CAJ | 학술논문

目的探讨短时间缺血预处理在诱导肾脏缺血耐受中的作用,及其对肾小管上皮细胞坏死、凋亡、增殖等的影响.方法雄性SD大鼠随机分为3组:假手术组(Sham),只分离两侧肾蒂,不进行夹闭;单纯缺血再灌注组(I/R),第0天假手术,第4天用尤损伤动脉夹夹闭两侧肾蒂40 min,然后恢复灌注;缺血预适应组(IPC),第O天预缺血20 rain,第4天再次缺血40 rain.PAS染色观察肾组织形态学,透射电镜观察小管上皮细胞超微结构,原位末端标记法(TUNEL)检测细胞凋亡情况,免疫组织化学法观察肾小管上皮细胞增殖核抗原(PCNA)的表达.结果　与单纯缺血再灌注组相比,缺血预适应组肾脏功能和病理性损伤显著减轻(P<0.01);大鼠死亡率从33%降低为0;肾小管上皮细胞凋亡和坏死显著减少(P<0.05),细胞增殖(PCNA阳性)显著增多(P<0.01).结论短时间缺血预处理能诱导肾脏耐受长时间缺血,减少小管上皮细胞死亡和促进其及时增殖修复可能是预缺血发挥肾脏保护作用的机制之一.
목적 탐토단시간결혈예처리재유도신장결혈내수중적작용,급기대신소관상피세포배사、조망、증식등적영향.방법 웅성SD대서수궤분위3조:가수술조(Sham),지분리량측신체,불진행협폐;단순결혈재관주조(I/R),제0천가수술,제4천용우손상동맥협협폐량측신체40 min,연후회복관주;결혈예괄응조(IPC),제O천예결혈20 rain,제4천재차결혈40 rain.PAS염색관찰신조직형태학,투사전경관찰소관상피세포초미결구,원위말단표기법(TUNEL)검측세포조망정황,면역조직화학법관찰신소관상피세포증식핵항원(PCNA)적표체.결과　여단순결혈재관주조상비,결혈예괄응조신장공능화병이성손상현저감경(P<0.01);대서사망솔종33%강저위0;신소관상피세포조망화배사현저감소(P<0.05),세포증식(PCNA양성)현저증다(P<0.01).결론 단시간결혈예처리능유도신장내수장시간결혈,감소소관상피세포사망화촉진기급시증식수복가능시예결혈발휘신장보호작용적궤제지일.
Objective To explore the role of brief ischemia pretreatment in the induction of renal ischemic tolerance,and investigate its effects on tubular cell necrosis,apoptosis and proliferation. Methods Male Sprague-Dawley rats were randomly divided into three groups,including sham-operated group (Sham),ischemia/reperfusion injured group subjected to theocclusion of both renal pedicles for 40 min followed by reperfusion(I/R),and preconditioned group with 20-min ischemia pretreatment induced 4 days before I/R(IPC).Histological changes were evaluated by PAS staining.The ultra-structure of tubular cells was observed by transmission electron microscopy(TEM).Apoptosis was confirmed by terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick end labeling (TUNEL).The proliferation of tubular cells was evaluated with proliferating cell nuclear antigen(PCNA). Results Twenty-minites ischemia pretreatment offered both promising functional and histological protection against 40-min ischemia/reperfusion injury (P<0.01).The mortality rate wag reduced from 33%in I/R group to 0 in IPC group.The renopmtection offered by 20-min ischemia pretreatment was accompanied with reduced postischemic tubular cell apoptosis and necrosis (P<0.05), and increased cell proliferation (PCNA positive) (P< 0.01). Conclusions Brief and sublethal prior ischemia can render the kidney more tolerant to subsequent prolonged I/R injury. Its ability to tilt the balance of tubular cell fate toward survival, reducing postischemic cell death and enhancing cell proliferation, may play an important role in renal protection of ischemic preconditioning.