中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2014年
10期
2244-2247,后插2
,共5页
刘桂勇%刘修恒%王磊%宋洪飞
劉桂勇%劉脩恆%王磊%宋洪飛
류계용%류수항%왕뢰%송홍비
右美托嘧啶%肾缺血%再灌注%Toll样受体4%核因子-κB
右美託嘧啶%腎缺血%再灌註%Toll樣受體4%覈因子-κB
우미탁밀정%신결혈%재관주%Toll양수체4%핵인자-κB
Dexmedetomidine%Renal schemia%Reperfusion injury%Toll-like receptor 4%Nuclear factor-κB
目的 探讨右美托嘧啶对大鼠肾脏缺血再灌注后炎性反应的保护作用及其机制.方法 将24只大鼠随机分为3组,每组8只.假手术组:游离双侧肾脏,切除右肾后缝合腹壁;缺血再灌注组:切除右肾,夹闭左肾动、静脉45 min后再灌注24 h,余同假手术组.右美托嘧啶组:夹闭左肾动、静脉前30 min,腹腔注射右美托嘧啶(100 μg/kg),余同缺血再灌注组.再灌注24 h后,检测各组大鼠血清肌酐、尿素氮,苏木素-伊红(HE)染色观察肾组织病理变化,实时荧光定量聚合酶链反应(FQ-PCR)检测肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)、细胞间黏附分子(ICAM-1)的水平,Western blot检测Toll样受体4(TLR4)和核因子-κB (NF-κB)的表达.结果 在假手术组、缺血再灌注组和右美托嘧啶组中,血清肌酐(μmol/L)分别为17.55±1.02、138.49±6.20、81.98 ±4.24,血清尿素氮(mmol/L)分别为7.00±2.06、27.38±4.37、13.75±3.54,假手术组的血清肌酐、尿素氮水平明显比缺血再灌注组和右美托嘧啶组低(P＜0.05),而缺血再灌注组的血清肌酐、尿素氮水平显著高于右美托嘧啶组(P＜0.05).HE染色可见缺血再灌注组的肾小管上皮细胞明显变性坏死,有大量炎性细胞浸润,而右美托嘧啶可以明显减轻损伤.与假手术组比较,缺血再灌注组和右美托嘧啶组TNF-α、IL-1β、ICAM-1、TLR4、NF-κB水平均显著升高,而右美托嘧啶组的上述指标明显低于缺血再灌注组.结论 右美托嘧啶可以减轻大鼠肾脏缺血再灌注损伤导致的炎性反应,其机制可能与抑制TLR4/NF-κB通路的表达有关.
目的 探討右美託嘧啶對大鼠腎髒缺血再灌註後炎性反應的保護作用及其機製.方法 將24隻大鼠隨機分為3組,每組8隻.假手術組:遊離雙側腎髒,切除右腎後縫閤腹壁;缺血再灌註組:切除右腎,夾閉左腎動、靜脈45 min後再灌註24 h,餘同假手術組.右美託嘧啶組:夾閉左腎動、靜脈前30 min,腹腔註射右美託嘧啶(100 μg/kg),餘同缺血再灌註組.再灌註24 h後,檢測各組大鼠血清肌酐、尿素氮,囌木素-伊紅(HE)染色觀察腎組織病理變化,實時熒光定量聚閤酶鏈反應(FQ-PCR)檢測腫瘤壞死因子-α(TNF-α)、白細胞介素-1β(IL-1β)、細胞間黏附分子(ICAM-1)的水平,Western blot檢測Toll樣受體4(TLR4)和覈因子-κB (NF-κB)的錶達.結果 在假手術組、缺血再灌註組和右美託嘧啶組中,血清肌酐(μmol/L)分彆為17.55±1.02、138.49±6.20、81.98 ±4.24,血清尿素氮(mmol/L)分彆為7.00±2.06、27.38±4.37、13.75±3.54,假手術組的血清肌酐、尿素氮水平明顯比缺血再灌註組和右美託嘧啶組低(P＜0.05),而缺血再灌註組的血清肌酐、尿素氮水平顯著高于右美託嘧啶組(P＜0.05).HE染色可見缺血再灌註組的腎小管上皮細胞明顯變性壞死,有大量炎性細胞浸潤,而右美託嘧啶可以明顯減輕損傷.與假手術組比較,缺血再灌註組和右美託嘧啶組TNF-α、IL-1β、ICAM-1、TLR4、NF-κB水平均顯著升高,而右美託嘧啶組的上述指標明顯低于缺血再灌註組.結論 右美託嘧啶可以減輕大鼠腎髒缺血再灌註損傷導緻的炎性反應,其機製可能與抑製TLR4/NF-κB通路的錶達有關.
목적 탐토우미탁밀정대대서신장결혈재관주후염성반응적보호작용급기궤제.방법 장24지대서수궤분위3조,매조8지.가수술조:유리쌍측신장,절제우신후봉합복벽;결혈재관주조:절제우신,협폐좌신동、정맥45 min후재관주24 h,여동가수술조.우미탁밀정조:협폐좌신동、정맥전30 min,복강주사우미탁밀정(100 μg/kg),여동결혈재관주조.재관주24 h후,검측각조대서혈청기항、뇨소담,소목소-이홍(HE)염색관찰신조직병리변화,실시형광정량취합매련반응(FQ-PCR)검측종류배사인자-α(TNF-α)、백세포개소-1β(IL-1β)、세포간점부분자(ICAM-1)적수평,Western blot검측Toll양수체4(TLR4)화핵인자-κB (NF-κB)적표체.결과 재가수술조、결혈재관주조화우미탁밀정조중,혈청기항(μmol/L)분별위17.55±1.02、138.49±6.20、81.98 ±4.24,혈청뇨소담(mmol/L)분별위7.00±2.06、27.38±4.37、13.75±3.54,가수술조적혈청기항、뇨소담수평명현비결혈재관주조화우미탁밀정조저(P＜0.05),이결혈재관주조적혈청기항、뇨소담수평현저고우우미탁밀정조(P＜0.05).HE염색가견결혈재관주조적신소관상피세포명현변성배사,유대량염성세포침윤,이우미탁밀정가이명현감경손상.여가수술조비교,결혈재관주조화우미탁밀정조TNF-α、IL-1β、ICAM-1、TLR4、NF-κB수평균현저승고,이우미탁밀정조적상술지표명현저우결혈재관주조.결론 우미탁밀정가이감경대서신장결혈재관주손상도치적염성반응,기궤제가능여억제TLR4/NF-κB통로적표체유관.
Objective To investigate the effect of dexmedetomidine on inflammation induced by renal ischemia and reperfusion injury (IRI) in rats.Methods Twenty SD rats were randomly divided into three groups:sham operated group,IRI group and dexmedetomidine group.Each group had 8 rats.In sham operated group,the right kidneys of rats were excised.In IRI group,with no wound vascular clamp,left renal arteries and veins of rats were clamped for 45 min,then vascular clamp was opened and the rats were subjected to repeffusion.In Dexmedetomidine groups,operation steps were the same as the IRI group,but at 30 min before ischemia,dexmedetomidine was given by intraperitoneal injection (100 μg/kg).The parameters [blood urea nitrogen (BUN) and ereatine (Cr)] for renal function were determined by auto-biochemieal analyzer.The expression levels of tumor necrosis factor (TNF)-α,interleukin (IL)-1 β and intercellular adhesion molecule-1 (ICAM-1) were measured by real-time fluorescent quantitative polymerase chain reaction (FQ-PCR) and the changes of renal tissue were examined by a microscope.The expression of Toll-like receptor4 (TLR4) and nuclear factor-κB (NF-κB) was detected by Western blotting.Results In sham group,IRI group and dexmedetomidine group,Cr levels (μmol/L) were 17.55 ± 1.02,138.49 ± 6.20 and 81.98 ±4.24,respectively,and BUN levels (mmol/L) were 7.00 ±2.06,27.38 ±4.37 and 13.75 ±3.54,respectively.Cr and BUN levels in sham operated group were obviously lower than in IRI group and dexmedetomidine group,and those in IRI group were significantly higher than in dexmedetomidine group.As compared with sham operated group,TNF-α,IL-1β,ICAM-1,TLR4 and NF-κB were significantly increased in IRI group and dexmedetomidine group.However,these targets in dexmedetomidine group were significantly decreased as compared with those in IRI group.Conclusion Dexmedetomidine can alleviate inflammation induced by renal IRI probably by inhibiting the expression of TLR4/NF-κB signaling pathway.
