心血管康复医学杂志
心血管康複醫學雜誌
심혈관강복의학잡지
JOURNAL OF CARDIOVASCULAR REHABILITATION MEDICINE
2012年
2期
117-122,封2
,共7页
徐锦春%陈思娇%熊盈%陈婕%宋今丹
徐錦春%陳思嬌%熊盈%陳婕%宋今丹
서금춘%진사교%웅영%진첩%송금단
糖尿病,2型%细胞凋亡%西罗莫司%大鼠
糖尿病,2型%細胞凋亡%西囉莫司%大鼠
당뇨병,2형%세포조망%서라막사%대서
Diabetes mellitus,type 2%Apoptosis%Sirolimus%Rats
目的:探讨糖尿病大鼠肾组织肿瘤坏死因子α(TNF-α)、核转录因子- κB (NF-κB)对肾组织细胞凋亡的诱导以及雷帕霉素干预的作用.方法:选择2型糖尿病大鼠(GK大鼠)20只,均分为糖尿病模型组(DM组),雷帕霉素治疗组(DMR组,建立糖尿病模型后给予雷帕霉素治疗);另选择10只Wistar雄性大鼠作为正常对照组.分别在4周、8周后检测各组肾组织细胞凋亡情况,NF- κB,TNF-α的表达水平以及血脂、血糖水平.结果:模型制作后4周、8周,与正常对照组和DMR组比较,DM组大鼠肾组织细胞凋亡数[RCA,4周(0.217±0.031)、(0.272±0.031)比(0.545±0.031)、8周(0.358±0.031)、(0.350±0.031)比(0.811±0.031)]均明显增多,NF-κBp65 [OD:4周(0.160±0.027)、(0.131±0.027)比(0.411±0.027)、8周(0.232±0.027)、(0.275±0.027)比(0.634±0.027)]、TNF-α [OD:4周(0.242±0.027)、 (0.275±0.027)比(0.617±0.027)、8周(0.385±0.027)、(0.342±0.027)比(0.912±0.027)]表达均明显升高(P均<0.01).相关分析显示,肾组织NF-κBp65与TNF -α,RCA与TNF-α,NF -κBp65均呈正相关关系(r=0.956,0.953,0.886,P均<0.01).结论:糖尿病病大鼠的肾细胞凋亡显著增加,雷帕霉素干预组肾细胞凋亡显著减少,NF- κB、TNF-α表达显著增加,其保护作用可能是NF- κB、TNF-α阻滞细胞的凋亡.
目的:探討糖尿病大鼠腎組織腫瘤壞死因子α(TNF-α)、覈轉錄因子- κB (NF-κB)對腎組織細胞凋亡的誘導以及雷帕黴素榦預的作用.方法:選擇2型糖尿病大鼠(GK大鼠)20隻,均分為糖尿病模型組(DM組),雷帕黴素治療組(DMR組,建立糖尿病模型後給予雷帕黴素治療);另選擇10隻Wistar雄性大鼠作為正常對照組.分彆在4週、8週後檢測各組腎組織細胞凋亡情況,NF- κB,TNF-α的錶達水平以及血脂、血糖水平.結果:模型製作後4週、8週,與正常對照組和DMR組比較,DM組大鼠腎組織細胞凋亡數[RCA,4週(0.217±0.031)、(0.272±0.031)比(0.545±0.031)、8週(0.358±0.031)、(0.350±0.031)比(0.811±0.031)]均明顯增多,NF-κBp65 [OD:4週(0.160±0.027)、(0.131±0.027)比(0.411±0.027)、8週(0.232±0.027)、(0.275±0.027)比(0.634±0.027)]、TNF-α [OD:4週(0.242±0.027)、 (0.275±0.027)比(0.617±0.027)、8週(0.385±0.027)、(0.342±0.027)比(0.912±0.027)]錶達均明顯升高(P均<0.01).相關分析顯示,腎組織NF-κBp65與TNF -α,RCA與TNF-α,NF -κBp65均呈正相關關繫(r=0.956,0.953,0.886,P均<0.01).結論:糖尿病病大鼠的腎細胞凋亡顯著增加,雷帕黴素榦預組腎細胞凋亡顯著減少,NF- κB、TNF-α錶達顯著增加,其保護作用可能是NF- κB、TNF-α阻滯細胞的凋亡.
목적:탐토당뇨병대서신조직종류배사인자α(TNF-α)、핵전록인자- κB (NF-κB)대신조직세포조망적유도이급뢰파매소간예적작용.방법:선택2형당뇨병대서(GK대서)20지,균분위당뇨병모형조(DM조),뢰파매소치료조(DMR조,건립당뇨병모형후급여뢰파매소치료);령선택10지Wistar웅성대서작위정상대조조.분별재4주、8주후검측각조신조직세포조망정황,NF- κB,TNF-α적표체수평이급혈지、혈당수평.결과:모형제작후4주、8주,여정상대조조화DMR조비교,DM조대서신조직세포조망수[RCA,4주(0.217±0.031)、(0.272±0.031)비(0.545±0.031)、8주(0.358±0.031)、(0.350±0.031)비(0.811±0.031)]균명현증다,NF-κBp65 [OD:4주(0.160±0.027)、(0.131±0.027)비(0.411±0.027)、8주(0.232±0.027)、(0.275±0.027)비(0.634±0.027)]、TNF-α [OD:4주(0.242±0.027)、 (0.275±0.027)비(0.617±0.027)、8주(0.385±0.027)、(0.342±0.027)비(0.912±0.027)]표체균명현승고(P균<0.01).상관분석현시,신조직NF-κBp65여TNF -α,RCA여TNF-α,NF -κBp65균정정상관관계(r=0.956,0.953,0.886,P균<0.01).결론:당뇨병병대서적신세포조망현저증가,뢰파매소간예조신세포조망현저감소,NF- κB、TNF-α표체현저증가,기보호작용가능시NF- κB、TNF-α조체세포적조망.
Objective:To investigate the apoptosis of renal cells induced by tumor necrosis factor alpha (TNF- a) and nuclear factor-κB (NF-κB) in diabetic rats and intervention of rapamycin.Methods:A total of 20 rats (GotoKakizaki rats) with type 2 diabetes mellitus (T2DM) were randomly and equally divided into DM model group (DM group) and rapamycin treatment group (DMR group,received rapamycin treatment after DM model was established) ; another 10 Wistar male rats were regard as normal control group.Apoptosis of renal cells,expression levels of TNF - α and NF- κB and levels of blood lipids,blood glucose were measured in all groups after four weeks and eight weeks.Results:Four and eight weeks after model was established,compared with normal control group and DMR group,there were significant increase in renal cells apoptosis [-RCA,four weeks:(0.217± 0.031),(0.272 ±0.031) vs.(0.545 ± 0.031),eight weeks:(0.358 ± 0.031),(0.350 ± 0.031) vs.(0.811 ± 0.031)] and expressions of NF-κB p65 [OD:four weeks:(0.160± 0.027),(0.131 ±0.027) vs.(0.411±0.027),eight weeks:(0.232± 0.027),(0.275 ± 0.027) vs.(0.634 ± 0.027)] and TNF- α [OD:four weeks:(0.242 ± 0.027),(0.275 ± 0.027)vs.(0.617 ± 0.027),eight weeks:(0.385 ± 0.027),(0.342 ± 0.027) vs.(0.912 ± 0.027)] in DM group (P<0.01all).Correlation analysis indicated that there were positive correlations between renal NF - κB p65 and TNF - α,among RCA and TN F- α,NF- κB p65 ( r =0.956,0.953,0.886,P<0.01 all).Conclusion:Renal cells apoptosis significant increase in rats with T2DM,but renal cells apoptosis significant decrease in DMR group,protection mechanism of rapamycin may be NF- κB、TNF- α inhibiting renal cells apoptosis.