中华肾脏病杂志
中華腎髒病雜誌
중화신장병잡지
2014年
10期
757-762
,共6页
魏盼%黄文娟%万辛%戴春%孙晴%陈文%夏文楷%曹长春
魏盼%黃文娟%萬辛%戴春%孫晴%陳文%夏文楷%曹長春
위반%황문연%만신%대춘%손청%진문%하문해%조장춘
巨噬细胞%再灌注损伤,肾脏%修复
巨噬細胞%再灌註損傷,腎髒%脩複
거서세포%재관주손상,신장%수복
Macrophages%Reperfusion injury,kidney%Repair
目的 探讨巨噬细胞在小鼠肾脏缺血/再灌注(IR)损伤修复期中的作用.方法 24只6~8周龄C57BL/6小鼠被分为假手术(Sham)组、缺血再灌注(IR)组、氯磷酸盐脂质体(LC)组、空白对照(Ctl)组.Sham组仅切开背部皮肤,暴露双侧肾蒂不予夹闭;其余3组小鼠均给予夹闭双侧肾蒂25 min后恢复血流,再灌注3d后留取肾脏标本.LC组和Ctl组在留取肾脏标本前1天分别经腹腔注射LC(0.15~ 0.2 ml/20 g)或PBS.HE染色观察肾脏组织形态学改变;免疫组化法检测巨噬细胞浸润情况,Ki67蛋白、肿瘤坏死因子(TNF-α)和白细胞介素(IL)10的表达;Western印迹法检测TNF-α和IL-10的改变.结果 与IR组和Ctl组相比,LC组肾组织巨噬细胞浸润明显减少,肾组织病理损伤加重,细胞增殖减少,TNF-α表达明显增多,IL-10表达明显减少(均P< 0.05).结论 在IR损伤修复期敲除巨噬细胞可加重小鼠缺血再灌注损伤,可能和巨噬细胞可抑制促炎因子TNF-α表达和促抗炎因子IL-10分泌有关.
目的 探討巨噬細胞在小鼠腎髒缺血/再灌註(IR)損傷脩複期中的作用.方法 24隻6~8週齡C57BL/6小鼠被分為假手術(Sham)組、缺血再灌註(IR)組、氯燐痠鹽脂質體(LC)組、空白對照(Ctl)組.Sham組僅切開揹部皮膚,暴露雙側腎蒂不予夾閉;其餘3組小鼠均給予夾閉雙側腎蒂25 min後恢複血流,再灌註3d後留取腎髒標本.LC組和Ctl組在留取腎髒標本前1天分彆經腹腔註射LC(0.15~ 0.2 ml/20 g)或PBS.HE染色觀察腎髒組織形態學改變;免疫組化法檢測巨噬細胞浸潤情況,Ki67蛋白、腫瘤壞死因子(TNF-α)和白細胞介素(IL)10的錶達;Western印跡法檢測TNF-α和IL-10的改變.結果 與IR組和Ctl組相比,LC組腎組織巨噬細胞浸潤明顯減少,腎組織病理損傷加重,細胞增殖減少,TNF-α錶達明顯增多,IL-10錶達明顯減少(均P< 0.05).結論 在IR損傷脩複期敲除巨噬細胞可加重小鼠缺血再灌註損傷,可能和巨噬細胞可抑製促炎因子TNF-α錶達和促抗炎因子IL-10分泌有關.
목적 탐토거서세포재소서신장결혈/재관주(IR)손상수복기중적작용.방법 24지6~8주령C57BL/6소서피분위가수술(Sham)조、결혈재관주(IR)조、록린산염지질체(LC)조、공백대조(Ctl)조.Sham조부절개배부피부,폭로쌍측신체불여협폐;기여3조소서균급여협폐쌍측신체25 min후회복혈류,재관주3d후류취신장표본.LC조화Ctl조재류취신장표본전1천분별경복강주사LC(0.15~ 0.2 ml/20 g)혹PBS.HE염색관찰신장조직형태학개변;면역조화법검측거서세포침윤정황,Ki67단백、종류배사인자(TNF-α)화백세포개소(IL)10적표체;Western인적법검측TNF-α화IL-10적개변.결과 여IR조화Ctl조상비,LC조신조직거서세포침윤명현감소,신조직병리손상가중,세포증식감소,TNF-α표체명현증다,IL-10표체명현감소(균P< 0.05).결론 재IR손상수복기고제거서세포가가중소서결혈재관주손상,가능화거서세포가억제촉염인자TNF-α표체화촉항염인자IL-10분비유관.
Objective To study the effect of macrophage on the repair phase of ischemic/ reperfusion (IR) renal injury in mice.Methods A total of 24 C57BL/6 mice aged 6 ~ 8 week-old were divided into 4 groups:the Sham group,IR group,LC group and Control group.For all the groups,the bilateral renal pedicles of the mice were clipped after dorsal skin dissection,except for the Sham group,then unclipped them 25 minutes later to restore blood flow to the kidney and collected the renal specimens after 3 days.The LC group and Control group each were injected intraperitoneally with 0.15 ~ 0.20 ml/20 g per day before kidney specimens were taken.The morphology changes of renal tissues were evaluated by HE staining.Immunohistochemical testing was performed to detect the infiltration of macrophages,the expression change of Ki67,TNF-α and IL-10.In addition TNF-o,IL 10 were measured using Western blotting.Results Compared to the IR group and the Control group,the infiltration of macrophages was markedly decreased,the damage of renal pathology was aggravated,the cell proliferation was significantly decreased,and the expression of IL-10 was also decreased (P < 0.05),while the expression of TNF-α were increased (P < 0.05).Conclusions Intraperitoneal LC injection can aggravate kidney damage on the repair phase of renal ischemic/reperfusion injury in mice,which is possibly related its inhibition of proinflammatory cytokines TNF-α and the secretion of antiinflammatory cytokine IL-10.