目的 探讨柴油废气颗粒的吸入对哮喘大鼠速发相反应的影响.方法 选择Wistar雄性大鼠60只,随机分为6组,每组各10只.A组用生理盐水攻击,B组用卵清蛋白攻击,C、D、E、F组用卵清蛋白攻击以后继续吸入柴油废气颗粒(DEP)各1周、2周、3周和4周.所有抗原攻击结束1周以后,除A组用生理盐水激发30 min以外其他组均用卵清蛋白激发30 min,之后测定并比较气道阻力,观察支气管肺泡灌洗液中炎症细胞的变化和肺组织病理学的改变,肺组织中自细胞介素5和γ干扰素的浓度,血清IgE变化等.结果 (1)A、B、C、D、E、F组在卵清蛋白激发后30 min时的气道阻力[cm H2O/(ml·s)]分别为(3.56±0.21)、(7.06±0.63)、(6.46±0.38)、(7.47±0.33)、(8.87±0.61)、(11.00±0.69).A组未发生气道高反应,B、C、D、E、F组的气道阻力均高于A组,E、F组高于B组,差异均有统计学意义.而各组在各时间点内的气道阻力比较同样有统计学意义(F=160.646,148.901,162.204,156.186,P均<0.01).DEP吸入的时间和气道阻力之间呈正相关(r=0.948,P<0.01).(2)血清IgE浓度在B、C、D、E、F组之间差异无统计学意义(P>0.05),但均高于A组(F=2.639,P<0.01).(3)支气管肺泡灌洗液中的炎症细胞有中性粒细胞、嗜酸性粒细胞和淋巴细胞等,以前者为主.中性粒细胞百分比(%)依次为(4.3±2.0)、(9.7±5.2)、(10.3±5.6)、(13.0±5.2)、(42.6±18.3)、(55.3±6.9),E、F组高于A组和B组,组间差异有统计学意义(F=114.226,P<0.01).(4)肺组织病理切片中可以看到A组上皮细胞完整,气道周围未见炎症细胞的浸润,以纤毛柱状上皮细胞为主,仅有少量的杯状细胞,基底膜未见纤维化.随着DEP吸入,逐渐出现上皮细胞的坏死、中断、脱落,杯状细胞增生,气道周围的炎症细胞浸润等改变.(5)肺组织中自细胞介素浓度(pg/mg)在B组(12.8±2.8)和C组(17.1±5.2)、E组(18.6±4.2)间差异有统计学意义(F=4.236,P<0.01),各组大鼠肺组织中γ干扰素的浓度之间比较差异无统计学意义(F=1.185,P>0.05).结论 DEP的吸入加重了哮喘大鼠的速发相反应.
目的 探討柴油廢氣顆粒的吸入對哮喘大鼠速髮相反應的影響.方法 選擇Wistar雄性大鼠60隻,隨機分為6組,每組各10隻.A組用生理鹽水攻擊,B組用卵清蛋白攻擊,C、D、E、F組用卵清蛋白攻擊以後繼續吸入柴油廢氣顆粒(DEP)各1週、2週、3週和4週.所有抗原攻擊結束1週以後,除A組用生理鹽水激髮30 min以外其他組均用卵清蛋白激髮30 min,之後測定併比較氣道阻力,觀察支氣管肺泡灌洗液中炎癥細胞的變化和肺組織病理學的改變,肺組織中自細胞介素5和γ榦擾素的濃度,血清IgE變化等.結果 (1)A、B、C、D、E、F組在卵清蛋白激髮後30 min時的氣道阻力[cm H2O/(ml·s)]分彆為(3.56±0.21)、(7.06±0.63)、(6.46±0.38)、(7.47±0.33)、(8.87±0.61)、(11.00±0.69).A組未髮生氣道高反應,B、C、D、E、F組的氣道阻力均高于A組,E、F組高于B組,差異均有統計學意義.而各組在各時間點內的氣道阻力比較同樣有統計學意義(F=160.646,148.901,162.204,156.186,P均<0.01).DEP吸入的時間和氣道阻力之間呈正相關(r=0.948,P<0.01).(2)血清IgE濃度在B、C、D、E、F組之間差異無統計學意義(P>0.05),但均高于A組(F=2.639,P<0.01).(3)支氣管肺泡灌洗液中的炎癥細胞有中性粒細胞、嗜痠性粒細胞和淋巴細胞等,以前者為主.中性粒細胞百分比(%)依次為(4.3±2.0)、(9.7±5.2)、(10.3±5.6)、(13.0±5.2)、(42.6±18.3)、(55.3±6.9),E、F組高于A組和B組,組間差異有統計學意義(F=114.226,P<0.01).(4)肺組織病理切片中可以看到A組上皮細胞完整,氣道週圍未見炎癥細胞的浸潤,以纖毛柱狀上皮細胞為主,僅有少量的杯狀細胞,基底膜未見纖維化.隨著DEP吸入,逐漸齣現上皮細胞的壞死、中斷、脫落,杯狀細胞增生,氣道週圍的炎癥細胞浸潤等改變.(5)肺組織中自細胞介素濃度(pg/mg)在B組(12.8±2.8)和C組(17.1±5.2)、E組(18.6±4.2)間差異有統計學意義(F=4.236,P<0.01),各組大鼠肺組織中γ榦擾素的濃度之間比較差異無統計學意義(F=1.185,P>0.05).結論 DEP的吸入加重瞭哮喘大鼠的速髮相反應.
목적 탐토시유폐기과립적흡입대효천대서속발상반응적영향.방법 선택Wistar웅성대서60지,수궤분위6조,매조각10지.A조용생리염수공격,B조용란청단백공격,C、D、E、F조용란청단백공격이후계속흡입시유폐기과립(DEP)각1주、2주、3주화4주.소유항원공격결속1주이후,제A조용생리염수격발30 min이외기타조균용란청단백격발30 min,지후측정병비교기도조력,관찰지기관폐포관세액중염증세포적변화화폐조직병이학적개변,폐조직중자세포개소5화γ간우소적농도,혈청IgE변화등.결과 (1)A、B、C、D、E、F조재란청단백격발후30 min시적기도조력[cm H2O/(ml·s)]분별위(3.56±0.21)、(7.06±0.63)、(6.46±0.38)、(7.47±0.33)、(8.87±0.61)、(11.00±0.69).A조미발생기도고반응,B、C、D、E、F조적기도조력균고우A조,E、F조고우B조,차이균유통계학의의.이각조재각시간점내적기도조력비교동양유통계학의의(F=160.646,148.901,162.204,156.186,P균<0.01).DEP흡입적시간화기도조력지간정정상관(r=0.948,P<0.01).(2)혈청IgE농도재B、C、D、E、F조지간차이무통계학의의(P>0.05),단균고우A조(F=2.639,P<0.01).(3)지기관폐포관세액중적염증세포유중성립세포、기산성립세포화림파세포등,이전자위주.중성립세포백분비(%)의차위(4.3±2.0)、(9.7±5.2)、(10.3±5.6)、(13.0±5.2)、(42.6±18.3)、(55.3±6.9),E、F조고우A조화B조,조간차이유통계학의의(F=114.226,P<0.01).(4)폐조직병리절편중가이간도A조상피세포완정,기도주위미견염증세포적침윤,이섬모주상상피세포위주,부유소량적배상세포,기저막미견섬유화.수착DEP흡입,축점출현상피세포적배사、중단、탈락,배상세포증생,기도주위적염증세포침윤등개변.(5)폐조직중자세포개소농도(pg/mg)재B조(12.8±2.8)화C조(17.1±5.2)、E조(18.6±4.2)간차이유통계학의의(F=4.236,P<0.01),각조대서폐조직중γ간우소적농도지간비교차이무통계학의의(F=1.185,P>0.05).결론 DEP적흡입가중료효천대서적속발상반응.
Objective The role of air pollution on asthma can not be ignored, diesel exhaust particles (DEP) in the air is one of the most important pollutants. This study aimed to investigate the effect and mechanism of DEP inhaled on immediate reaction in the asthma rats. Method Sixty male Wistar rats of "Clean" grade, 6-7 week-old, with an average weight of (140±20) g were used in this study. The rats were randomly divided into 6 groups, 10 in each. Group A was treated with normal saline attack as a negative control, Group B with ovalbumin attack as a positive control. After ovalbumin attack, groups C, D, E, F continued to inhale DEP for 1 week, 2 weeks, 3 weeks and 4 weeks, respectively. The concentration of DEP was 200 μg/ml, the animals were subjected to inhalation of ultrasound nebulized DEP for 30 min per day. One week after all the attacks were concluded, Group A was stimulated with normal saline for 30 min, other groups were stimulated with ovalbumin. Then the airway resistance was determined with multi-channel signal acquisition and processing system and compared. The changes in neutrephils, eosinophils, and other inflammatory cells of BALF and the pathological changes in lung tissue, including epithelial cells loss, the inflammatory cells infiltration around the airway, basement membrane fibrosis, goblet cell hyperplasia etc. were observed. The concentration of IL-5 and γ-interferon in the lung tissues, and the changes of serum IgE etc. were determined. Result Airway resistance values of group A, B, C, D, E, F after ovalbumin excitation for 30 min were (3.56±0.21), (7.06±0.63), (6.46±0.38), (7.47±0.33), (8.87±Groups B, C, D, E, F had higher airway resistance than group A, group E and F had higher airway resistance than that of group B, the differences were statistically significant. And the airway resistance was different in each group among 0 min, 10 min, 20 min and 30 min (F=160. 646, 148. 901, 162.204, 156. 186, P<0.01 for both). The time of DEP inhalation and the airway resistance was positively correlated (r=0.948, P<0.01); IgE concentrations of the serum between groups B, C, D, E, F was not significantly different (P>0.05), but higher than that of group A (F=2.639, P<0.01). The infiltrated inflammatory cells included eesinophils and lymphocytes, etc. The percentages of neutrophil (%) were (4.3±2.0), (9.7±5.2), (10.3±5.6), (13.0±5.2), (42.6±18.3), (55.3±6.9). The groups E and F had higher percentage than Group A and Group B (F=114.226, P<0.01). The percentages of eosinophils (%) were 0, (11.9±3.8), (15.8±6.3), (13.0±4.9), (21.1±5.6), (27.1±4.8). The difference between Groups B, C, D, E, F and Group A was statistically significant. There was significant difference between groups C, D, E, F and group B (F=46.462, P<0.05); Lung tissue biopsy in group A showed that the epithelial cells were intact, no inflammatory cells infiltrations were found around the airways, instead, mainly ciliated columnar epithelial cells and only a small number of goblet cells were seen without basement membrane fibrosis. With the inhalation of DEP, the epithelial cells showed gradual necrosis, disruption and loss, goblet cells showed hyperplasia, and infiltrations with inflammatory cells were seen around the airway. In the lung tissue, concentrations of IL-5 in group B,C, and E were (12.8±2.8), (17.1±5.2), (18.6±4.2) pg/mg, the difference between groups C, E and group B was statistically significant (F=4.236, P<0.01), the difference in γ-interferon concentration among all groups was not statistically significance (F=1.185, P>0.05). Conclusion DEP inhalation increased the airway responsiveness of asthma rats in immediate reaction, promoted the lung epithelial cell loss, inflammatory cell infiltration, basement membrane fibrosis and goblet cell hyperplasia.
