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Abstract：
BACKGROUND: This study evaluated the effects of concurrent isolated training (T) or training combined with the antioxidant N-acetylcysteine (NAC) on cardiac remodeling and oxidative stress in spontaneously hypertensive rats (SHR).
METHODS: Six-month-old male SHR were divided into sedentary (S, n = 12), concurrent training (T, n = 13), sedentary supplemented with NAC (SNAC, n = 13), and concurrent training with NAC supplementation (TNAC, n = 14) groups. T and TNAC rats were trained three times a week on a treadmill and ladder; NAC supplemented groups received 120 mg/kg/day NAC in rat chow for eight weeks. Myocardial antioxidant enzyme activity and lipid hydroperoxide concentration were assessed by spectrophotometry. Gene expression of NADPH oxidase subunits Nox2, Nox4, p22 phox, and p47 phox was evaluated by real time RT-PCR. Statistical analysis was performed using ANOVA and Bonferroni or Kruskal-Wallis and Dunn.
RESULTS: Echocardiogram showed concentric remodeling in TNAC, characterized by increased relative wall thickness (S 0.40 ± 0.04; T 0.39 ± 0.03; SNAC 0.40 ± 0.04; TNAC 0.43 ± 0.04 *; * p < 0.05 vs T and SNAC) and diastolic posterior wall thickness (S 1.50 ± 0.12; T 1.52 ± 0.10; SNAC 1.56 ± 0.12; TNAC 1.62 ± 0.14 * mm; * p < 0.05 vs T), with improved contractile function (posterior wall shortening velocity: S 39.4 ± 5.01; T 36.4 ± 2.96; SNAC 39.7 ± 3.44; TNAC 41.6 ± 3.57 * mm/s; * p < 0.05 vs T). Myocardial lipid hydroperoxide concentration was lower in NAC treated groups (S 210 ± 48; T 182 ± 43; SNAC 159 ± 33 *; TNAC 110 ± 23 *# nmol/g tissue; * p < 0.05 vs S, # p < 0.05 vs T and SNAC). Nox 2 and p22 phox expression was higher and p47 phox lower in T than S [S 1.37 (0.66-1.66); T 0.78 (0.61-1.04) *; SNAC 1.07 (1.01-1.38); TNAC 1.06 (1.01-1.15) arbitrary units; * p < 0.05 vs S]. NADPH oxidase subunits did not differ between TNAC, SNAC, and S groups.
CONCLUSIONS: N-acetylcysteine supplementation alone reduces oxidative stress in untreated spontaneously hypertensive rats. The combination of N-acetylcysteine and concurrent exercise further decreases oxidative stress. However, the lower oxidative stress does not translate into improved cardiac remodeling and function in untreated spontaneously hypertensive rats.
METHODS: Six-month-old male SHR were divided into sedentary (S, n = 12), concurrent training (T, n = 13), sedentary supplemented with NAC (SNAC, n = 13), and concurrent training with NAC supplementation (TNAC, n = 14) groups. T and TNAC rats were trained three times a week on a treadmill and ladder; NAC supplemented groups received 120 mg/kg/day NAC in rat chow for eight weeks. Myocardial antioxidant enzyme activity and lipid hydroperoxide concentration were assessed by spectrophotometry. Gene expression of NADPH oxidase subunits Nox2, Nox4, p22 phox, and p47 phox was evaluated by real time RT-PCR. Statistical analysis was performed using ANOVA and Bonferroni or Kruskal-Wallis and Dunn.
RESULTS: Echocardiogram showed concentric remodeling in TNAC, characterized by increased relative wall thickness (S 0.40 ± 0.04; T 0.39 ± 0.03; SNAC 0.40 ± 0.04; TNAC 0.43 ± 0.04 *; * p < 0.05 vs T and SNAC) and diastolic posterior wall thickness (S 1.50 ± 0.12; T 1.52 ± 0.10; SNAC 1.56 ± 0.12; TNAC 1.62 ± 0.14 * mm; * p < 0.05 vs T), with improved contractile function (posterior wall shortening velocity: S 39.4 ± 5.01; T 36.4 ± 2.96; SNAC 39.7 ± 3.44; TNAC 41.6 ± 3.57 * mm/s; * p < 0.05 vs T). Myocardial lipid hydroperoxide concentration was lower in NAC treated groups (S 210 ± 48; T 182 ± 43; SNAC 159 ± 33 *; TNAC 110 ± 23 *# nmol/g tissue; * p < 0.05 vs S, # p < 0.05 vs T and SNAC). Nox 2 and p22 phox expression was higher and p47 phox lower in T than S [S 1.37 (0.66-1.66); T 0.78 (0.61-1.04) *; SNAC 1.07 (1.01-1.38); TNAC 1.06 (1.01-1.15) arbitrary units; * p < 0.05 vs S]. NADPH oxidase subunits did not differ between TNAC, SNAC, and S groups.
CONCLUSIONS: N-acetylcysteine supplementation alone reduces oxidative stress in untreated spontaneously hypertensive rats. The combination of N-acetylcysteine and concurrent exercise further decreases oxidative stress. However, the lower oxidative stress does not translate into improved cardiac remodeling and function in untreated spontaneously hypertensive rats.
摘要：
背景：这项研究评估了同时进行的孤立训练（T）或与抗氧化剂N-乙酰半胱氨酸（NAC）结合的训练对自发性高血压大鼠（SHR）心脏重塑和氧化应激的影响。
方法：将六个月大的男性SHR分为久坐（S，n=12),并发训练(T，n=13),久坐辅以NAC(SNAC，n=13),并同时进行NAC补充培训(TNAC，n=14)组。T和TNAC大鼠每周在跑步机和梯子上训练三次；补充NAC的组在大鼠食物中接受120mg/kg/天的NAC，持续八周。通过分光光度法评估心肌抗氧化酶活性和脂质过氧化氢浓度。NADPH氧化酶亚基Nox2,Nox4,p22phox,通过实时RT-PCR评估p47phox。使用ANOVA和Bonferroni或Kruskal-Wallis和Dunn进行统计分析。
结果：超声心动图显示TNAC同心重构，特征为相对壁厚增加（S0.40±0.04；T0.39±0.03；SNAC0.40±0.04；TNAC0.43±0.04*；*p<0.05vs.T和SNAC）和舒张后壁厚度（S1.50±0.12；T1.52±0.10；SNAC1.56±0.12；TNAC1.62±0.14*mm；*p<0.05vsT），收缩功能改善(后壁缩短速度:S39.4±5.01;T36.4±2.96;SNAC39.7±3.44;TNAC41.6±3.57*mm/s;*p<0.05vsT)。NAC治疗组心肌脂质过氧化氢浓度较低(S210±48;T182±43;SNAC159±33*;TNAC110±23*#nmol/g组织;*p<0.05vs.S,#p<0.05vs.T和SNAC)。T中Nox2和p22phox表达高于S，p47phox表达低于S[S1.37（0.66-1.66）；T0.78（0.61-1.04）*；SNAC1.07（1.01-1.38）；TNAC1.06（1.01-1.15）任意单位；*p<0.05vs.S]。NADPH氧化酶亚基在TNAC之间没有差异，SNAC,S组。
结论：单独补充N-乙酰半胱氨酸可降低未经治疗的自发性高血压大鼠的氧化应激。N-乙酰半胱氨酸和同时运动的组合进一步降低了氧化应激。然而,在未经治疗的自发性高血压大鼠中，较低的氧化应激不能转化为改善的心脏重塑和功能。
方法：将六个月大的男性SHR分为久坐（S，n=12),并发训练(T，n=13),久坐辅以NAC(SNAC，n=13),并同时进行NAC补充培训(TNAC，n=14)组。T和TNAC大鼠每周在跑步机和梯子上训练三次；补充NAC的组在大鼠食物中接受120mg/kg/天的NAC，持续八周。通过分光光度法评估心肌抗氧化酶活性和脂质过氧化氢浓度。NADPH氧化酶亚基Nox2,Nox4,p22phox,通过实时RT-PCR评估p47phox。使用ANOVA和Bonferroni或Kruskal-Wallis和Dunn进行统计分析。
结果：超声心动图显示TNAC同心重构，特征为相对壁厚增加（S0.40±0.04；T0.39±0.03；SNAC0.40±0.04；TNAC0.43±0.04*；*p<0.05vs.T和SNAC）和舒张后壁厚度（S1.50±0.12；T1.52±0.10；SNAC1.56±0.12；TNAC1.62±0.14*mm；*p<0.05vsT），收缩功能改善(后壁缩短速度:S39.4±5.01;T36.4±2.96;SNAC39.7±3.44;TNAC41.6±3.57*mm/s;*p<0.05vsT)。NAC治疗组心肌脂质过氧化氢浓度较低(S210±48;T182±43;SNAC159±33*;TNAC110±23*#nmol/g组织;*p<0.05vs.S,#p<0.05vs.T和SNAC)。T中Nox2和p22phox表达高于S，p47phox表达低于S[S1.37（0.66-1.66）；T0.78（0.61-1.04）*；SNAC1.07（1.01-1.38）；TNAC1.06（1.01-1.15）任意单位；*p<0.05vs.S]。NADPH氧化酶亚基在TNAC之间没有差异，SNAC,S组。
结论：单独补充N-乙酰半胱氨酸可降低未经治疗的自发性高血压大鼠的氧化应激。N-乙酰半胱氨酸和同时运动的组合进一步降低了氧化应激。然而,在未经治疗的自发性高血压大鼠中，较低的氧化应激不能转化为改善的心脏重塑和功能。
