中国男科学杂志
中國男科學雜誌
중국남과학잡지
CHINESE JOURNAL OF ANDROLOGY
2009年
10期
5-9,17
,共6页
姚乐申%李燕%陈赟%戴玉田
姚樂申%李燕%陳赟%戴玉田
요악신%리연%진빈%대옥전
糖尿病%糖尿病性勃起功能障碍(DMED)%氧化损伤%还原型谷胱甘肽(GSH)
糖尿病%糖尿病性勃起功能障礙(DMED)%氧化損傷%還原型穀胱甘肽(GSH)
당뇨병%당뇨병성발기공능장애(DMED)%양화손상%환원형곡광감태(GSH)
diabetes%diabetic erection disfunction(DMED)%oxidative damnification%reducedglutathione sodium (GSH)
目的 探讨氧化损伤在糖尿病性ED发病机制中的作用,以及还原型谷胱甘肽(GSH)对氧化损伤的干预作用,为临床治疗提供新的手段.方法 成年雄性SD大鼠50只,随机分为4组:A组为对照组(N=10),B组为糖尿病无干预组(N=13),C组为糖尿病胰岛素干预组(N=13)和D组为糖尿病胰岛素+GSH干预组(N=14).采用腹腔注射STZ法制作糖尿病模型并进行筛选.8周后取大鼠阴茎海绵体组织进行组织匀浆,采用黄嘌呤氧化法测定阴茎海绵体组织中超氧化物岐化酶(SOD)活性:用TBA法测定丙二醛(MDA)含量;RT-PCR法检测胞外型SOD基因(SOD_(EX)基因)的表达;WESTERN-BLOT法检测CUZNSOD蛋白含量.结果 A组大鼠海绵体组织基本无过氧化产物蓄积.与A组相比,B、C、D组的SOD活性显著下降(P<0.05),MDA含量均显著升高(P<0.05),B、C、D组SOD_(EX)基因的表达、CUZNSOD蛋白含量显著下降(P<0.05);与B组相比,C、D组的SOD活性显著升高(P<0.05),MDA含量显著下降(P<0.05),SOD_(EX)基因的表达及CUZNSOD蛋白含量显著升高(P<0.05).与C组相比,D组SOD_(EX)基因的表达及CUZNSOD蛋白含量显著升高(P<0.05).结论 糖尿病性雄性大鼠阴茎海绵体组织自由基代谢明显障碍,脂质过氧化产物增加,同时氧自由基清除能力下降;而抗氧化剂GSH的应用能部分减弱氧化损伤.提示氧化损伤可能在糖尿病性ED的发生发展中起一定作用.本研究为糖尿病性ED的预防和治疗提供新的策略.
目的 探討氧化損傷在糖尿病性ED髮病機製中的作用,以及還原型穀胱甘肽(GSH)對氧化損傷的榦預作用,為臨床治療提供新的手段.方法 成年雄性SD大鼠50隻,隨機分為4組:A組為對照組(N=10),B組為糖尿病無榦預組(N=13),C組為糖尿病胰島素榦預組(N=13)和D組為糖尿病胰島素+GSH榦預組(N=14).採用腹腔註射STZ法製作糖尿病模型併進行篩選.8週後取大鼠陰莖海綿體組織進行組織勻漿,採用黃嘌呤氧化法測定陰莖海綿體組織中超氧化物岐化酶(SOD)活性:用TBA法測定丙二醛(MDA)含量;RT-PCR法檢測胞外型SOD基因(SOD_(EX)基因)的錶達;WESTERN-BLOT法檢測CUZNSOD蛋白含量.結果 A組大鼠海綿體組織基本無過氧化產物蓄積.與A組相比,B、C、D組的SOD活性顯著下降(P<0.05),MDA含量均顯著升高(P<0.05),B、C、D組SOD_(EX)基因的錶達、CUZNSOD蛋白含量顯著下降(P<0.05);與B組相比,C、D組的SOD活性顯著升高(P<0.05),MDA含量顯著下降(P<0.05),SOD_(EX)基因的錶達及CUZNSOD蛋白含量顯著升高(P<0.05).與C組相比,D組SOD_(EX)基因的錶達及CUZNSOD蛋白含量顯著升高(P<0.05).結論 糖尿病性雄性大鼠陰莖海綿體組織自由基代謝明顯障礙,脂質過氧化產物增加,同時氧自由基清除能力下降;而抗氧化劑GSH的應用能部分減弱氧化損傷.提示氧化損傷可能在糖尿病性ED的髮生髮展中起一定作用.本研究為糖尿病性ED的預防和治療提供新的策略.
목적 탐토양화손상재당뇨병성ED발병궤제중적작용,이급환원형곡광감태(GSH)대양화손상적간예작용,위림상치료제공신적수단.방법 성년웅성SD대서50지,수궤분위4조:A조위대조조(N=10),B조위당뇨병무간예조(N=13),C조위당뇨병이도소간예조(N=13)화D조위당뇨병이도소+GSH간예조(N=14).채용복강주사STZ법제작당뇨병모형병진행사선.8주후취대서음경해면체조직진행조직균장,채용황표령양화법측정음경해면체조직중초양화물기화매(SOD)활성:용TBA법측정병이철(MDA)함량;RT-PCR법검측포외형SOD기인(SOD_(EX)기인)적표체;WESTERN-BLOT법검측CUZNSOD단백함량.결과 A조대서해면체조직기본무과양화산물축적.여A조상비,B、C、D조적SOD활성현저하강(P<0.05),MDA함량균현저승고(P<0.05),B、C、D조SOD_(EX)기인적표체、CUZNSOD단백함량현저하강(P<0.05);여B조상비,C、D조적SOD활성현저승고(P<0.05),MDA함량현저하강(P<0.05),SOD_(EX)기인적표체급CUZNSOD단백함량현저승고(P<0.05).여C조상비,D조SOD_(EX)기인적표체급CUZNSOD단백함량현저승고(P<0.05).결론 당뇨병성웅성대서음경해면체조직자유기대사명현장애,지질과양화산물증가,동시양자유기청제능력하강;이항양화제GSH적응용능부분감약양화손상.제시양화손상가능재당뇨병성ED적발생발전중기일정작용.본연구위당뇨병성ED적예방화치료제공신적책략.
Objective To investigate the mechanism of oxidative damnification during the developement of diabetic erection dysfunction(DMED) and explore the effect of reduced glutathione on oxidative damnification. Methods Fifty male Sptague-Dawley rats were randomly divided into 4 groups including group A(control group, n=10), group B(no intervention diabetic group,n=13), C group(insulin intervention diabetic group, n=13) and D group(diabetic insulin and GSH intervention group,n=14). The diabetic model was established by the intraperitoneal injection of streptozotoc. Homogenates of corpus cavernosum tissue of rats was ready for next analysis. The thiobarbaturic acid (TBA) method was used to determine the lipid peroxidation, SOD activity was measured using the xanthine-oxidase cytochrome c method. The expression of SODex gene was detected by RT-PCR and level of CuZnSOD protein by Western-blot. Results There was almost no lipid peroxidation product detected in the corpus cavernosum tissue of the rats in group A. Compare with that of group A, SOD activity, the expression of SODex gene and CuZnSOD protein significantly decreased in B, C, D groups (P<0.05) whereas MDA level significantly increased(P<0.05). Compare with that of group B, SOD activity, the expression of SOD_(ex) gene and CuZnSOD protein in C, D groups significantly increased (P<0.05) whereas MDA level significantly decreased (P<0.05). Compare with that of C group, the expression of SOD_(ex) gene of D groups, and CuZnSOD protein significantly increased (P<0.05). Conclusion The metabolism was distinctly disturbed in the corpus cavernosum tissue of the diabetic male rats such as increase of the lipid peroxidation product and decrease of the free radical eliminating. Reduced GSH could reduced the oxidative damnification partly, which indicated that oxidative damnification might be involved in the development of DMED. Our study might provide a new insight for prevention and treatment of DMED.
