广东医学
廣東醫學
엄동의학
GUNAGDONG MEDICAL JOURNAL
2015年
9期
1318-1321
,共4页
睾酮%血管平滑肌细胞%线粒体%线粒体融合素2
睪酮%血管平滑肌細胞%線粒體%線粒體融閤素2
고동%혈관평활기세포%선립체%선립체융합소2
testosterone%vascular smooth muscle cell%mitochondrial%mitofusin 2
目的:研究生理剂量睾酮对去势大鼠主动脉血管平滑肌细胞线粒体损伤的保护作用,并探讨其可能机制。方法选取8周龄雄性 SD 大鼠30只,随机分为假手术组,去势组和去势﹢睾酮组,每组10只。去势组行睾丸切除术,去势﹢睾酮组在去势后每天给予丙酸睾酮5.0 mg/ kg 肌肉注射。12周后测定各组血清睾酮浓度,并取大鼠胸主动脉,免疫印迹法检测血管平滑肌组织线粒体融合素2蛋白表达,激光共聚焦显微镜观察线粒体形态变化;JC -1检测线粒体膜电位;测定细胞总三磷酸腺苷(ATP)含量,超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH - Px)活性以及丙二醛(MDA)水平。结果与假手术组比较,去势组大鼠血清睾酮水平降低( P <0.05),线粒体融合素2表达降低(P <0.05),线粒体聚集呈团块状,线粒体膜电位减低(P <0.05),ATP 含量、SOD 和GSH - Px 活性降低(P <0.05),MDA 水平增加(P <0.05)。与去势组相比,去势﹢睾酮组大鼠血清睾酮水平升高(P <0.05),线粒体融合素2表达增加(P <0.05),线粒体呈管状分布,线粒体膜电位增高(P <0.05),ATP 含量、SOD 和 GSH - Px 活性增加(P <0.05),MDA 水平降低(P <0.05),与假手术组比较差异无统计学意义(P >0.05)。结论生理剂量睾酮可维持去势大鼠血管平滑肌细胞的线粒体形态和膜电位水平,增加细胞 ATP 含量,降低氧化应激水平,对线粒体损伤具有保护作用,上调线粒体融合素2表达是其可能机制之一。
目的:研究生理劑量睪酮對去勢大鼠主動脈血管平滑肌細胞線粒體損傷的保護作用,併探討其可能機製。方法選取8週齡雄性 SD 大鼠30隻,隨機分為假手術組,去勢組和去勢﹢睪酮組,每組10隻。去勢組行睪汍切除術,去勢﹢睪酮組在去勢後每天給予丙痠睪酮5.0 mg/ kg 肌肉註射。12週後測定各組血清睪酮濃度,併取大鼠胸主動脈,免疫印跡法檢測血管平滑肌組織線粒體融閤素2蛋白錶達,激光共聚焦顯微鏡觀察線粒體形態變化;JC -1檢測線粒體膜電位;測定細胞總三燐痠腺苷(ATP)含量,超氧化物歧化酶(SOD)、穀胱甘肽過氧化物酶(GSH - Px)活性以及丙二醛(MDA)水平。結果與假手術組比較,去勢組大鼠血清睪酮水平降低( P <0.05),線粒體融閤素2錶達降低(P <0.05),線粒體聚集呈糰塊狀,線粒體膜電位減低(P <0.05),ATP 含量、SOD 和GSH - Px 活性降低(P <0.05),MDA 水平增加(P <0.05)。與去勢組相比,去勢﹢睪酮組大鼠血清睪酮水平升高(P <0.05),線粒體融閤素2錶達增加(P <0.05),線粒體呈管狀分佈,線粒體膜電位增高(P <0.05),ATP 含量、SOD 和 GSH - Px 活性增加(P <0.05),MDA 水平降低(P <0.05),與假手術組比較差異無統計學意義(P >0.05)。結論生理劑量睪酮可維持去勢大鼠血管平滑肌細胞的線粒體形態和膜電位水平,增加細胞 ATP 含量,降低氧化應激水平,對線粒體損傷具有保護作用,上調線粒體融閤素2錶達是其可能機製之一。
목적:연구생리제량고동대거세대서주동맥혈관평활기세포선립체손상적보호작용,병탐토기가능궤제。방법선취8주령웅성 SD 대서30지,수궤분위가수술조,거세조화거세﹢고동조,매조10지。거세조행고환절제술,거세﹢고동조재거세후매천급여병산고동5.0 mg/ kg 기육주사。12주후측정각조혈청고동농도,병취대서흉주동맥,면역인적법검측혈관평활기조직선립체융합소2단백표체,격광공취초현미경관찰선립체형태변화;JC -1검측선립체막전위;측정세포총삼린산선감(ATP)함량,초양화물기화매(SOD)、곡광감태과양화물매(GSH - Px)활성이급병이철(MDA)수평。결과여가수술조비교,거세조대서혈청고동수평강저( P <0.05),선립체융합소2표체강저(P <0.05),선립체취집정단괴상,선립체막전위감저(P <0.05),ATP 함량、SOD 화GSH - Px 활성강저(P <0.05),MDA 수평증가(P <0.05)。여거세조상비,거세﹢고동조대서혈청고동수평승고(P <0.05),선립체융합소2표체증가(P <0.05),선립체정관상분포,선립체막전위증고(P <0.05),ATP 함량、SOD 화 GSH - Px 활성증가(P <0.05),MDA 수평강저(P <0.05),여가수술조비교차이무통계학의의(P >0.05)。결론생리제량고동가유지거세대서혈관평활기세포적선립체형태화막전위수평,증가세포 ATP 함량,강저양화응격수평,대선립체손상구유보호작용,상조선립체융합소2표체시기가능궤제지일。
Objective To investigate the protective effect of testosterone on the mitochondrial damage of vascular smooth muscle cells of castrated rats,and to explore its possible mechanisms. Methods A total of 30 male Sprague -Dawley(SD)rats were randomly divided into sham - operated group,castrated group(treated with normal saline),and castrated ﹢ testosterone group(treated with testosterone 5. 0mg/ kg daily). After treatment for 12 weeks,the rats were sac-rificed,and blood samples were drawn for measurement of plasma testosterone. The expression of Mitofusin 2(Mfn2)was detected by western blotting. The mitochondrial morphology and distribution was observed through laser confocal microsco-py. The mitochondrial membrane potential(ΔΨm)was detected by JC - 1 staining method. The total contents of ATP, superoxide dismutase(SOD),glutathione peroxidase(GSH - Px),and malondialdehyde(MDA)were determined by as-say kits. Results Compared with the sham group,the plasma testosterone level and Mfn2 protein expression in castrated group were significantly reduced(P < 0. 05);so were the ΔΨm,and the total contents of ATP,SOD,and GSH - Px;while the MDA was significantly increased(P < 0. 05). Mitochondrial fusion and morphology was dramatically altered in castrated group. Compared with the castrated group,significant increase in the plasma testosterone level,Mfn2 protein ex-pression,ΔΨm,and the total contents of ATP,SOD,and GSH - Px in castrated ﹢ testosterone group(P < 0. 05);so was the reduction in MDA level(P < 0. 05). No significant difference in mitochondrial morphology or distribution was ob-served between the sham and the castrated ﹢ testosterone groups. Conclusion Testosterone at physiological concentration plays a protective role in the mitochondrial damage of vascular smooth muscle cells of castrated rats,which may relate to up - regulation of mitofusin 2.