CAJ | 학술논문

目的：观察硫氧环蛋白过氧化物酶3（Prdx-3）在血管紧张素Ⅱ（AngⅡ）诱导心肌细胞肥大中的作用，并探讨其作用机制。方法体外培养心肌细胞（H9C2）随机分为对照组、AngⅡ组、AngⅡ+转染对照组和AngⅡ+Prdx-3转染组。脂质体转染法将Prdx-3表达质粒转染心肌细胞，Western blot法检测Prdx-3蛋白表达，Real-time PCR法检测脑钠素（BNP）mRNA表达，二氯荧光素二乙酸（DCFH-DA）检测活性氧（ROS）水平。结果 Prdx-3表达质粒转染心肌细胞后，Prdx-3蛋白表达值为（0.88±0.12），高于转染对照组（0.38±0.05），差异有统计学意义（P<0.05）。与对照组比较，AngⅡ组BNP mRNA[（1.00±0.00）比（1.72±0.29）]、ROS[（3473±81）比（4439±111）]及Prdx-3蛋白表达水平[（0.33±0.05）比（0.72±0.14）]均明显增加，差异均有统计学意义（均P<0.05）。 AngⅡ+转染对照组和AngⅡ组的BNP mRNA [（1.72±0.29）比（1.94±0.34）]、ROS [（4439±111）比（4285±167）]及Prdx-3蛋白水平[（0.72±0.14）比（0.75±0.11）]比较，差异无统计学意义（P>0.05）。与AngⅡ组比较，AngⅡ+Prdx-3转染组BNP mRNA [（1.72±0.29）比（1.29±0.15）]和ROS水平[（4439±111）比（3648±254）]明显下降，但Prdx-3蛋白水平[（0.72±0.14）比（1.89±0.37）]显著增高，差异均有统计学意义（均P<0.05）。结论 AngⅡ可通过ROS诱导心肌细胞肥大，而Prdx-3通过降低ROS抑制AngⅡ的作用。
목적：관찰류양배단백과양화물매3（Prdx-3）재혈관긴장소Ⅱ（AngⅡ）유도심기세포비대중적작용，병탐토기작용궤제。방법체외배양심기세포（H9C2）수궤분위대조조、AngⅡ조、AngⅡ+전염대조조화AngⅡ+Prdx-3전염조。지질체전염법장Prdx-3표체질립전염심기세포，Western blot법검측Prdx-3단백표체，Real-time PCR법검측뇌납소（BNP）mRNA표체，이록형광소이을산（DCFH-DA）검측활성양（ROS）수평。결과 Prdx-3표체질립전염심기세포후，Prdx-3단백표체치위（0.88±0.12），고우전염대조조（0.38±0.05），차이유통계학의의（P<0.05）。여대조조비교，AngⅡ조BNP mRNA[（1.00±0.00）비（1.72±0.29）]、ROS[（3473±81）비（4439±111）]급Prdx-3단백표체수평[（0.33±0.05）비（0.72±0.14）]균명현증가，차이균유통계학의의（균P<0.05）。 AngⅡ+전염대조조화AngⅡ조적BNP mRNA [（1.72±0.29）비（1.94±0.34）]、ROS [（4439±111）비（4285±167）]급Prdx-3단백수평[（0.72±0.14）비（0.75±0.11）]비교，차이무통계학의의（P>0.05）。여AngⅡ조비교，AngⅡ+Prdx-3전염조BNP mRNA [（1.72±0.29）비（1.29±0.15）]화ROS수평[（4439±111）비（3648±254）]명현하강，단Prdx-3단백수평[（0.72±0.14）비（1.89±0.37）]현저증고，차이균유통계학의의（균P<0.05）。결론 AngⅡ가통과ROS유도심기세포비대，이Prdx-3통과강저ROS억제AngⅡ적작용。
Objective To study the effect of peroxiredoxin-3 (Prdx-3, a noval type of peroxidase) on AngiotensinII(AngII)-induced cardiomyocytes hypertrophy and explore the precious mechanism. Methods Cultured cardiomyocytes (H9C2) were randomly divided into four groups: control group, AngII group, Ang II+vehicle (plasmid without prdx-3 gene) group, AngII+Prdx-3 plasmid group. Prdx-3 was transfected into cardiomyocytes using the liposome infection. Western blot was used to evaluate Prdx-3 expression in cardiomyocytes, while levels of brain natriuretic peptide (BNP) mRNA and reactive oxygen species (ROS) were measured by Real-time PCR and DCFH-DA. Results The expression of Prdx-3 protein in transfected cardiomyocytes (0.88±0.12) was significantly higher than vehicle (0.38±0.05, P<0.05). Compared with control group, expressions of BNP mRNA, ROS and Prdx-3 in AngII group all increased [(1.00±0.00) vs (1.72±0.29), (3473±81) vs (4439±111), (0.33±0.05) vs (0.72±0.14), P< 0.05]. The difference of expressions of BNP mRNA [(1.72±0.29) vs (1.94±0.34)], ROS [(4439±111) vs (4285±167)] and Prdx-3[(0.72±0.14) vs (0.75±0.11)] between AngII and AngII+vehicle groups were not statistically significant (P> 0.05). Compared with Ang II, expressions of BNP mRNA and ROS in AngII+Prdx-3 plasmid group were lower [(1.72±0.29) vs (1.29±0.15), (4439±111) vs (3648±254), P<0.05], while Prdx-3 level was further higher [(0.72±0.14) vs (1.89±0.37), P<0.05]. Conclusion AngII in-duced cardiomyocytes to generate ROS, which contributes to cell hypertrophy;however, Prdx-3 over-expression inhibits these changes by decreasing ROS level.