中华老年医学杂志
中華老年醫學雜誌
중화노년의학잡지
Chinese Journal of Geriatrics
2014年
7期
788-791
,共4页
衰老%肌细胞,心脏%睾酮%受体,雄激素
衰老%肌細胞,心髒%睪酮%受體,雄激素
쇠로%기세포,심장%고동%수체,웅격소
Aging%Myocytes cardiac%Testosterone%Receptor,androgen
目的 探讨睾酮治疗是否通过其经典的雄激素受体(AR)途径影响心肌细胞衰老的发生. 方法 雄性C57BL/6J鼠和睾丸女性化鼠(Tfm)分为正常组(8只)、去势组(8只)、Tfm组(7只)、去势+睾酮(T)组(8只)、Tfm+T组(8只).分离左心室心肌细胞测定超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量及测定p16 INK4a和去磷酸化Rb蛋白表达量. 结果 与正常组比较,去势组和Tfm组SOD活性减弱[(16.55±1.18) U/ml、(17.30±1.32) U/ml比(21.57±2.21)U/ml,P＜0.05];MDA含量增加[(7.78±1.27) μmol/L、(6.52±0.82) μmol/L比(3.48±0.70) μmol/L,P＜0.01];p16INK4a(0.37±0.08、0.45±0.06比0.14±0.02)和去磷酸化Rb(0.74±0.05、0.79±0.08比0.40±0.05)蛋白表达水平上调(P＜0.05).与去势组比较,去势+T组SOD活性[(23.00±0.58)U/mD增加(P＜0.01);MDA含量[(2.63±0.90)μmol/L]、p16INK4a(0.13±0.03)和去磷酸化Rb(0.45±0.05)蛋白表达水平均下降(P＜0.05).与Tfm组比较,Tfm+T组SOD活性增加,MDA含量、p16INK4a和去磷酸化Rb蛋白表达水平下降(P＜0.05).去势+T组与Tfm+T组比较差异无统计学意义(P＞0.05). 结论 生理剂量睾酮治疗通过非AR依赖的机制延缓心肌细胞衰老.
目的 探討睪酮治療是否通過其經典的雄激素受體(AR)途徑影響心肌細胞衰老的髮生. 方法 雄性C57BL/6J鼠和睪汍女性化鼠(Tfm)分為正常組(8隻)、去勢組(8隻)、Tfm組(7隻)、去勢+睪酮(T)組(8隻)、Tfm+T組(8隻).分離左心室心肌細胞測定超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量及測定p16 INK4a和去燐痠化Rb蛋白錶達量. 結果 與正常組比較,去勢組和Tfm組SOD活性減弱[(16.55±1.18) U/ml、(17.30±1.32) U/ml比(21.57±2.21)U/ml,P＜0.05];MDA含量增加[(7.78±1.27) μmol/L、(6.52±0.82) μmol/L比(3.48±0.70) μmol/L,P＜0.01];p16INK4a(0.37±0.08、0.45±0.06比0.14±0.02)和去燐痠化Rb(0.74±0.05、0.79±0.08比0.40±0.05)蛋白錶達水平上調(P＜0.05).與去勢組比較,去勢+T組SOD活性[(23.00±0.58)U/mD增加(P＜0.01);MDA含量[(2.63±0.90)μmol/L]、p16INK4a(0.13±0.03)和去燐痠化Rb(0.45±0.05)蛋白錶達水平均下降(P＜0.05).與Tfm組比較,Tfm+T組SOD活性增加,MDA含量、p16INK4a和去燐痠化Rb蛋白錶達水平下降(P＜0.05).去勢+T組與Tfm+T組比較差異無統計學意義(P＞0.05). 結論 生理劑量睪酮治療通過非AR依賴的機製延緩心肌細胞衰老.
목적 탐토고동치료시부통과기경전적웅격소수체(AR)도경영향심기세포쇠로적발생. 방법 웅성C57BL/6J서화고환녀성화서(Tfm)분위정상조(8지)、거세조(8지)、Tfm조(7지)、거세+고동(T)조(8지)、Tfm+T조(8지).분리좌심실심기세포측정초양화물기화매(SOD)활성화병이철(MDA)함량급측정p16 INK4a화거린산화Rb단백표체량. 결과 여정상조비교,거세조화Tfm조SOD활성감약[(16.55±1.18) U/ml、(17.30±1.32) U/ml비(21.57±2.21)U/ml,P＜0.05];MDA함량증가[(7.78±1.27) μmol/L、(6.52±0.82) μmol/L비(3.48±0.70) μmol/L,P＜0.01];p16INK4a(0.37±0.08、0.45±0.06비0.14±0.02)화거린산화Rb(0.74±0.05、0.79±0.08비0.40±0.05)단백표체수평상조(P＜0.05).여거세조비교,거세+T조SOD활성[(23.00±0.58)U/mD증가(P＜0.01);MDA함량[(2.63±0.90)μmol/L]、p16INK4a(0.13±0.03)화거린산화Rb(0.45±0.05)단백표체수평균하강(P＜0.05).여Tfm조비교,Tfm+T조SOD활성증가,MDA함량、p16INK4a화거린산화Rb단백표체수평하강(P＜0.05).거세+T조여Tfm+T조비교차이무통계학의의(P＞0.05). 결론 생리제량고동치료통과비AR의뢰적궤제연완심기세포쇠로.
Objective To explore whether physiological doses of testosterone therapy can modulate cardiomyocyte aging via classical androgen receptor (AR) dependent pathways.Methods Male C57BL/6J mice and testicular feminized (Tfm) mice were divided into five experimental groups:the control group (n=8),the castrated group (n=8),the Tfm group (n=7),the testosterone treated castrated group (n=8),and the testosterone-treated Tfm group (n =8).After isolation of cardiomyocytes from the left ventricle,the activity of superoxide dismutase (SOD) and the amount of malondialdehyde (MDA) were measured using colorimetry,and the expression of the p16INK4a and retinoblastoma (Rb) proteins was detected by Western blotting.Results Compared with the control group,the activity of SOD in the castrated group and the Tfm group declined [(16.55±1.18) U/ml,(17.30±1.32) U/ml vs.(21.57±2.21)U/ml,P＜0.05)],the amount of MDA increased [(7.78±1.27)μmol/L,(6.52±0.82)μmol/L vs.(3.48±0.70)μmol/L],P＜0.01,and the expression of both the p16INK4aand Rb proteins increased [(0.37±0.08),(0.45±0.06) vs.(0.14±0.02),forp16INK4a,P＜0.05; (0.74±0.05),(0.79±0.08) vs.(0.40±0.05),for Rb,P＜0.05].Compared with the castrated group,the activity of SOD in the testosterone treated castrated group increased [(23.00±0.58)U/ml vs.(16.55±1.18) U/ml,P＜0.01],the amount of MDA decreased [(2.63±0.90) μmol/L vs.(7.78±1.27) μmol/L,P＜0.01],and the p16INK4a and Rb proteins were both downregulated (0.13 ± 0.03 vs.0.37± 0.08),for p16INK4a,P＜0.05; (0.45 ±0.05) vs.(0.79±0.08),for Rb P＜0.05.Compared with the Tfm group,the activity of SOD in testosterone-treated Tfm group increased,the amount of MDA decreased,and the p16IN4a and Rb proteins were both downregulated (P＜ 0.05).No significant differences in these markers were detected between the testosterone-treated castrated group and the testosterone-treated Tfm group.Conclusions Physiological doses of testosterone can retard cardiomyocyte aging via androgen receptor independent pathways.
