Cerebral ischemia/reperfusion injury induces airway mucus hypersecretion in rats and activates IL‑13‑associated inflammatory mechanisms.

Abstract

The majority of patients that suffer a stroke have excessive sputum, which accelerates the development of pulmonary complications. However, it is unclear whether cerebral ischemia and reperfusion (I/R) injury induces mucus hypersecretion, and the potential role of inflammation remains unknown. In the present study, the reversible middle cerebral artery occlusion model was applied in rats to induce cerebral I/R injury. The rats were grouped according to the duration of reperfusion (6, 12, 24, 48 and 72h). Neurological dysfunction was evaluated by Longa scoring and lung dry‑to‑wet weight (dw/ww) ratios were determined to reflect the degree of mucus secretion. Inflammatory factor interleukin‑13 (IL‑13) and tumor necrosis factor‑α (TNF‑α) levels in serum and bronchoalveolar lavage fluid (BALF) were determined by enzyme‑linked immunosorbent assay. Pulmonary levels of mucin 5AC (MUC5AC) and key molecules involved in nuclear factor‑κB (NF‑κB) signaling were determined by western blotting and immunohistochemistry. Rats with cerebral I/R had impaired neurological function, which was associated with the length of reperfusion time. In addition, the dw/ww lung ratio decreased and the pulmonary expression of MUC5AC increased with the increase in severity of neurological dysfunction, indicating that cerebral I/R may induce mucus hypersecretion in a reperfusion time‑dependent manner. IL‑13 and TNF‑α levels in serum and BALF, as well as the nuclear translocation of NF‑κB p65 in pulmonary tissues, significantly increased following cerebral I/R, which suggests that the activation of IL‑13 and NF‑κB inflammatory pathways may be involved. The present study concluded that cerebral I/R injury may induce airway mucus hypersecretion by activating IL‑13 and NF‑κB inflammatory pathways.