中华围产医学杂志
中華圍產醫學雜誌
중화위산의학잡지
CHINESE JOURNAL OF PERINATAL MEDICINE
2014年
2期
104-108
,共5页
硫化氢%高氧症%肺疾病%动物,新生
硫化氫%高氧癥%肺疾病%動物,新生
류화경%고양증%폐질병%동물,신생
Hydrogen sulfide%Hyperoxia%Lung diseasea%Animals,newborn
目的 探讨硫化氢(hydrogen sulfide,H2S)在新生大鼠高氧肺损伤中的作用.方法 80只足月自然分娩娩出12h内的Sprague-Dawley大鼠随机分为对照组、高氧组、硫氢化钠(sodium hydrosulfide,NaHS)+高氧组以及胱硫脒-γ-裂解酶(cystathionine-γ lyase,CSE)抑制剂——炔丙基甘氨酸(propargylglycine,PPG)+高氧组.NaHS+高氧组大鼠腹腔注射1次NaHS(90μmol/kg),PPG+高氧组注射PPG(50 mg/kg).对照组在空气中饲养,其余各组均置于持续高浓度氧(95％O2)环境中饲养.7d后,HE染色观察肺组织形态学改变,光镜下计数支气管肺泡灌洗液中白细胞计数及分类计数,采用Lowry法测定其中的蛋白含量;采用去蛋白法测定血浆中H2S含量,分光光度计检测肺组织CSE活性及丙二醛(malondialdehyde,MDA)含量.多组间比较采用方差分析,两两比较采用LSD-t检验. 结果 (1)高氧组光镜下可见肺泡内出血、炎症细胞浸润;肺泡灌洗液中白细胞总数[(130.2±15.3)×107/L]、中性粒细胞数[(64.6±12.4)×107/L]及蛋白含量[(934.6±106.4) mg/L]较对照组[分别为(15.1±2.5)×107/L、(2.1±0.5)×107/L和(254.3±50.7) mg/L]升高(LSD f值分别为14.65、5.78和2.97,P值均＜0.01);血浆中H2S含量[(112.6±20.4)μmol/L]和肺组织CSE活性[(3.4±0.4) μmol/ (min·g)]较对照组[分别为(182.3±15.7)μmol/L和(6.8±1.4) μmol/ (min·g)]降低(LSD-t值分别为-9.90和-4.59,P值均＜0.01),肺组织MDA含量较对照组升高[(1.7±0.3)nmol/ml与(0.9±0.1)nmol/ml,LSD t=3.03,P＜0.01].(2)与高氧组比较,NaHS+高氧组肺组织炎性渗出及结构紊乱减轻;肺泡灌洗液中白细胞总数[(56.3±11.6)×107/L]、中性粒细胞数[(34.8±7.8)×107/L]及蛋白含量[(753.8±89.6) mg/L]均下降(LSD-t值分别为-9.66、-11.81和-5.78,P值均＜0.01);血浆中H2S含量[(235.7±32.7)μmol/L]和肺组织CSE活性[(5.8±1.1)μmol/(min·g)]均升高(LSD t值分别为11.34和5.98,P值均＜0.01).(3)与高氧组比较,PPG+高氧组光镜下肺泡炎性渗出及结构紊乱加重,肺泡灌洗液中白细胞总数、中性粒细胞数及蛋白含量升高(LSD-t值分别为5.52、6.37和8.23,P值均＜0.01);血浆中H2S含量和肺组织CSE活性降低(LSD-t值分别为-4.29和-3.97,P值均＜0.01),肺组织MDA含量升高(LSD-t=3.02,P＜0.01). 结论 H2S参与了新生大鼠高氧肺损伤的病理生理过程.外源性补充H2S可通过抑制炎症和氧化应激反应从而减轻高氧肺损伤.
目的 探討硫化氫(hydrogen sulfide,H2S)在新生大鼠高氧肺損傷中的作用.方法 80隻足月自然分娩娩齣12h內的Sprague-Dawley大鼠隨機分為對照組、高氧組、硫氫化鈉(sodium hydrosulfide,NaHS)+高氧組以及胱硫脒-γ-裂解酶(cystathionine-γ lyase,CSE)抑製劑——炔丙基甘氨痠(propargylglycine,PPG)+高氧組.NaHS+高氧組大鼠腹腔註射1次NaHS(90μmol/kg),PPG+高氧組註射PPG(50 mg/kg).對照組在空氣中飼養,其餘各組均置于持續高濃度氧(95％O2)環境中飼養.7d後,HE染色觀察肺組織形態學改變,光鏡下計數支氣管肺泡灌洗液中白細胞計數及分類計數,採用Lowry法測定其中的蛋白含量;採用去蛋白法測定血漿中H2S含量,分光光度計檢測肺組織CSE活性及丙二醛(malondialdehyde,MDA)含量.多組間比較採用方差分析,兩兩比較採用LSD-t檢驗. 結果 (1)高氧組光鏡下可見肺泡內齣血、炎癥細胞浸潤;肺泡灌洗液中白細胞總數[(130.2±15.3)×107/L]、中性粒細胞數[(64.6±12.4)×107/L]及蛋白含量[(934.6±106.4) mg/L]較對照組[分彆為(15.1±2.5)×107/L、(2.1±0.5)×107/L和(254.3±50.7) mg/L]升高(LSD f值分彆為14.65、5.78和2.97,P值均＜0.01);血漿中H2S含量[(112.6±20.4)μmol/L]和肺組織CSE活性[(3.4±0.4) μmol/ (min·g)]較對照組[分彆為(182.3±15.7)μmol/L和(6.8±1.4) μmol/ (min·g)]降低(LSD-t值分彆為-9.90和-4.59,P值均＜0.01),肺組織MDA含量較對照組升高[(1.7±0.3)nmol/ml與(0.9±0.1)nmol/ml,LSD t=3.03,P＜0.01].(2)與高氧組比較,NaHS+高氧組肺組織炎性滲齣及結構紊亂減輕;肺泡灌洗液中白細胞總數[(56.3±11.6)×107/L]、中性粒細胞數[(34.8±7.8)×107/L]及蛋白含量[(753.8±89.6) mg/L]均下降(LSD-t值分彆為-9.66、-11.81和-5.78,P值均＜0.01);血漿中H2S含量[(235.7±32.7)μmol/L]和肺組織CSE活性[(5.8±1.1)μmol/(min·g)]均升高(LSD t值分彆為11.34和5.98,P值均＜0.01).(3)與高氧組比較,PPG+高氧組光鏡下肺泡炎性滲齣及結構紊亂加重,肺泡灌洗液中白細胞總數、中性粒細胞數及蛋白含量升高(LSD-t值分彆為5.52、6.37和8.23,P值均＜0.01);血漿中H2S含量和肺組織CSE活性降低(LSD-t值分彆為-4.29和-3.97,P值均＜0.01),肺組織MDA含量升高(LSD-t=3.02,P＜0.01). 結論 H2S參與瞭新生大鼠高氧肺損傷的病理生理過程.外源性補充H2S可通過抑製炎癥和氧化應激反應從而減輕高氧肺損傷.
목적 탐토류화경(hydrogen sulfide,H2S)재신생대서고양폐손상중적작용.방법 80지족월자연분면면출12h내적Sprague-Dawley대서수궤분위대조조、고양조、류경화납(sodium hydrosulfide,NaHS)+고양조이급광류미-γ-렬해매(cystathionine-γ lyase,CSE)억제제——결병기감안산(propargylglycine,PPG)+고양조.NaHS+고양조대서복강주사1차NaHS(90μmol/kg),PPG+고양조주사PPG(50 mg/kg).대조조재공기중사양,기여각조균치우지속고농도양(95％O2)배경중사양.7d후,HE염색관찰폐조직형태학개변,광경하계수지기관폐포관세액중백세포계수급분류계수,채용Lowry법측정기중적단백함량;채용거단백법측정혈장중H2S함량,분광광도계검측폐조직CSE활성급병이철(malondialdehyde,MDA)함량.다조간비교채용방차분석,량량비교채용LSD-t검험. 결과 (1)고양조광경하가견폐포내출혈、염증세포침윤;폐포관세액중백세포총수[(130.2±15.3)×107/L]、중성립세포수[(64.6±12.4)×107/L]급단백함량[(934.6±106.4) mg/L]교대조조[분별위(15.1±2.5)×107/L、(2.1±0.5)×107/L화(254.3±50.7) mg/L]승고(LSD f치분별위14.65、5.78화2.97,P치균＜0.01);혈장중H2S함량[(112.6±20.4)μmol/L]화폐조직CSE활성[(3.4±0.4) μmol/ (min·g)]교대조조[분별위(182.3±15.7)μmol/L화(6.8±1.4) μmol/ (min·g)]강저(LSD-t치분별위-9.90화-4.59,P치균＜0.01),폐조직MDA함량교대조조승고[(1.7±0.3)nmol/ml여(0.9±0.1)nmol/ml,LSD t=3.03,P＜0.01].(2)여고양조비교,NaHS+고양조폐조직염성삼출급결구문란감경;폐포관세액중백세포총수[(56.3±11.6)×107/L]、중성립세포수[(34.8±7.8)×107/L]급단백함량[(753.8±89.6) mg/L]균하강(LSD-t치분별위-9.66、-11.81화-5.78,P치균＜0.01);혈장중H2S함량[(235.7±32.7)μmol/L]화폐조직CSE활성[(5.8±1.1)μmol/(min·g)]균승고(LSD t치분별위11.34화5.98,P치균＜0.01).(3)여고양조비교,PPG+고양조광경하폐포염성삼출급결구문란가중,폐포관세액중백세포총수、중성립세포수급단백함량승고(LSD-t치분별위5.52、6.37화8.23,P치균＜0.01);혈장중H2S함량화폐조직CSE활성강저(LSD-t치분별위-4.29화-3.97,P치균＜0.01),폐조직MDA함량승고(LSD-t=3.02,P＜0.01). 결론 H2S삼여료신생대서고양폐손상적병리생리과정.외원성보충H2S가통과억제염증화양화응격반응종이감경고양폐손상.
Objective To explore the effects of hydrogen sulfide (H2S) on hyperoxia-induced lung injury in neonatal rats.Methods Eighty full-term Sprague-Dawley rats within 12 hours after birth were randomly divided into control group,hyperoxia group,sodium hydrosulfide (NaHS) + hyperoxia group (NaHS 90 μmol/kg injected intraperitoneally) and propargylglycine (PPG) +hyperoxia group (PPG 50 mg/kg injected intraperitoneally).Except for the control group,the other three groups were exposed to 95％ O2 for seven days.Pulmonary histopathology was observed after HE staining,numeration of leukocyte and albumin in bronchoalveolar lavage fluid (BALF) were processed by optical microscope and Lowry methods.The plasma H2S concentration,activity of cystathionine-γ-lyase (CSE) and contents of malondialdehyde (MDA) in lung tissues were also detected.Analysis of variance and LSD-t test were used for statistics.Results (1) Compared with the control group,alveolar hemorrhage,interstitial edema,inflammatory cell infiltration were observed in the hyperoxia group.The number of white blood cells,neutrophils and albumin content in BALF increased in the hyperoxia group [(130.2± 15.3) × 107/L vs (15.1 ±2.5) × 107/L; (64.6± 12.4) × 107/L vs (2.1 ±0.5) × 107/L; (934.6± 106.4) mg/L vs (254.3±50.7) mg/L,respectively.LSD-t=-14.65,5.78 and 2.97,all P＜0.01],but the plasma H2S concentration and the activity of CSE in lung tissue decreased [(112.6± 20.4) μmol/Lvs (182.3±15.7) μ mol/L,LSD-t=-9.90; (3.4±0.4) μmol/ (min·g) vs (6.8± 1.4) μ mol/ (min · g),LSD-t=-4.59; both P＜0.01].However,the contents of MDA increased [(1.7± 0.3) nmol/ml vs (0.9±0.1) nmol/ml,LSD-t=3.03,P＜0.01].(2) Compared with the hyperoxia group,inflammatory exudation and structural disorder of lung tissue were alleviated in the NaHS+hyperoxia group.White blood cells [(56.3± 11.6) × 107/L],neutrophils [(34.8±7.8) × 107/L] and albumin content [(753.8± 89.6) mg/L] in BALF decreased significantly (LSD-t=-9.66,-11.81 and-5.78,P＜0.01).The plasma H2S concentration [(235.7±32.7) μ mol/L] and the activity ofCSE [(5.8± 1.1) μ mol/(min · g)] increased significantly (LSD-t=11.34 and 5.98,P＜0.01) in the NaHS+hyperoxia group.(3) Compared with the hyperoxia group,inflammatory exudation and structural disorder of lung tissue were more severe in PPG+ hyperoxia group.White blood cells,neutrophils and albumin content in BALF increased significantly (LSD-t=5.52,6.37 and 8.23,P＜0.01),the plasma H2S concentration and the activity of CSE decreased (LSD-t=-4.29 and-3.97,P＜0.01),the contents of MDA increased (LSD-t=3.02,P＜0.01).Conclusions H2S is involved in the pathophysiological process of hyperoxia-induced lung injury in neonatal rats.Exogenous H2S can alleviate the pulmonary injury by inhibiting inflammatory reaction and oxidative stress.
