CAJ | 학술논문

目的探讨甲醛预暴露与微生物气溶胶吸入对大鼠呼吸系统的协同损伤效应.方法 6周龄雄性Wistar大鼠25只(购自中国科学院实验动物中心),体质量(160±10)g,按数字表法随机分为正常对照组(6只)、甲醛吸入组(6只)、微生物气溶胶吸入组(6只)、甲醛与微生物气溶胶联合吸入组(7只).正常对照组:普通室内环境中饲养生长28 d.甲醛吸入组:以舱内(3.1 ±0.2) mg/m3为稳定暴露浓度,每天吸入2h,连续吸入28 d.微生物气溶胶吸入组:吸入舱内微生物气溶胶浓度稳定在(0.5～1.0)×107 cfu/m3,每天吸入2h,连续吸入暴露28 d.甲醛与微生物气溶胶联合吸入组:每天甲醛暴露2h后,暴露舱通新鲜空气45 min,再行微生物暴露2h,连续暴露28 d.采用动态气溶胶染毒暴露系统建立大鼠染毒暴露模型,用ELISA方法测血清免疫球蛋白M,发光比色法检测血清超氧化物歧化酶活性,HE染色法检测肺组织结构损伤,TUNNEL原位显色法检测肺组织细胞凋亡情况,Gram染色检测大鼠各级支气管及肺泡腔细菌残留情况.结果与对照组相比,微生物气溶胶吸入组,大鼠血清IgM水平升高明显,甲醛和微生物联合吸入组升高更显著[(0.35 ±0.09) g/L];3个实验组大鼠血清SOD活性增加,其中甲醛和微生物联合吸入组SOD活性[(2.22 ±0.25)×106 U/L]明显高于其他两单因素暴露组[(1.50±0.37) ×106 U/L与(1.58 ±0.34)×106 U/L].形态学观察结果显示,3个实验组大鼠肺泡间隔增宽、肺间质水肿、肺组织内炎性细胞侵润,以甲醛和微生物联合吸入组病理学改变最明显.TUNNEL检测结果表明,甲醛和微生物联合吸入组大鼠肺组织内凋亡细胞数明显增加.Gram染色结果显示,甲醛和微生物联合暴露后经2h正常通气停留,大鼠细支气管及肺泡腔内残留细菌数较微生物单因素暴露组明显增多.结论甲醛预暴露明显促进微生物气溶胶吸入暴露后对大鼠肺组织的损伤效应,并降低肺组织对异源性污染物的清除能力. 目的探討甲醛預暴露與微生物氣溶膠吸入對大鼠呼吸繫統的協同損傷效應.方法 6週齡雄性Wistar大鼠25隻(購自中國科學院實驗動物中心),體質量(160±10)g,按數字錶法隨機分為正常對照組(6隻)、甲醛吸入組(6隻)、微生物氣溶膠吸入組(6隻)、甲醛與微生物氣溶膠聯閤吸入組(7隻).正常對照組:普通室內環境中飼養生長28 d.甲醛吸入組:以艙內(3.1 ±0.2) mg/m3為穩定暴露濃度,每天吸入2h,連續吸入28 d.微生物氣溶膠吸入組:吸入艙內微生物氣溶膠濃度穩定在(0.5～1.0)×107 cfu/m3,每天吸入2h,連續吸入暴露28 d.甲醛與微生物氣溶膠聯閤吸入組:每天甲醛暴露2h後,暴露艙通新鮮空氣45 min,再行微生物暴露2h,連續暴露28 d.採用動態氣溶膠染毒暴露繫統建立大鼠染毒暴露模型,用ELISA方法測血清免疫毬蛋白M,髮光比色法檢測血清超氧化物歧化酶活性,HE染色法檢測肺組織結構損傷,TUNNEL原位顯色法檢測肺組織細胞凋亡情況,Gram染色檢測大鼠各級支氣管及肺泡腔細菌殘留情況.結果與對照組相比,微生物氣溶膠吸入組,大鼠血清IgM水平升高明顯,甲醛和微生物聯閤吸入組升高更顯著[(0.35 ±0.09) g/L];3箇實驗組大鼠血清SOD活性增加,其中甲醛和微生物聯閤吸入組SOD活性[(2.22 ±0.25)×106 U/L]明顯高于其他兩單因素暴露組[(1.50±0.37) ×106 U/L與(1.58 ±0.34)×106 U/L].形態學觀察結果顯示,3箇實驗組大鼠肺泡間隔增寬、肺間質水腫、肺組織內炎性細胞侵潤,以甲醛和微生物聯閤吸入組病理學改變最明顯.TUNNEL檢測結果錶明,甲醛和微生物聯閤吸入組大鼠肺組織內凋亡細胞數明顯增加.Gram染色結果顯示,甲醛和微生物聯閤暴露後經2h正常通氣停留,大鼠細支氣管及肺泡腔內殘留細菌數較微生物單因素暴露組明顯增多.結論甲醛預暴露明顯促進微生物氣溶膠吸入暴露後對大鼠肺組織的損傷效應,併降低肺組織對異源性汙染物的清除能力.
목적 탐토갑철예폭로여미생물기용효흡입대대서호흡계통적협동손상효응.방법 6주령웅성Wistar대서25지(구자중국과학원실험동물중심),체질량(160±10)g,안수자표법수궤분위정상대조조(6지)、갑철흡입조(6지)、미생물기용효흡입조(6지)、갑철여미생물기용효연합흡입조(7지).정상대조조:보통실내배경중사양생장28 d.갑철흡입조:이창내(3.1 ±0.2) mg/m3위은정폭로농도,매천흡입2h,련속흡입28 d.미생물기용효흡입조:흡입창내미생물기용효농도은정재(0.5～1.0)×107 cfu/m3,매천흡입2h,련속흡입폭로28 d.갑철여미생물기용효연합흡입조:매천갑철폭로2h후,폭로창통신선공기45 min,재행미생물폭로2h,련속폭로28 d.채용동태기용효염독폭로계통건립대서염독폭로모형,용ELISA방법측혈청면역구단백M,발광비색법검측혈청초양화물기화매활성,HE염색법검측폐조직결구손상,TUNNEL원위현색법검측폐조직세포조망정황,Gram염색검측대서각급지기관급폐포강세균잔류정황.결과 여대조조상비,미생물기용효흡입조,대서혈청IgM수평승고명현,갑철화미생물연합흡입조승고경현저[(0.35 ±0.09) g/L];3개실험조대서혈청SOD활성증가,기중갑철화미생물연합흡입조SOD활성[(2.22 ±0.25)×106 U/L]명현고우기타량단인소폭로조[(1.50±0.37) ×106 U/L여(1.58 ±0.34)×106 U/L].형태학관찰결과현시,3개실험조대서폐포간격증관、폐간질수종、폐조직내염성세포침윤,이갑철화미생물연합흡입조병이학개변최명현.TUNNEL검측결과표명,갑철화미생물연합흡입조대서폐조직내조망세포수명현증가.Gram염색결과현시,갑철화미생물연합폭로후경2h정상통기정류,대서세지기관급폐포강내잔류세균수교미생물단인소폭로조명현증다.결론 갑철예폭로명현촉진미생물기용효흡입폭로후대대서폐조직적손상효응,병강저폐조직대이원성오염물적청제능력.
Objective To investigate the synergistic effect of formaldehyde pre-exposure on the damage to the respiratory system in rats after microbial aerosol inhalation.Methods The intoxication model was established in rats by the dynamic aerosol exposure system.Serum IgM concentration and SOD activity were measured by ELISA and luminescence assay respectively.Morphologic injury of the lung tissue was detected by HE staining.Tunnel chromogenic in-situ detection was used to detect the apoptosis of lung epithelial cells and Gram staining was performed to detect the capacity of lung epithelial cells in bacterial clearance.Results Serum IgM levels in rats increased significantly,after microbial aerosol inhalation,when compared with that of the control group,with the serum IgM levels of the formaldehyde combined with microbial aerosol inhalation group increased more significantly [(0.35 ±0.09) g/L].The serum SOD activity of the experimental groups all increased,with the level of the formaldehyde combined with microbial aerosol inhalation group [(2.22 ± 0.25) × 106 U/L] being significantly higher than that of the 2 other groups [(1.50 ±0.37) × 106 U/L] and [(1.58 ± 0.34) × 106 U/L].Morphological observation showed that widened alveolar septum,interstitial edema and inflammatory cell infiltration could be clearly noted in the lung tissue of the 3 experimental groups,with the pathological changes in the formaldehyde combined with microbial aerosol inhalation group being most significant.Tunnel detection also indicated that the nnmber of apoptotic cells in the lung tissue for the formaldehyde combined with microbial aerosol inhalation group increased significantly.Gram staining showed that the number of residue bacteria in the rat bronchiole for the rats of the formaldehyde combined with microbial aerosol inhalation group after 2-hour air intervention was significantly more than that of the simple bacteria exposure group.Conclusions Formaldehyde pre-exposure combined with microbial aerosol inhalation could induce synergistic damage to the rat lung tissue and decrease the capacity of the lung tissue to clear out heterogeneous pollutants.