中华劳动卫生职业病杂志
中華勞動衛生職業病雜誌
중화노동위생직업병잡지
Chinese Journal of Industrial Hygiene and Occupational Diseases
2015年
9期
658-662
,共5页
支绍册%吴冬%李玲文%洪广亮%李萌芳%吴斌%卢中秋
支紹冊%吳鼕%李玲文%洪廣亮%李萌芳%吳斌%盧中鞦
지소책%오동%리령문%홍엄량%리맹방%오빈%로중추
百草枯%兔%炎症%灌流%肾脏
百草枯%兔%炎癥%灌流%腎髒
백초고%토%염증%관류%신장
Paraquat%Rabbits%Inflammation%Perfusion%Kidney
目的 观察血液灌流(hemoperfusion,HP)对急性百草枯(paraquat,PQ)中毒兔肾组织炎症损伤影响,并探讨可能的机制.方法 将60只普通级雄性日本大耳白兔随机分为4组,正常对照组(6只,生理盐水灌胃),空白对照组(18只,生理盐水灌胃后1h给予血液灌流治疗2h),百草枯染毒组(PQ染毒组,18只,20%百草枯溶液按50 mg/kg灌胃),血液灌流治疗组(HP治疗组,18只,20%百草枯溶液按50 mg/kg灌胃后1h给予血液灌流治疗2h).空白对照组、PQ染毒组、HP治疗组兔分为3个观察时间亚组(1、3、7d),每组6只.处理后,第1、3、7d麻醉处死,并留取肾脏.ELISA检测肾脏TNF-α、IL-6和iNOS的表达量,逆转录-聚合酶链式反应法(RT-PCR)和蛋白印迹法(Western blot)分别检测核转录因子NF-κB基因和蛋白的表达.光镜下观察肾脏组织病理改变.结果 与正常对照组比较,空白对照组各观察指标无变化,PQ染毒组TNF-α、IL-6和iNOS的表达量、NF-κB蛋白和NF-κB基因表达均明显上升,差异有统计学意义(P<0.05).与PQ染毒组比较,在1、3、7天HP治疗组TNF-α、IL-6的表达量、NF-κB蛋白和NF-κB基因均明显下降,差异有统计学意义(P<0.05),iNOS活力在第1天无明显变化,而在第3、7天明显降低,差异有统计学意义(P<0.05).光学显微镜下观察,正常对照组和空白对照组兔肾脏病理切片未见异常表现.PQ染毒组兔肾组织病理损害在染毒后第3天最严重,在第1、3、7天HP治疗组肾脏病理损害较PQ染毒组轻.结论 HP治疗可能够降低PQ对家兔肾脏的炎症损伤,对PQ中毒所致的兔肾脏损伤有保护作用.
目的 觀察血液灌流(hemoperfusion,HP)對急性百草枯(paraquat,PQ)中毒兔腎組織炎癥損傷影響,併探討可能的機製.方法 將60隻普通級雄性日本大耳白兔隨機分為4組,正常對照組(6隻,生理鹽水灌胃),空白對照組(18隻,生理鹽水灌胃後1h給予血液灌流治療2h),百草枯染毒組(PQ染毒組,18隻,20%百草枯溶液按50 mg/kg灌胃),血液灌流治療組(HP治療組,18隻,20%百草枯溶液按50 mg/kg灌胃後1h給予血液灌流治療2h).空白對照組、PQ染毒組、HP治療組兔分為3箇觀察時間亞組(1、3、7d),每組6隻.處理後,第1、3、7d痳醉處死,併留取腎髒.ELISA檢測腎髒TNF-α、IL-6和iNOS的錶達量,逆轉錄-聚閤酶鏈式反應法(RT-PCR)和蛋白印跡法(Western blot)分彆檢測覈轉錄因子NF-κB基因和蛋白的錶達.光鏡下觀察腎髒組織病理改變.結果 與正常對照組比較,空白對照組各觀察指標無變化,PQ染毒組TNF-α、IL-6和iNOS的錶達量、NF-κB蛋白和NF-κB基因錶達均明顯上升,差異有統計學意義(P<0.05).與PQ染毒組比較,在1、3、7天HP治療組TNF-α、IL-6的錶達量、NF-κB蛋白和NF-κB基因均明顯下降,差異有統計學意義(P<0.05),iNOS活力在第1天無明顯變化,而在第3、7天明顯降低,差異有統計學意義(P<0.05).光學顯微鏡下觀察,正常對照組和空白對照組兔腎髒病理切片未見異常錶現.PQ染毒組兔腎組織病理損害在染毒後第3天最嚴重,在第1、3、7天HP治療組腎髒病理損害較PQ染毒組輕.結論 HP治療可能夠降低PQ對傢兔腎髒的炎癥損傷,對PQ中毒所緻的兔腎髒損傷有保護作用.
목적 관찰혈액관류(hemoperfusion,HP)대급성백초고(paraquat,PQ)중독토신조직염증손상영향,병탐토가능적궤제.방법 장60지보통급웅성일본대이백토수궤분위4조,정상대조조(6지,생리염수관위),공백대조조(18지,생리염수관위후1h급여혈액관류치료2h),백초고염독조(PQ염독조,18지,20%백초고용액안50 mg/kg관위),혈액관류치료조(HP치료조,18지,20%백초고용액안50 mg/kg관위후1h급여혈액관류치료2h).공백대조조、PQ염독조、HP치료조토분위3개관찰시간아조(1、3、7d),매조6지.처리후,제1、3、7d마취처사,병류취신장.ELISA검측신장TNF-α、IL-6화iNOS적표체량,역전록-취합매련식반응법(RT-PCR)화단백인적법(Western blot)분별검측핵전록인자NF-κB기인화단백적표체.광경하관찰신장조직병리개변.결과 여정상대조조비교,공백대조조각관찰지표무변화,PQ염독조TNF-α、IL-6화iNOS적표체량、NF-κB단백화NF-κB기인표체균명현상승,차이유통계학의의(P<0.05).여PQ염독조비교,재1、3、7천HP치료조TNF-α、IL-6적표체량、NF-κB단백화NF-κB기인균명현하강,차이유통계학의의(P<0.05),iNOS활력재제1천무명현변화,이재제3、7천명현강저,차이유통계학의의(P<0.05).광학현미경하관찰,정상대조조화공백대조조토신장병리절편미견이상표현.PQ염독조토신조직병리손해재염독후제3천최엄중,재제1、3、7천HP치료조신장병리손해교PQ염독조경.결론 HP치료가능구강저PQ대가토신장적염증손상,대PQ중독소치적토신장손상유보호작용.
Objective To investigate the effect of hemoperfusion on paraquat-Induced kidney inflammation injury of rabbit and the mechanism of it.Methods 60 male rabbits were randomly divided into 4 groups,the normal control group (n=6,the rabbits were given NS by gavage),blank control group (n=18,he rabbits were given 2 hours hemoperfusion once within 1 hour after given NS by gavage),paraquat poisoning group (n=18,the rabbits were given 50 mg/kg 20% paraquat solution by gavage),hemoperfusion treatment group (n=18,the rabbits were given 2 hours hemoperfusion once within 1 hour after 20% paraquat solution espoused).The last 3 groups were divided into 3 observation time groups (1,3,7 day),contained 6 rabbits each group.On days 1,3,7 all groups rabbits were anesthetized and sacrificed,and their kidney tissues collected.The levels of NF-κB mRNA by RT-PCR,and the expression of NF-κB protein was measured by Western blotting,The expression levels of TNF-α,IL-6,iNOS measured by chemical colorimetric method to to observe inflammatory injury.Results Compared with the normal control group rabbits,there were no changes in the TNF-α,IL-6,iNOS,NF-κB mRNA and protein of blank control group (P>0.05),while the expression of TNF-α,IL-6,NF-κB mRNA and protein in the kidney tissue of PQ group and were significantly increased (P<0.05).The pathological results of kidney tissues were no abnormalities onnormal control group and blank control group.Conclusion HP significantly increase resistance to PQ-induced inflammation injury in the rabbit kidney and exert a protective effect on PQ-induced kidney injury.