. The present study aimed to determine the role of sevoflurane in AQPs (AQP1,3,4,5) expression in mice with allergic airway inflammation and the probable mechanism. The increased number of inflammatory cells infiltrating the lung tissue, and the elevated levels of tumor necrosis factor-α (TNF-α) and interleukin (IL) 13 (IL-13) were all decreased after sevoflurane treatment (all P<0.05). Meanwhile, mRNA levels of AQP1 and AQP5 but not AQP3 and AQP4 were decreased in ovalbumin (OVA)-induced allergic mice lung. Both the decreased mRNA expression and protein levels of AQP1 and AQP5 in allergic lung tissues were reversed by sevoflurane treatment. Furthermore, we established that sevoflurane inhibited the OVA-induced protein increase in the endoplasmic reticulum (ER) stress markers BiP and C/EBP homologous protein (CHOP). Collectively, these findings suggested that sevoflurane modulated the expression and protein level of AOPs (AQP1, AQP5) as well as inhibited ER stress response in OVA-induced allergic airway inflammation of mice.
七氟醚被发现对哮喘小鼠具有保护作用，但具体机制仍需进一步研究。水通道蛋白（AQP）已被证明与哮喘的发病机制有关，而内质网应激已被报道与许多炎症性疾病有关，并参与包括 AQP 在内的蛋白质加工。本研究旨在确定七氟醚在变应性气道炎症小鼠 AQP（AQP1、3、4、5）表达中的作用及其可能的机制。七氟醚处理后，肺组织中炎性细胞浸润数量增加，肿瘤坏死因子-α（TNF-α）和白细胞介素-13（IL-13）水平升高，均降低（均 P<0.05）。同时，卵清蛋白（OVA）诱导的过敏性小鼠肺中 AQP1 和 AQP5 的 mRNA 水平降低，但 AQP3 和 AQP4 的 mRNA 水平未降低。变应性肺组织中 AQP1 和 AQP5 的 mRNA 表达和蛋白水平降低均被七氟醚治疗逆转。此外，我们发现七氟醚抑制了内质网（ER）应激标志物 BiP 和 C/EBP 同源蛋白（CHOP）诱导的 OVA 蛋白增加。综上所述，这些发现表明，七氟醚调节 AOPs（AQP1、AQP5）的表达和蛋白水平，并抑制 OVA 诱导的过敏性气道炎症小鼠的 ER 应激反应。
