南方医科大学学报
南方醫科大學學報
남방의과대학학보
JOURNAL OF SOUTHERN MEDICAL UNIVERSITY
2015年
1期
149-153
,共5页
鄢娜%冯泽国%颜光涛%岳剑虹%赵艳军%耿娜
鄢娜%馮澤國%顏光濤%嶽劍虹%趙豔軍%耿娜
언나%풍택국%안광도%악검홍%조염군%경나
重复性低氧预处理%肾%缺血%再灌注损伤%肝损伤
重複性低氧預處理%腎%缺血%再灌註損傷%肝損傷
중복성저양예처리%신%결혈%재관주손상%간손상
repetitive hypoxic preconditioning%nephrology%ischemia%reperfusion injury%hepatic dysfunction
目的:探究重复性低氧预处理(RHP)对大鼠肾脏缺血再灌注损伤(IRI)所致的肝脏损伤的影响并初步探讨其机制。方法120只雄性SD大鼠随机分为4组(n=30):低氧预处理手术组(RHP组),低氧预处理假手术组(RHPS组),常压手术组(IRI组)及常压假手术组(S组)。低压氧舱预处理大鼠5 d,建立肾IRI模型,RHP组及IRI组统一切除右肾、夹闭左肾肾门45 min后放开建立肾缺血再灌注模型,而RHPS组及S组仅切除右肾,不进行左肾缺血再灌注处理。于再灌注后2、8、24 h检测血清谷丙转氨酶(ALT)、IL-17A、TNF-α浓度,酶标仪检测肝脏匀浆超氧化物歧化酶(SOD)及一氧化氮(NO)的含量,Western blot检测测肝脏p-PI3K、p-AKT水平,病理组织形态学检查观察肝脏结构变化。结果与IRI组相比,RHP组大鼠再灌注后2、8、24 h病理组织形态学检查显示损伤减轻,血清ALT浓度降低,TNF-α水平于再灌注后24 h降低(P<0.05)肝组织NO含量升高(P<0.05),SOD含量于再灌注后8 h升高(P<0.05);与S组相比,IRI组及RHP组血清IL-17A浓度均显著升高(P<0.05),但两组间差异无统计学意义(P>0.05);RHP组P-PI3K及P-AKT表达均高于IRI组(P<0.05),且差异于再灌注后8 h尤为显著(P<0.05)。结论 RHP对大鼠肾脏IRI所致的肝脏损伤具有保护作用,但并非通过抑制IL-17A来实现。
目的:探究重複性低氧預處理(RHP)對大鼠腎髒缺血再灌註損傷(IRI)所緻的肝髒損傷的影響併初步探討其機製。方法120隻雄性SD大鼠隨機分為4組(n=30):低氧預處理手術組(RHP組),低氧預處理假手術組(RHPS組),常壓手術組(IRI組)及常壓假手術組(S組)。低壓氧艙預處理大鼠5 d,建立腎IRI模型,RHP組及IRI組統一切除右腎、夾閉左腎腎門45 min後放開建立腎缺血再灌註模型,而RHPS組及S組僅切除右腎,不進行左腎缺血再灌註處理。于再灌註後2、8、24 h檢測血清穀丙轉氨酶(ALT)、IL-17A、TNF-α濃度,酶標儀檢測肝髒勻漿超氧化物歧化酶(SOD)及一氧化氮(NO)的含量,Western blot檢測測肝髒p-PI3K、p-AKT水平,病理組織形態學檢查觀察肝髒結構變化。結果與IRI組相比,RHP組大鼠再灌註後2、8、24 h病理組織形態學檢查顯示損傷減輕,血清ALT濃度降低,TNF-α水平于再灌註後24 h降低(P<0.05)肝組織NO含量升高(P<0.05),SOD含量于再灌註後8 h升高(P<0.05);與S組相比,IRI組及RHP組血清IL-17A濃度均顯著升高(P<0.05),但兩組間差異無統計學意義(P>0.05);RHP組P-PI3K及P-AKT錶達均高于IRI組(P<0.05),且差異于再灌註後8 h尤為顯著(P<0.05)。結論 RHP對大鼠腎髒IRI所緻的肝髒損傷具有保護作用,但併非通過抑製IL-17A來實現。
목적:탐구중복성저양예처리(RHP)대대서신장결혈재관주손상(IRI)소치적간장손상적영향병초보탐토기궤제。방법120지웅성SD대서수궤분위4조(n=30):저양예처리수술조(RHP조),저양예처리가수술조(RHPS조),상압수술조(IRI조)급상압가수술조(S조)。저압양창예처리대서5 d,건립신IRI모형,RHP조급IRI조통일절제우신、협폐좌신신문45 min후방개건립신결혈재관주모형,이RHPS조급S조부절제우신,불진행좌신결혈재관주처리。우재관주후2、8、24 h검측혈청곡병전안매(ALT)、IL-17A、TNF-α농도,매표의검측간장균장초양화물기화매(SOD)급일양화담(NO)적함량,Western blot검측측간장p-PI3K、p-AKT수평,병리조직형태학검사관찰간장결구변화。결과여IRI조상비,RHP조대서재관주후2、8、24 h병리조직형태학검사현시손상감경,혈청ALT농도강저,TNF-α수평우재관주후24 h강저(P<0.05)간조직NO함량승고(P<0.05),SOD함량우재관주후8 h승고(P<0.05);여S조상비,IRI조급RHP조혈청IL-17A농도균현저승고(P<0.05),단량조간차이무통계학의의(P>0.05);RHP조P-PI3K급P-AKT표체균고우IRI조(P<0.05),차차이우재관주후8 h우위현저(P<0.05)。결론 RHP대대서신장IRI소치적간장손상구유보호작용,단병비통과억제IL-17A래실현。
Objective To explore the effect of repeated hypoxic preconditioning (RHP) on renal ischemia-reperfusion-induced hepatic dysfunction in rats and the underlying mechanism. Methods A total of 120 normal SD rats were randomly divided into 4 groups (n=40), namely RHP surgical group, RHP sham-operated (RHPS) group, nonhypoxic surgical group (IRI group), and nonhypoxic sham-operated group (S group). The rats in the hypoxic groups were exposed to hypoxia in a hypoxic chamber for 5 days prior to establishment of renal ischemia-reperfusion model by resection of the right kidney and clamping the left renal hilum. Serum alanine aminotransferase (ALT), IL-17A, TNF-α, liver superoxide dismutase (SOD) and nitric oxide (NO) were detected at 2, 8 and 24h after reperfusion, and Western blotting was used to determine the expression of p-PI3K and p-AKT;HE staining was used to observe the structural changes in the liver. Results Compared with IRI group, RHP group showed significantly milder hepatic damage, lower ALT levels and higher NO levels at 2, 8, and 24 after reperfusion (P<0.05);TNF-αlevels were lowered at 24 h (P<0.05) and SOD increased at 8 h after the reperfusion (P<0.05). Compared with S group, IRI group and RHP group showed significantly higher IL-17A levels (P<0.05) but without significant difference between the latter two groups (P>0.05). The expressions of p-PI3K and P-Akt in RHP group were significantly higher than those in IRI group (P<0.05), especially at 8 h after reperfusion (P<0.05). Conclusion Repeated hypoxic preconditioning can attenuate hepatic injury induced by renal ischemia-reperfusion injury in rats.