Abstract:Objective: To investigate the expression of Toll-like receptor 2 (TLR2) in the serum of patients with obstructive sleep apnea syndrome (OSAS) and its effect on lung injury. Methods: Enzyme-linked immunosorbent assay (ELISA) was used to detect the expression level of TLR2 in the patients’serum. Wistar rats were divided into Control group, chronic intermittent hypoxia group (CIH group) and TLR2 antagonist T2.5 group (T2.5 group), the hypoxic chamber was used to establish the CIH model and it was identified. The animal lung function analysis system was used to measure the lung function indexes changes of each group of rats[inspiratory capacity (IC), volume after forced exhalation in 0.3 s (FEV0.3), breath volume per minute (MV) and peak expiratory flow (PEF) ]. HE staining was used to detect the pathological changes of lung tissue in each group of rats; qRT-PCR and Western blot were used to detect the expression level of TLR2 in the lung tissue of each group of rats; ELISA was used to detect the expression changes of superoxidedismutase (SOD) activity, malondialdehyde (MDA), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in the lung tissue of each group and ELISA was used to de tect changes in the expression of TLR2, TNF-α and IL-6 in serum of rats in each group. Results: With the aggravation of OSAS, the TLR2 content in the serum of OSAS patients increased (P<0.05). The physiological characteristics of the model rats were close to the pathophysiological characteristics of OSAHS, so the CIH rat model was successfully established. Compared with CIH group (IC: 4.71±0.28, FEV0.3:4.48±0.31, MV:156.78±6.11, PEF:20.89±1.37), T2.5 increased the IC (6.01±0.32), FEV0.3 (5.51±0.38), MV (187.56±5.53) and PEF (29.75±1.43) of rats (all P<0.05); T2.5 inhibited lung tissue damage in rats, neutrophil infiltration was less, and capillaries only expanded slightly; the expression level of TLR2 protein in lung tissue of T2.5 group was down-regulated (P<0.05), the SOD activity increased (P<0.05), the MDA content decreased (P<0.05), and the TNF-α and IL-6 levels decreased (all P<0.05) in the lung tissue; the serum levels of TLR2, TNF-α and IL-6 in the T2.5 group decreased (all P<0.05). Conclusion: OSAS can cause lung damage, oxidative stress and inflammatory response, while TLR2 antagonists can improve lung function in rats and reduce the expression of oxidative stress and inflammatory factors.
