To evaluate the activation effect of α7 nicotinic acetylcholine receptor (α7-nAChR) on ventilator-induced lung injury in rats.

Thirty-two male Sprague Dawley rats were randomly divided into four groups: the control group (C group), mechanical ventilation group (V group), nicotine pretreatment and mechanical ventilation group (N group), and methylbovine (MLA), nicotine and ventilation group (MLA group), with 8 rats in each group. Rats in the C group did not undergo mechanical ventilation after tracheal intubation, while the rest were mechanically ventilated for 2 hours. Rats in the N group were intraperitoneally injected with 1 mg/kg nicotine 30 min before mechanical ventilation, rats in MLA group were injected with 1 mg/kg MLA 30 min before intraperitoneal injection of niacin, and rats in other groups were intraperitoneally injected with isotonic sodium chlorrde solution. Rats were sacrificed immediately after mechanical ventilation. The wet/dry weight of lung tissue, hematoxylin eosin (HE) staining and pathological score of lung injury were calculated. The expression levels of interleukin-1beta (IL-1β), IL-6, and tumor necrosis factor-alpha (TNF-α) protein were detected by Western-blotting.

The alveolar morphology of rats was normal in the C group; alveolar morphology was destroyed, and a large number of inflammatory cells infiltrated in V group. The alveolar morphology was slightly destroyed, and a small number of inflammatory cells infiltrated in N group. The alveolar structure was destroyed, alveolus collapsed, and more inflammatory cells infiltrated in MLA group. There were significant differences in the wet/dry weight, injury score, and expressions of IL-1β, IL-6 and TNF-α protein of lung tissue among these four groups (F = 168.009, 647.579, 138.005, 192.706, 178.094; all P < 0.05). Further comparison showed that the wet/dry weight, injury score, and expressions of IL-1β, IL-6 and TNF-α protein of lung tissue were significantly higher in the V group than in C group (all P < 0.05), significantly lower in N group than in V group (all P < 0.05), and significantly higher in MLA group than in N group (all P < 0.05).

Nicotine has a protective effect on ventilator-induced lung injury in rats, and its mechanism is related to the activation of α7-nAChR.