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Oxid Med Cell Longev
2020 Jun 26;2020:4604387. doi: 10.1155/2020/4604387.
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Sea Cucumber Peptides Improved the Mitochondrial Capacity of Mice: A Potential Mechanism to Enhance Gluconeogenesis and Fat Catabolism during Exercise for Improved Antifatigue Property.
Yu Y
,
Wu G
,
Jiang Y
,
Li B
,
Feng C
,
Ge Y
,
Le H
,
Jiang L
,
Liu H
,
Shi Y
,
Le G
.
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Sea cucumber promotes multifaceted health benefits. However, the mechanisms of sea cucumber peptides (Scp) regulating the antifatigue capacity is still unknown. The present study is aimed at further elucidating the effects and mechanisms of Scp on the antifatigue capacity of mice. At first, C57BL/6J mice were assigned into four groups named Con, L-Scp, M-Scp, and H-Scp and received diets containing Scp (0%, 0.15%, 0.3%, and 0.5%, respectively) for continuous 30 days. On the 21th day, a fore grip test was conducted on mice. On the 25th day, a rotating rod test was conducted on mice. On the 30th day, the quantities of glycogen and mitochondrial DNA (mtDNA) were determined in 8 random mice and another 8 mice were forced to swim for 1 hour before slaughter for detecting biochemical indicators. It was observed that the Scp groups significantly prolonged the running time in rotarod, increased forelimb grip strength, improved lactic acid (LD) and urea nitrogen (BUN) levels in the serum, decreased lactic dehydrogenase (LDH) and glutamic oxalacetic transaminase (GOT) activities in the serum, increased blood glucose (BG) and glycogen (GN) levels in the liver and skeletal muscle after swimming, increased the activity of Na+-K+-ATPase and Ca2+-Mg2+-ATPase in the skeletal muscle and heart, and improved antioxidant capacity. Furthermore, Scp treatment significantly elevated the mRNA and protein relative levels of power-sensitive factors, lipid catabolism, and mitochondrial biogenesis and significantly upregulated mRNA levels of gluconeogenesis. Besides, mtDNA before the swimming test was increased in the three Scp groups. These results show that Scp treatment has antifatigue capacity. Furthermore, these results suggest that improved energy regulation and antioxidant capacity may be the result of improved mitochondrial function.
Figure 1. The molecular weight distribution of SCP.
Figure 2. Effects of Scp on body weight, exercise-related organ weight, and feed intake. (a) Bodyweight, (b) daily feed intake, (c) the actual Scp daily intake, (d) heart weight, and (e) skeletal muscle weight. Con: the control group; L-Scp: Scp low-dose group; M-Scp: Scp moderate-dose group; H-Scp: Scp high-dose group. All data are presented as mean ± SEM (n = 16).
Figure 3. Effects of Scp on the forelimb grip strength (a) and rotarod performance (b). All data are presented as mean ± SEM (n = 16). Con: the control group; L-Scp: Scp low-dose group; M-Scp: Scp moderate-dose group; H-Scp: Scp high-dose group. The means marked with superscript letters are significantly different relative to others.
Figure 4. Effects of Scp on fatigue-related biochemical indicators. (a) Muscular LD, (b) plasma LD, (c) plasma BUN, (d) plasma LDH, (e) plasma GOT, (f) BG, (g) liver glycogen before and after exercise, and (h) muscle glycogen before and after exercise. Con: the control group; L-Scp: Scp low-dose group; M-Scp: Scp moderate-dose group; H-Scp: Scp high-dose group. All data are presented as mean ± SEM (n = 8). The means marked with superscript letters are significantly different relative to others.
Figure 5. Effects of Scp on the levels of mRNA expression and protein expression of lipid metabolism and glycometabolism. (a–d) mRNA expression levels: (a) hepatic lipid metabolism, (b) heart lipid metabolism, (c) muscle lipid metabolism, and (d) liver gluconeogenesis. Protein levels of the lipid metabolism and gluconeogenesis regulatory elements: (e) the western band and (f) relative protein expression levels of PGC1α and PPARα in the liver, PPARα in the heart, and PPARδ in the muscle. Con: the control group; L-Scp: Scp low-dose group; M-Scp: Scp moderate-dose group; H-Scp: Scp high-dose group. All data are presented as mean ± SEM (n = 8). The means marked withsuperscript letters are significantly different relative to others.
Figure 6. Effects of Scp on cell energy sensors. (a–f) mRNA expression levels: (a) liver AMPK, (b) muscle AMPK, (c) heart AMPK, (d) liver SIRT1, (e) muscle SIRT1, and (f) heart SIRT1. (g) pAMPK, AMPK, and SIRT1 Western blotting bands in the liver, skeletal muscle, and heart. (h) Relative protein expression levels of AMPK and SIRT1 in the liver, skeletal muscle, and heart. Con: the control group; L-Scp: Scp low-dose group; M-Scp: Scp moderate-dose group; H-Scp: Scp high-dose group. All data are presented as mean ± SEM (n = 8). The means marked with superscript letters are significantly different relative to others.
Figure 7. Effects of Scp on the mitochondrial biogenesis and adaptions. (a, b) ATPase activity, the activity of Na+K+ATPase and Ca2+Mg2+ATPase in muscle (a) and heart (b). (c) mtDNA content. (d) mRNA expression levels regarding mitochondrial biogenesis and adaption in skeletal muscle. (e) mRNA expression levels regarding mitochondrial biogenesis and adaption in the heart. (f) PGC1α and TFAM Western blotting bands in the skeletal muscle and heart. (g) relative protein expression levels of PGC1α and TFAM in skeletal muscle. (h) Relative protein expression levels of PGC1α TFAM in heart. Con: the control group; L-Scp: Scp low-dose group; M-Scp: Scp moderate-dose group; H-Scp: Scp high-dose group. All data are presented as mean ± SEM (n = 8). The means marked with superscript letters are significantly different relative to others.
Figure 8. Effects of Scp on oxidative stress and antioxidant-related biochemical indicators. (a) MDA levels in plasma and tissues. (b) TAC levels in plasma and tissues. (c) GPX activities in plasma and tissues. (d) CAT activities in tissues. All data are presented as mean ± SEM (n = 8). The means marked with superscript letters are significantly different relative to others.
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