中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2012年
2期
330-332
,共3页
刘韦成%罗学来%李兆明%邓豫%曹小年%杨熹%李川%金源%李小兰%陶德定%胡俊波%王晶
劉韋成%囉學來%李兆明%鄧豫%曹小年%楊熹%李川%金源%李小蘭%陶德定%鬍俊波%王晶
류위성%라학래%리조명%산예%조소년%양희%리천%금원%리소란%도덕정%호준파%왕정
急性肝损伤%模型,动物%脂多糖
急性肝損傷%模型,動物%脂多糖
급성간손상%모형,동물%지다당
Acute liver injury%Model,animal%Lipopolysaccharide
目的 建立脂多糖(内毒素,LPS)单独诱导小鼠急性肝损伤模型及致死模型.方法 分别以生理盐水、LPS 10、30、50、80 mg/kg腹腔注射小鼠,筛选LPS诱导小鼠急性肝损伤和致死剂量.分别以生理盐水、LPS 30、50 mg/kg腹腔注射小鼠,绘制各组小鼠的生存曲线,苏木素-伊红(HE)染色观察各组肝组织损伤情况,免疫组织化学染色检测肝组织核因子(NF) -κB p65蛋白的表达和核转位变化,酶联免疫吸附试验(ELISA)检测小鼠血清中肿瘤坏死因子(TNF)-α含量.结果 对照组小鼠无死亡和肝组织损伤,肝组织内NF-κB p65蛋白表达水平低,无核转位现象,血清中TNF-α含量低.腹腔注射LPS 30 mg/kg组小鼠无死亡,出现肝组织损伤,肝组织内NF-κB p65蛋白表达水平增加、出现核转位,血清中TNF-α含量升高,与对照组比较差异有统计学意义(P＜0.01).腹腔注射LPS 50 mg/kg组小鼠存活不超过120 h,肝组织严重损伤,肝组织内NF-κB p65蛋白表达水平以及核转位显著增加,血清中TNF-α含量显著增高,与对照组比较差异有统计学意义(P＜0.01).结论 成功建立脂多糖诱导肝损伤动物模型和致死模型,为在体内进一步研究p55PIK对LPS-NF-κB通路奠定基础.
目的 建立脂多糖(內毒素,LPS)單獨誘導小鼠急性肝損傷模型及緻死模型.方法 分彆以生理鹽水、LPS 10、30、50、80 mg/kg腹腔註射小鼠,篩選LPS誘導小鼠急性肝損傷和緻死劑量.分彆以生理鹽水、LPS 30、50 mg/kg腹腔註射小鼠,繪製各組小鼠的生存麯線,囌木素-伊紅(HE)染色觀察各組肝組織損傷情況,免疫組織化學染色檢測肝組織覈因子(NF) -κB p65蛋白的錶達和覈轉位變化,酶聯免疫吸附試驗(ELISA)檢測小鼠血清中腫瘤壞死因子(TNF)-α含量.結果 對照組小鼠無死亡和肝組織損傷,肝組織內NF-κB p65蛋白錶達水平低,無覈轉位現象,血清中TNF-α含量低.腹腔註射LPS 30 mg/kg組小鼠無死亡,齣現肝組織損傷,肝組織內NF-κB p65蛋白錶達水平增加、齣現覈轉位,血清中TNF-α含量升高,與對照組比較差異有統計學意義(P＜0.01).腹腔註射LPS 50 mg/kg組小鼠存活不超過120 h,肝組織嚴重損傷,肝組織內NF-κB p65蛋白錶達水平以及覈轉位顯著增加,血清中TNF-α含量顯著增高,與對照組比較差異有統計學意義(P＜0.01).結論 成功建立脂多糖誘導肝損傷動物模型和緻死模型,為在體內進一步研究p55PIK對LPS-NF-κB通路奠定基礎.
목적 건립지다당(내독소,LPS)단독유도소서급성간손상모형급치사모형.방법 분별이생리염수、LPS 10、30、50、80 mg/kg복강주사소서,사선LPS유도소서급성간손상화치사제량.분별이생리염수、LPS 30、50 mg/kg복강주사소서,회제각조소서적생존곡선,소목소-이홍(HE)염색관찰각조간조직손상정황,면역조직화학염색검측간조직핵인자(NF) -κB p65단백적표체화핵전위변화,매련면역흡부시험(ELISA)검측소서혈청중종류배사인자(TNF)-α함량.결과 대조조소서무사망화간조직손상,간조직내NF-κB p65단백표체수평저,무핵전위현상,혈청중TNF-α함량저.복강주사LPS 30 mg/kg조소서무사망,출현간조직손상,간조직내NF-κB p65단백표체수평증가、출현핵전위,혈청중TNF-α함량승고,여대조조비교차이유통계학의의(P＜0.01).복강주사LPS 50 mg/kg조소서존활불초과120 h,간조직엄중손상,간조직내NF-κB p65단백표체수평이급핵전위현저증가,혈청중TNF-α함량현저증고,여대조조비교차이유통계학의의(P＜0.01).결론 성공건립지다당유도간손상동물모형화치사모형,위재체내진일보연구p55PIK대LPS-NF-κB통로전정기출.
Objective To establish mouse acute liver injury model and lethal model induced by lipopolysaccharide (LPS) injection alone.Methods Mice were injected intraperitoneally ( i.p.) with different concentrations of LPS (0,10,30,50,80 mg/kg).The physiological statuses of mice were observed.The liver tissue of mice was stained by Hematoxylin and Eosin (HE) to examine the injury of the liver.The levels of tumor necrosis factor (TNF)-α in mouse serum were detected by enzyme linked immunosorbent assay (ELISA).The expression and nuclear translocation of nuclear factor (NF)-κB p65 in mouse liver tissue were measured by immunohistochemistry staining.Results No death and liver injury were found in control group mice.No increased NF-κB p65 protein expression and nuclear translocation in liver tissue and increased serum TNF-α levels were detected in control group mice.No deaths of mice were found in group with intraperitoneal injection of LPS at a concentration of 30 mg/kg.As compared with the control group,liver injury,increased NF-κB p65 protein expression and nuclear translocation in liver tissue and increased serum TNF-α levels were detected in this group ( P ＜ 0.01 ).Mice with intraperitoneal injection of LPS at a concentration of LPS 50mg/kg survived no more than 120 h.As compared with the control group,liver injury,significantly increased NF-κB p65 protein expression and nuclear translocation in liver tissue and significantly increased serum TNF-α levels were detected in this group (P ＜0.01 ).Conclusion Our research successfully establishes mice liver injury model and lethal model induced by LPS intraperitoneal injection alone,which provides stable research platform for further medical treatment.
