中国糖尿病杂志
中國糖尿病雜誌
중국당뇨병잡지
CHINESE JOURNAL OF DIABETES
2006年
6期
438-441
,共4页
毛永辉%大高澈也%佐藤博%伊藤貞嘉%王梅
毛永輝%大高澈也%佐籐博%伊籐貞嘉%王梅
모영휘%대고철야%좌등박%이등정가%왕매
糖尿病肾病%糖基化终产物%表型转化
糖尿病腎病%糖基化終產物%錶型轉化
당뇨병신병%당기화종산물%표형전화
Phenotype transformation
目的 观察糖基化终产物(AGEs)在肾脏组织中的沉积及其与肾脏固有细胞表型转化的关系. 方法 采用免疫组化染色法观察AGEs:羧甲基赖氨酸(CML)、吡咯素、戊糖苷素和细胞骨架蛋白:α-肌动蛋白(α-SMA)、L-收缩平滑肌蛋白(L-CLD)在28例2型糖尿病肾病(DN)患者肾活检组织(疾病组)的沉积,分析二者间及其与肾脏病理改变和临床表现的关系.4例增生硬化型IgA肾病及4例轻微病变型和2例正常肾组织作为对照组. 结果 (1)四组均可见CML、吡咯素分别沉积在系膜区和肾间质,但对照组明显弱于DN组;戊糖苷素只沉积在DN肾小球基底膜(GBM).(2)系膜区α-SMA、L-CLD的表达与戊糖苷素呈正相关,吡咯素的沉积与间质L-CLD有关.(3)α-SMA和L-CLD及戊糖苷素的沉积与肾小球硬化指数、间质纤维化百分数及蛋白尿、Scr正相关. 结论 戊糖苷素在GBM的沉积是糖尿病肾小球硬化的重要原因;AGEs对肾脏的影响部分可能是通过引起肾脏固有细胞的表型转化而起作用的.
目的 觀察糖基化終產物(AGEs)在腎髒組織中的沉積及其與腎髒固有細胞錶型轉化的關繫. 方法 採用免疫組化染色法觀察AGEs:羧甲基賴氨痠(CML)、吡咯素、戊糖苷素和細胞骨架蛋白:α-肌動蛋白(α-SMA)、L-收縮平滑肌蛋白(L-CLD)在28例2型糖尿病腎病(DN)患者腎活檢組織(疾病組)的沉積,分析二者間及其與腎髒病理改變和臨床錶現的關繫.4例增生硬化型IgA腎病及4例輕微病變型和2例正常腎組織作為對照組. 結果 (1)四組均可見CML、吡咯素分彆沉積在繫膜區和腎間質,但對照組明顯弱于DN組;戊糖苷素隻沉積在DN腎小毬基底膜(GBM).(2)繫膜區α-SMA、L-CLD的錶達與戊糖苷素呈正相關,吡咯素的沉積與間質L-CLD有關.(3)α-SMA和L-CLD及戊糖苷素的沉積與腎小毬硬化指數、間質纖維化百分數及蛋白尿、Scr正相關. 結論 戊糖苷素在GBM的沉積是糖尿病腎小毬硬化的重要原因;AGEs對腎髒的影響部分可能是通過引起腎髒固有細胞的錶型轉化而起作用的.
목적 관찰당기화종산물(AGEs)재신장조직중적침적급기여신장고유세포표형전화적관계. 방법 채용면역조화염색법관찰AGEs:최갑기뢰안산(CML)、필각소、무당감소화세포골가단백:α-기동단백(α-SMA)、L-수축평활기단백(L-CLD)재28례2형당뇨병신병(DN)환자신활검조직(질병조)적침적,분석이자간급기여신장병리개변화림상표현적관계.4례증생경화형IgA신병급4례경미병변형화2례정상신조직작위대조조. 결과 (1)사조균가견CML、필각소분별침적재계막구화신간질,단대조조명현약우DN조;무당감소지침적재DN신소구기저막(GBM).(2)계막구α-SMA、L-CLD적표체여무당감소정정상관,필각소적침적여간질L-CLD유관.(3)α-SMA화L-CLD급무당감소적침적여신소구경화지수、간질섬유화백분수급단백뇨、Scr정상관. 결론 무당감소재GBM적침적시당뇨병신소구경화적중요원인;AGEs대신장적영향부분가능시통과인기신장고유세포적표형전화이기작용적.
Objective To investigate the distribution of AGEs in renal tissue and to study the interrelationship of AGEs and phenotypic changes of kidney cells in patients with diabetic nephropathy(DN).Methods The locations of AGEs and cytoskeletal proteins were evaluated by immunohistochemical method and the relationship between them were analyzed in 28 DN patients.Results The carboxymethyl lysine(CML) and pyrraline were localized in mesangial area(especially in nodular area) and renal interstitium respectively and the similar areas of positive staining were found in IgA nephropathy,minor lesion and normal renal tissue,but in less degree of staining.Pentosidine was localized only in glomerular basement membrane(GBM) in DN and this deposition significantly correlated with diabetic glomerulosclerotic index,24-h urinary protein and serum creatinine level.The positive staining of α-smooth muscle actin(α-SMA),and low molecular caldesmon(L-CLD)were found in the mesangial area,and the expression significantly correlated with pentosidine,but not with CML.The α-SMA in interstitial area significantly correlated with pyrraline.Conclusions AGEs are involved in renal injury in DN.Their effect on kidney is,at least in part,produced via phenotypic changes of intrinsic cells.Pentosidine deposition in DN may be specific.
