Nicotine plays a protective role in rats with induced viral pneumonia with polyinosinic-polycytidylic acid through α7nAChR

Pre-administration of nicotine improved Poly (I:C)-induced pneumonia by activating the cholinergic anti-inflammatory pathway.

Twenty-four healthy adult male Sprague-Dawley (SD) rats (200-250 g) were randomly divided into normal saline control group (NS group); Poly (I:C) group; nicotine group (NIC group); and α7 nicotinic acetylcholine receptor (α7nAChR) antagonist group (α-BGT group) (n = 6 each). Rats in the Poly (I: C), NIC, and α-BGT groups were administered 1.5 mg/mL 100 μL Poly (I:C) intranasally to establish pneumonia model. In α-BGT group, 1 μg/kg α-bungarotoxin (α-BGT) was intraperitoneally injected 45 min before intranasal Poly (I:C), and 400 μg/kg nicotine was intraperitoneally injected 15 min after α-BGT injection. The NIC group received an equal volume of NS in place of α-BGT while the other treatments were same. The Poly (I:C) group received equal volume of NS in place of nicotine while the other treatments were same as in NIC group. In the NS group, only NS was administered at all three time points. PaCO2, PaO2, and PaO2/FiO2 levels were determined 24 h after administration of Poly (I:C). After euthanization, rat lung tissues were extracted for pathological examination, and wet weight/dry weight (W/D ratio) was determined. Expression of tumor necrosis factor-α (TNF-α), interleukin (IL)-6, IL-1β, and interferon (IFN)-γ in lung tissue was determined by ELISA. q-PCR was used to detect nuclear factor kappa-B P65 (NF-κBP65).

To study the effect of nicotine in rat model of pneumonia induced by polyinosinic-polycytidylic acid [Poly (I:C)] and explore the underlying mechanism.

Compared with NS group, Poly (I:C) and α-BGT groups showed significantly increased W/D ratio, PaCO2, TNF-α, IL-6, IL-1β, and IFN-γ content, NF-κB P65 expression, and reduced PaO2 and PaO2/FiO2 (p < 0.05), along with obvious signs of pathological injury. Nicotine pre-treatment reduced W/D ratio, PaCO2, proinflammatory cytokines, NF-κBP65 expression, and increased PaO2 and PaO2/FiO2 levels. The above effects were negated in α-BGT group.