Mechanism of lung injury of rats induced by inhalation of white smoke from burning smoke pot
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摘要: 目的 探讨吸入发烟罐燃烧产生的白烟致大鼠肺损伤的机制。 方法 将48只SD大鼠按照随机数字表法分为对照组12只和致伤组36只。致伤组大鼠置于充满发烟罐燃烧产生的白烟的烟雾致伤实验设备中5 min,造成肺损伤。对照组大鼠置于充满空气的烟雾致伤实验设备中5 min致假伤。分别于伤后6、24、72 h取6只致伤组大鼠,于伤后72 h取6只对照组大鼠,苏木素-伊红染色观察大鼠肺组织病理变化并进行病理学评分,反转录PCR检测大鼠肺组织中核因子κB p65 mRNA表达,酶联免疫吸附法检测大鼠肺组织中TNF-α、IL-1β、IL-6含量。对数据行单因素方差分析、
t 检验。 结果 对照组大鼠伤后72 h肺组织结构清晰完整,无炎性细胞浸润。致伤组大鼠伤后6 h肺组织出现水肿、出血和炎性细胞浸润,伤后24 h肺组织水肿、出血、炎性细胞浸润加剧,伤后72 h肺组织水肿范围增大,炎性细胞浸润和出血依然明显。伤后6、24、72 h,致伤组大鼠肺组织病理学评分分别为(3.43±0.86)、(5.39±0.93)、(9.99±0.84)分,明显高于对照组伤后72 h的(2.11±0.20)分,t =3.659、8.450、22.355,P <0.05。随着致伤时间延长,致伤组大鼠肺组织病理学评分明显升高(F =121.244,P <0.01)。伤后6、24、72 h,致伤组大鼠肺组织核因子κB p65 mRNA的表达量分别为15.5±4.3、25.9±1.8、30.9±3.5,明显高于对照组伤后72 h的7.8±0.8(t =4.315、20.445、14.408,P <0.01)。随着致伤时间的延长,致伤组大鼠肺组织核因子κB p65 mRNA的表达量逐渐增加(F =32.691,P <0.01)。伤后6、24、72 h,致伤组大鼠肺组织TNF-α、IL-1β和IL-6含量明显高于对照组伤后72 h(t =7.650、8.968、6.827、6.726、8.978、3.460、5.420、13.289、16.438,P <0.01)。伤后24 h,致伤组大鼠肺组织TNF-α、IL-1β含量明显高于组内伤后6、72 h(t =3.409、-2.549、4.047、-4.100,P <0.05);伤后24、72 h,致伤组大鼠肺组织IL-6含量明显高于组内伤后6 h(t =8.273、9.711,P <0.05)。 结论 大鼠吸入发烟罐燃烧产生的白烟后,可能通过促进肺组织中核因子κB p65 mRNA的表达,提高TNF-α、IL-1β和IL-6的含量,导致肺损伤,并引起肺组织水肿、出血、炎性细胞浸润等病理变化。Abstract: 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 andt 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.-
Key words:
- Burns, inhalation /
- Lung injury /
- Inflammation /
- NF-kappa B /
- White smoke /
- Smoke pot
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