PL-011 Astaxanthin Reduces High Intensity Training Induced Myocardial Cell Apoptosis Via Activating Nrf2 in Rats

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Abstract

Objective Long-term intensive training may led to ischemia oxygen reaction and increase the ROS. Astaxanthin, as the super antioxidant, was investigated to against anti-oxidative stress. By supplementing the astaxanthin, we wanted to observe if it can mediated Nrf2 reduces myocardial cell oxidative injury in rats after high intensity training of 6 weeks. 

Methods 7-week SD male rats were divided into 3 groups randomly: control group ( C group，n =10)，high intensity training group ( HT group，n = 15)，astaxanthin and high intensity training group (HTA group，n = 15) . The rats in HTA group were given with astaxanthin 20 mg /kg·d and in HT group were given with oil during the training day．The serum cTnI，myocardial apoptosis index,  the expression of myocardial BAX, Bcl2, Nrf2, HO-1, myocardial MDA，SOD and T- AOC activity were measured 24 hours after the last training．

Results After 6-week tranning of high intensity, compared with group C, the serum cTNI, myocardial apoptosis index, the expression of BAX and myocardial MDA were significantly higher in group HT(P<0.01).The Bcl2/Bax, the expression of HO-1, SOD and T-AOC activity were significantly declined (P<0.01). After the intervention of 6-week astaxanthin, compared with group HT, the serum cTNI, myocardial MDA, the myocardial apoptosis index, the expression of BAX were significantly lower in HTA group (cTNI(ng/ml): 1.16±0.27 VS 2.47±0.39, P<0.05; myocardial apoptosis index: 164.27±3.98 VS 196.20±9.65, P<0.01; BAX: 58.40±5.95 VS 78.03±3.80, P<0.01 ). Finally, Bcl2/Bax, SOD, T-AOC activity, the expression of Nrf2 and HO-1 were significantly higher  (Bcl2/Bax : 1.92±0.10 VS 1.19±0.18, P<0.01; SOD(U/mg): 52.38±6.15 VS 38.32±3.36, P<0.01; T-AOC(U/mg): 30.22±4.07 VS 23.76±3.20, P<0.01; Nrf2: 93.61±8.53 VS 74.26±6.69, P<0.01; HO-1: 84.99±13.78 VS 64.22±11.39, P<0.05). 

Conclusions The supplement of astaxanthin can mediate Nrf2 signaling pathway, and elevate the expression of Nrf2 and HO-1. Then it can increase the activity of SOD and T-AOC and reduce the myocardial oxidative level and myocardial apoptosis in rats caused by 6-week high intensity training. Finally, the structure and function of heart tissue are back to normal.