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Mar Drugs
2014 Aug 21;128:4602-15. doi: 10.3390/md12084602.
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Echinochrome a increases mitochondrial mass and function by modulating mitochondrial biogenesis regulatory genes.
Jeong SH
,
Kim HK
,
Song IS
,
Noh SJ
,
Marquez J
,
Ko KS
,
Rhee BD
,
Kim N
,
Mishchenko NP
,
Fedoreyev SA
,
Stonik VA
,
Han J
.
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Echinochrome A (Ech A) is a natural pigment from sea urchins that has been reported to have antioxidant properties and a cardio protective effect against ischemia reperfusion injury. In this study, we ascertained whether Ech A enhances the mitochondrial biogenesis and oxidative phosphorylation in rat cardio myoblast H9c2 cells. To study the effects of Ech A on mitochondrial biogenesis, we measured mitochondrial mass, level of oxidative phosphorylation, and mitochondrial biogenesis regulatory gene expression. Ech A treatment did not induce cytotoxicity. However, Ech A treatment enhanced oxygen consumption rate and mitochondrial ATP level. Likewise, Ech A treatment increased mitochondrial contents in H9c2 cells. Furthermore, Ech A treatment up-regulated biogenesis of regulatory transcription genes, including proliferator-activated receptor gamma co-activator (PGC)-1α, estrogen-related receptor (ERR)-α, peroxisome proliferator-activator receptor (PPAR)-γ, and nuclear respiratory factor (NRF)-1 and such mitochondrial transcription regulatory genes as mitochondrial transcriptional factor A (TFAM), mitochondrial transcription factor B2 (TFB2M), mitochondrial DNA direct polymerase (POLMRT), single strand binding protein (SSBP) and Tu translation elongation factor (TUFM). In conclusion, these data suggest that Ech A is a potentiated marine drug which enhances mitochondrial biogenesis.
Figure 5. Echinochrome A modulated proliferator-activated receptor gamma co-activator (PGC)-1α expression via phosphorylation of CREB. Ech A treatment increased phosphorylation of CREB. Also PGC-1α was increased.
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