*P < 0.05 and # P < 0.01 vs CS; ★ P < 0.05 and ※< 0.01 vs SE; △ P < 0.01 vs ES. Exhaustive QNZ order exercise induces the generation of free radicals which may cause an increase in lipid peroxidation [21]. Measuring MDA is one of the most widely used approaches for evaluating oxidative damage to lipids. Figure 3b illustrates that the plasmic MDA levels of SE or ES-LBP rats significantly decreased compared with that of ES rats (P<0.05 and P< 0.01 respectively). This result indicates that LBPs can attenuate lipid peroxidation. NO is an important vasodiator factor produced by vascular endothelial cells. We found that there was a significant increase in the SE

group. As expected, the NO level was significantly reduced by exhaustive exercise. Further, Epoxomicin mw we found this reduction induced by exhaustive exercise could be reversed by LBPs treatment (Figure 3c). The expression of heat shock proteins (HSPs) is induced by hyperthermia GW786034 concentration ischemia, oxidative cytokine, muscular stress, glucose deprivation, alterations in calcium and pH [22]. HSP70 is a group of binding proteins with molecular weight of 70 KD, which is significantly increased by high-intensity exercise [23]. To determine the expression of HSP70 after exercise and supplement with LBPs, the plasmic level of HSP70, analyzed by ELISA, showed

an immediate increase after both exercise sessions. As shown in Figure 3d, the HSP70 levels of SE or ES rats were increased. Furthermore, LBPs treatment induced a much higher increase in the ES group (P< 0.01). Expression of eNOS mRNA As the NO level can be up-regulated by LBPs, we therefore examined the effect of LBPs on the expression of eNOS in the aorta after exhaustive exercise. The expression of eNOS mRNA in aorta of four groups was shown Mirabegron in Figure 4. There were significant differences in the eNOS mRNA expression level among different groups. The eNOS expression was increased in both SE and ES-LBP groups (P < 0.01). However, the level of eNOS expression was significantly attenuated in rats after exhaustive exercise (P < 0.01). LBPs treatment significantly

reversed the inhibition of the eNOS expression in rats from ES group (p < 0.01). Figure 4 Effects of LBPs on eNOS mRNA expression in thoracic aorta separated from rats in different groups. Values are expressed as mean ± SD (n = 10). # P<0.01 vs CS; △ P<0.01 vs ES. Discussion The effects of LBPs on vascular vasoreactivity in exhaustive exercise rats were investigated. The major finding of this study was that the contraction induced by NA in thoracic aorta was increased in the presence of exhaustive exercise. Furthermore, supplementation with the LBPs for 4 weeks remarkably improved the vascular reactivity of ES-LBP rats compared to the ES rats (Figure 1). As the arterial compliance is judged by the responsiveness to NA, the results showed that the compliance or distensibility of aorta was increased in LBPs treated animals [24].