中华老年医学杂志
中華老年醫學雜誌
중화노년의학잡지
Chinese Journal of Geriatrics
2012年
4期
335-338
,共4页
牟亚汝%周颖%张钟文%周晓君%廖琳
牟亞汝%週穎%張鐘文%週曉君%廖琳
모아여%주영%장종문%주효군%료림
前列腺素E类%糖尿病肾病%肾小球%肾小管%细胞凋亡
前列腺素E類%糖尿病腎病%腎小毬%腎小管%細胞凋亡
전렬선소E류%당뇨병신병%신소구%신소관%세포조망
Prostaglandin E%Diabetic nephropathies%Kidney glomerulus%Kidney tubules%Apoptosis
目的 观察前列腺素E1 (PGE1)对糖尿病肾病(DN)大鼠肾脏细胞凋亡的影响. 方法 雄性Wistar大鼠65只,单次腹腔注射链脲佐菌素(STZ)制备DN大鼠模型.将造模成功的46只大鼠随机分为4组,PGE1组12只:前列地尔注射液(凯时)10 μg/d,静脉推注,10 d；血管紧张素转换酶抑制剂(ACEI)组12只:盐酸贝那普利片(洛汀新)10 mg/d,灌胃,8w;联合用药组11只:给予PGE1和ACEI联合治疗,剂量及时间同上；肾病对照组11只:仅给予相同体积生理盐水；另设正常对照组10只,处理同肾病对照组.治疗8 w后处死所有动物并测定24 h尿微量白蛋白、血尿素和血肌酐；HE染色观察肾脏病理和原位末端转移酶标记法(TUNEL)法检测细胞凋亡. 结果 治疗后8w,ACE1组、PGE1组、联合用药组24 h尿白蛋白水平均低于肾病对照组[(374.6±54.1)μg,(570.0±72.5)μg,(253.1±28.9)μg 比(1123.4±106.2 )μg,P＜0.01或P＜0.05]；血尿素[(9.3±2.6)mmol/L,(11.0±3.5)mmol/L.(8.4±2.2)mmol/L比(15.1±4.0)mmol/L]和血肌酐[(74.5±19.2)μmol/L,(83.5±15.8) μmol/L,(64.6±17.3)μ mol/L比(117.7±33.0)μmol/L]水平均低于肾病对照组(P＜0.01或P＜0.05)；与肾病对照组比较,各用药组肾脏组织病理改变减轻,联合用药组病理形态最佳.细胞凋亡在肾小球区域不明显.各组间差异无统计学意义(P＞0.05)；除正常对照组外,各组肾小管细胞凋亡数显著多于肾小球. 结论 PGE1减少尿白蛋白的机制与肾小球细胞凋亡无明显相关,可能与肾小管细胞凋亡有关.
目的 觀察前列腺素E1 (PGE1)對糖尿病腎病(DN)大鼠腎髒細胞凋亡的影響. 方法 雄性Wistar大鼠65隻,單次腹腔註射鏈脲佐菌素(STZ)製備DN大鼠模型.將造模成功的46隻大鼠隨機分為4組,PGE1組12隻:前列地爾註射液(凱時)10 μg/d,靜脈推註,10 d；血管緊張素轉換酶抑製劑(ACEI)組12隻:鹽痠貝那普利片(洛汀新)10 mg/d,灌胃,8w;聯閤用藥組11隻:給予PGE1和ACEI聯閤治療,劑量及時間同上；腎病對照組11隻:僅給予相同體積生理鹽水；另設正常對照組10隻,處理同腎病對照組.治療8 w後處死所有動物併測定24 h尿微量白蛋白、血尿素和血肌酐；HE染色觀察腎髒病理和原位末耑轉移酶標記法(TUNEL)法檢測細胞凋亡. 結果 治療後8w,ACE1組、PGE1組、聯閤用藥組24 h尿白蛋白水平均低于腎病對照組[(374.6±54.1)μg,(570.0±72.5)μg,(253.1±28.9)μg 比(1123.4±106.2 )μg,P＜0.01或P＜0.05]；血尿素[(9.3±2.6)mmol/L,(11.0±3.5)mmol/L.(8.4±2.2)mmol/L比(15.1±4.0)mmol/L]和血肌酐[(74.5±19.2)μmol/L,(83.5±15.8) μmol/L,(64.6±17.3)μ mol/L比(117.7±33.0)μmol/L]水平均低于腎病對照組(P＜0.01或P＜0.05)；與腎病對照組比較,各用藥組腎髒組織病理改變減輕,聯閤用藥組病理形態最佳.細胞凋亡在腎小毬區域不明顯.各組間差異無統計學意義(P＞0.05)；除正常對照組外,各組腎小管細胞凋亡數顯著多于腎小毬. 結論 PGE1減少尿白蛋白的機製與腎小毬細胞凋亡無明顯相關,可能與腎小管細胞凋亡有關.
목적 관찰전렬선소E1 (PGE1)대당뇨병신병(DN)대서신장세포조망적영향. 방법 웅성Wistar대서65지,단차복강주사련뇨좌균소(STZ)제비DN대서모형.장조모성공적46지대서수궤분위4조,PGE1조12지:전렬지이주사액(개시)10 μg/d,정맥추주,10 d；혈관긴장소전환매억제제(ACEI)조12지:염산패나보리편(락정신)10 mg/d,관위,8w;연합용약조11지:급여PGE1화ACEI연합치료,제량급시간동상；신병대조조11지:부급여상동체적생리염수；령설정상대조조10지,처리동신병대조조.치료8 w후처사소유동물병측정24 h뇨미량백단백、혈뇨소화혈기항；HE염색관찰신장병리화원위말단전이매표기법(TUNEL)법검측세포조망. 결과 치료후8w,ACE1조、PGE1조、연합용약조24 h뇨백단백수평균저우신병대조조[(374.6±54.1)μg,(570.0±72.5)μg,(253.1±28.9)μg 비(1123.4±106.2 )μg,P＜0.01혹P＜0.05]；혈뇨소[(9.3±2.6)mmol/L,(11.0±3.5)mmol/L.(8.4±2.2)mmol/L비(15.1±4.0)mmol/L]화혈기항[(74.5±19.2)μmol/L,(83.5±15.8) μmol/L,(64.6±17.3)μ mol/L비(117.7±33.0)μmol/L]수평균저우신병대조조(P＜0.01혹P＜0.05)；여신병대조조비교,각용약조신장조직병리개변감경,연합용약조병리형태최가.세포조망재신소구구역불명현.각조간차이무통계학의의(P＞0.05)；제정상대조조외,각조신소관세포조망수현저다우신소구. 결론 PGE1감소뇨백단백적궤제여신소구세포조망무명현상관,가능여신소관세포조망유관.
Objective To investigate the effects of prostaglandin E1 (PGE1) on renal cell apoptosis in rats with diabetic nephropathy(DN). Methods Totally 55 male Wistar rats were intraperitoneally injected with streptozotocin (STZ) to develop DN model.46 successfully established DN rat models were randomly divided into 4 groups:PGE1 group received PGE1 intravenously at dose of 10 μg · kg-1 · d-1 for 10 d (n=12),angiotensin converting enzyme inhibitors(ACEI) group given ACEI orally at dose of 10 mg kg-1·d-1 for 8 W(n=12),PGE1+ACEI group given both PGE1 and ACEI (n=11),DN control group(n=11) and normal control group(n=10) given saline only.All rats were killed after 8 weeks and blood samples or kidney tissue were collected.Blood urea nitrogen (BUN),serum creatine(Scr),albuminuria of 24 h were detected.Renal pathological morphology and apoptosis of renal cells were observed by HE staining and terminal deoxynucleotidyl transferase-mediated dUTP nick-end-labeling (TUNEL) test. Results At 8 week after treatment,the 24-hour urinary albumin levels were decreased significantly in the following order:DN control group＞ PGE1 group ＞ ACEI group ＞PGE1+ ACEI group＞ control group[(374.6±54.1)μg,(570.0±72.5)μg,(253.1±28.9)μg vs.(1123.4±106.2)μg,P＜0.01 or P＜0.05].BUN[(9.3±2.6)mmol/L,(11.0±3.5)mmol/L,(8.4±2.2)mmol/Lvs.(15.1±4.0)mmol/L]and Scr [(74.5±19.2) umol/L,(83.5± 15.8)μmol/L,(64.6±17.3) μmol/L vs.(117.7±33.0)μmol/L]levels after treatment were also reduced in PGE1,ACEI and PGE1 + ACEI groups as compared with DN control group (P＜0.01or P＜ 0.05). Pathological manifestations of all treatment groups showed better results than DN group,and PGE1 + ACEI group was the best.There was no obvious apoptosis in glomerular area with on significant differences between groups.While apoptosis of renal tubules was observed in DN rats. Conclusions Renal tubule but not glomerular cell apoptosis may play some role in Prostaglandin E1 reduciug albuminuria.
