中国社区医师
中國社區醫師
중국사구의사
Chinese Community Doctors
2014年
36期
9-10
,共2页
肝%HIRI%NF-κB%ω-3 PUFAs
肝%HIRI%NF-κB%ω-3 PUFAs
간%HIRI%NF-κB%ω-3 PUFAs
Liver%HIRI%NF-κB%ω-3 PUFAs
目的：应用大鼠肝缺血再灌注损伤(HIRI)模型，探讨ω-3脂肪酸预处理对其保护机制。方法：将60只大鼠随机分为假手术组(S组)、肝缺血再灌注损伤模型组(HIRI组)及缺血再灌注前ω-3多不饱和脂肪酸(ω-3 PUFAs)预处理组(ω组)，建立大鼠HIRI模型，予缺血60 min，恢复血流后再灌注1 h和6 h后取材。各组分别于再灌注末抽取静脉血、处死大鼠，收集肝组织。观察血清中谷草转氨酶(AST)、谷丙转氨酶(ALT)含量；HE染色观察肝组织病理学改变；酶联免疫吸附法测定大鼠血清超氧化物歧化酶(SOD)含量；免疫组化方法检测肝组织中核转录因子(NF-κB)的表达水平。结果：与S组比较，HIRI组和ω组血清ALT、AST水平、血清MDA含量及NF-κB表达均显著升高，而血清SOD活性明显下降(P＜0.05)，肝组织病理学损伤明显；与HIRI组比较，ω组血清ALT、AST的活性及NF-κB表达均显著降低，而血清 SOD 活性则明显升高(P＜0.05)，肝组织病理学损伤较轻。结论：ω-3 PUFAs 预处理对大鼠HIRI具有保护作用，机制可能是通过减少氧自由基的产生以及降低脂质过氧化反应，进而抑制NF-κB的活化来实现。
目的：應用大鼠肝缺血再灌註損傷(HIRI)模型，探討ω-3脂肪痠預處理對其保護機製。方法：將60隻大鼠隨機分為假手術組(S組)、肝缺血再灌註損傷模型組(HIRI組)及缺血再灌註前ω-3多不飽和脂肪痠(ω-3 PUFAs)預處理組(ω組)，建立大鼠HIRI模型，予缺血60 min，恢複血流後再灌註1 h和6 h後取材。各組分彆于再灌註末抽取靜脈血、處死大鼠，收集肝組織。觀察血清中穀草轉氨酶(AST)、穀丙轉氨酶(ALT)含量；HE染色觀察肝組織病理學改變；酶聯免疫吸附法測定大鼠血清超氧化物歧化酶(SOD)含量；免疫組化方法檢測肝組織中覈轉錄因子(NF-κB)的錶達水平。結果：與S組比較，HIRI組和ω組血清ALT、AST水平、血清MDA含量及NF-κB錶達均顯著升高，而血清SOD活性明顯下降(P＜0.05)，肝組織病理學損傷明顯；與HIRI組比較，ω組血清ALT、AST的活性及NF-κB錶達均顯著降低，而血清 SOD 活性則明顯升高(P＜0.05)，肝組織病理學損傷較輕。結論：ω-3 PUFAs 預處理對大鼠HIRI具有保護作用，機製可能是通過減少氧自由基的產生以及降低脂質過氧化反應，進而抑製NF-κB的活化來實現。
목적：응용대서간결혈재관주손상(HIRI)모형，탐토ω-3지방산예처리대기보호궤제。방법：장60지대서수궤분위가수술조(S조)、간결혈재관주손상모형조(HIRI조)급결혈재관주전ω-3다불포화지방산(ω-3 PUFAs)예처리조(ω조)，건립대서HIRI모형，여결혈60 min，회복혈류후재관주1 h화6 h후취재。각조분별우재관주말추취정맥혈、처사대서，수집간조직。관찰혈청중곡초전안매(AST)、곡병전안매(ALT)함량；HE염색관찰간조직병이학개변；매련면역흡부법측정대서혈청초양화물기화매(SOD)함량；면역조화방법검측간조직중핵전록인자(NF-κB)적표체수평。결과：여S조비교，HIRI조화ω조혈청ALT、AST수평、혈청MDA함량급NF-κB표체균현저승고，이혈청SOD활성명현하강(P＜0.05)，간조직병이학손상명현；여HIRI조비교，ω조혈청ALT、AST적활성급NF-κB표체균현저강저，이혈청 SOD 활성칙명현승고(P＜0.05)，간조직병이학손상교경。결론：ω-3 PUFAs 예처리대대서HIRI구유보호작용，궤제가능시통과감소양자유기적산생이급강저지질과양화반응，진이억제NF-κB적활화래실현。
Objective:Using the rat hepatic ischemia reperfusion injury(HIRI) model,to investigate the ω-3 fatty acid pretreatment on the protective mechanism.Methods:60 rats were randomly divided into the sham operation group(S group),the liver ischemia reperfusion injury model group(HIRI group) and ω-3 polyunsaturated fatty acids(ω-3 PUFAs) pretreatment before ischemia-reperfusion group(ω group),HIRI rat model was established,it was given the ischemia 60 min,samples were prepared after the restoration of blood flow after reperfusion for 1 and 6 hours.In each group,venous blood was drawn at the end of reperfusion,rats were sacrificed to collect the liver tissue.We observed the serum aspartate aminotransferase(AST),alanine aminotransferase(ALT) content;we observed the pathological changes of liver tissue stained by HE;enzyme linked immunosorbent assay was used to measure the rat serum superoxide dismutase(SOD) content;immunohistochemistry method was used to detect the expression level of nuclear transcription factor(NF-κ B) in liver tissue.Results:Compared with S group,in HIRI group and ωgroup,serum ALT,AST level,MDA content and NF-κB expression were increased significantly,while serum SOD activity was significantly decreased(P<0.05),liver tissue pathology damage was obvious;compared with HIRI group,in the ω group,serum ALT,AST activity and NF-κB expression were significantly reduced,and the activity of serum SOD was significantly elevated(P<0.05),liver histopathological injury was lighter.Conclusion: ω-3 PUFAs preconditioning had protective effect on rats HIRI,the mechanism may be to reduce the production of oxygen free radicals and reduce lipid peroxidation,and then make inhibition of NF-κB activation.
