Objective To explore mechanism of lung injury of rats induced by inhalation of white smoke from burning smoke pot.
Methods Forty-eight Sprague Dawley rats were divided into control group (
n=12) and injury group (
n=36) according to the random number table. Rats in injury group were placed in smoke-induced injury experimental equipment fulled with white smoke from burning smoke pot for 5 minutes to make lung injury, and rats in control group were placed in smoke-induced injury experimental equipment fulled with air for 5 minutes to make sham injury. Six rats in injury group at post injury hour (PIH) 6, 24, and 72 and six rats in control group at PIH 72 were collected to observe pathological changes of lung tissue and pathological score of rats in the two groups by hematoxylin-eosin staining, to detect expression of nuclear factor-κB (NF-κB) p65 mRNA in lung tissue of rats by reverse transcriptional polymerase chain reaction, and to detect content of tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β), and IL-6 in lung tissue of rats by enzyme-linked immunosorbent assay. Data were processed with one-way analysis of variance and
t test.
Results At PIH 72, lung tissue structure of rats in control group was clear and complete, with no inflammatory cell infiltration. At PIH 6, there was edema, hemorrhage, and inflammatory cell infiltration in lung tissue of rats in injury group. At PIH 24, edema, hemorrhage, and inflammatory cell infiltration in lung tissue of rats in injury group aggravated. At PIH 72, area of edema in lung tissue of rats in injury group was enlarged, with obvious hemorrhage and inflammatory cell infiltration. At PIH 6, 24, and 72, pathological score of lung tissue of rats in injury group was (3.43±0.86), (5.39±0.93), and (9.99±0.84) points, respectively, obviously higher than that of rats in control group at PIH 72 [(2.11±0.20) points,
t=3.659, 8.450, 22.355,
P<0.05]. As time post injury prolonged, pathological scores of lung tissue of rats in injury group were significantly increased (
F=121.244,
P<0.01). At PIH 6, 24, and 72, expression of NF-κB p65 mRNA in lung tissue of rats in injury group was 15.5±4.3, 25.9±1.8, 30.9±3.5 respectively, significantly higher than that of rats in control group at PIH 72 (7.8±0.8,
t=4.315, 20.445, 14.408,
P<0.01). As time post injury prolonged, expression of NF-κB p65 mRNA in lung tissue of rats in injury group gradually increased (
F=32.691,
P<0.01). At PIH 6, 24, and 72, content of TNF-α, IL-1β, and IL-6 in lung tissue of rats in injury group was significantly higher than that of rats in control group at PIH 72, respectively (
t=7.650, 8.968, 6.827, 6.726, 8.978, 3.460, 5.420, 13.289, 16.438,
P<0.01). At PIH 24, content of TNF-α and IL-1β in lung tissue of rats in injury group was higher than that of rats in the same group at PIH 6 and 72, respectively (
t=3.409, -2.549, 4.047, -4.100,
P<0.05). At PIH 24 and 72, content of IL-6 in lung tissue of rats in injury group was respectively higher than that of rats in the same group at PIH 6 (
t=8.273, 9.711,
P<0.05).
Conclusions After inhaling white smoke from burning smoke pot, rats are inflicted with lung injury by increasing expression of NF-κB p65 mRNA and content of TNF-α, IL-1β, and IL-6, and induce pathological changes of edema, hemorrhage, and inflammatory cell infiltration of lung tissue.
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