中国病理生理杂志
中國病理生理雜誌
중국병리생리잡지
CHINESE JOURNAL OF PATHOPHYSIOLOGY
2015年
1期
166-171
,共6页
陈达%张洪颖%贾浩%朱杰
陳達%張洪穎%賈浩%硃傑
진체%장홍영%가호%주걸
乌司他丁%急性肺损伤%百草枯%丝裂原活化蛋白激酶%金属蛋白酶组织抑制物%基质金属蛋白酶
烏司他丁%急性肺損傷%百草枯%絲裂原活化蛋白激酶%金屬蛋白酶組織抑製物%基質金屬蛋白酶
오사타정%급성폐손상%백초고%사렬원활화단백격매%금속단백매조직억제물%기질금속단백매
KEY WORDS] Ulinastatin%Acute lung injury%Paraquat%Mitogen-activated protein kinases%Tissue inhibitor of metalloproteinases%Matrix metalloproteinases
目的:探讨乌司他丁保护百草枯中毒大鼠肺免受损伤的作用及其机制。方法: Wistar大鼠108只,随机分为对照组、百草枯组和乌司他丁组。百草枯组和乌司他丁组给予百草枯灌胃染毒,对照组给予无菌生理盐水灌胃,乌司他丁组同时给予乌司他丁治疗。1、3、7、14、21、28 d测血清中的MDA、SOD、IL-6、IL-10和TNF-α水平,以及肺组织中的p38 MAPK、MMP-2和TIMP-1表达水平。结果:1、3、7 d百草枯组和乌司他丁组的SOD均较对照组下降(P<0.01),乌司他丁组SOD明显高于百草枯组(P<0.05)。1、3、7 d百草枯组和乌司他丁组的MDA、IL-6、IL-10及TNF-α均较对照组增高(P<0.01),乌司他丁组各指标明显低于百草枯组(P<0.05)。1、3、7、14、21、28 d百草枯组和乌司他丁组肺组织中的p38 MAPK及TIMP-1均较对照组增高( P<0.01),乌司他丁组各指标明显低于百草枯组(P<0.05)。1、3、7、14、21 d百草枯组和乌司他丁组肺组织中的MMP-2均较对照组增高(P<0.01),乌司他丁组MMP-2明显低于百草枯组(P<0.05)。结论:乌司他丁通过抑制p38 MAPK信号通路及抗炎、抗氧化作用保护百草枯中毒大鼠肺免受损伤的作用。
目的:探討烏司他丁保護百草枯中毒大鼠肺免受損傷的作用及其機製。方法: Wistar大鼠108隻,隨機分為對照組、百草枯組和烏司他丁組。百草枯組和烏司他丁組給予百草枯灌胃染毒,對照組給予無菌生理鹽水灌胃,烏司他丁組同時給予烏司他丁治療。1、3、7、14、21、28 d測血清中的MDA、SOD、IL-6、IL-10和TNF-α水平,以及肺組織中的p38 MAPK、MMP-2和TIMP-1錶達水平。結果:1、3、7 d百草枯組和烏司他丁組的SOD均較對照組下降(P<0.01),烏司他丁組SOD明顯高于百草枯組(P<0.05)。1、3、7 d百草枯組和烏司他丁組的MDA、IL-6、IL-10及TNF-α均較對照組增高(P<0.01),烏司他丁組各指標明顯低于百草枯組(P<0.05)。1、3、7、14、21、28 d百草枯組和烏司他丁組肺組織中的p38 MAPK及TIMP-1均較對照組增高( P<0.01),烏司他丁組各指標明顯低于百草枯組(P<0.05)。1、3、7、14、21 d百草枯組和烏司他丁組肺組織中的MMP-2均較對照組增高(P<0.01),烏司他丁組MMP-2明顯低于百草枯組(P<0.05)。結論:烏司他丁通過抑製p38 MAPK信號通路及抗炎、抗氧化作用保護百草枯中毒大鼠肺免受損傷的作用。
목적:탐토오사타정보호백초고중독대서폐면수손상적작용급기궤제。방법: Wistar대서108지,수궤분위대조조、백초고조화오사타정조。백초고조화오사타정조급여백초고관위염독,대조조급여무균생리염수관위,오사타정조동시급여오사타정치료。1、3、7、14、21、28 d측혈청중적MDA、SOD、IL-6、IL-10화TNF-α수평,이급폐조직중적p38 MAPK、MMP-2화TIMP-1표체수평。결과:1、3、7 d백초고조화오사타정조적SOD균교대조조하강(P<0.01),오사타정조SOD명현고우백초고조(P<0.05)。1、3、7 d백초고조화오사타정조적MDA、IL-6、IL-10급TNF-α균교대조조증고(P<0.01),오사타정조각지표명현저우백초고조(P<0.05)。1、3、7、14、21、28 d백초고조화오사타정조폐조직중적p38 MAPK급TIMP-1균교대조조증고( P<0.01),오사타정조각지표명현저우백초고조(P<0.05)。1、3、7、14、21 d백초고조화오사타정조폐조직중적MMP-2균교대조조증고(P<0.01),오사타정조MMP-2명현저우백초고조(P<0.05)。결론:오사타정통과억제p38 MAPK신호통로급항염、항양화작용보호백초고중독대서폐면수손상적작용。
AIM: To investigate the protective effects of ulinastatin on the rats with paraquat-induced acute lung injury and its mechanisms .METHODS:The Wistar rats ( n=108 ) were randomly divided into control group , pa-raquat group and ulinastatin group .The rats in paraquat group and ulinastatin group were given paraquat by gavage , while the rats in control group were given sterile saline by gavage .The rats in ulinastatin group were also given ulinastatin treat-ment.The serum levels of MDA, SOD, IL-6, IL-10 and TNF-αwere measured after 1 d, 3 d, 7 d, 14 d, 21 d and 28 d. The expression levels of p 38 MAPK, MMP-2 and TIMP-1 in the lung were also measured .RESULTS:The levels of SOD in 1 d, 3 d and 7 d in paraquat group and ulinastatin group were significantly lower than those in control group ( P<0.01).The level of SOD in ulinastatin group was significantly higher than that in paraquat group (P<0.05).The levels of MDA, IL-6, IL-10 and TNF-αin 1 d, 3 d and 7 d in paraquat group and ulinastatin group increased compared with con-trol group (P<0.01), and those in ulinastatin group were significantly lower than those in paraquat group (P<0.05). The levels of p38 MAPK and TIMP-1 in 1 d, 3 d, 7 d, 14 d, 21 d and 28 d in paraquat group and ulinastatin group were higher than those in control group (P<0.01), and those in ulinastatin group was significantly lower than those in paraquat group ( P<0.05) .The level of MMP-2 in 1 d, 3 d, 7 d, 14 d and 21 d in paraquat group and ulinastatin group increased compared with control group (P<0.01), and that in ulinastatin group was significantly lower than that in paraquat group (P<0.05).CONCLUSION:Ulinastatin protects the lung tissues of rats from paraquat-induced acute lung injury by in-hibiting p38 MAPK signaling pathway and ameliorating inflammatory and oxidative responses .