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KMID : 0387420090200010147
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Korean Society of Oriental Neuropsychiatry
2009 Volume.20 No. 1 p.147 ~ p.164
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A Molecular Study of Sopungsungi-won(Shufengshunqiyuan) about Regulation of PPARs in Mouse NMu2Li Liver Cells and C2C12 Skeletal Muscle Myogenic Progenital Cells
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Oh Young-Jin
Shin Soon-Shik
Yoon Mi-Chung
Kim Bo-Kyung
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Abstract
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Objective: We investigated the effects of Sopungsungi-won(Shufengshunqiyuan) (SSEx1, SSEx2) to treat the metabolic syndrome by the molecular mechanism of regulation of PPAR and modulation of mitochondrial MCAD, VLCAD mRNA expression.
Methods: Mouse NMu2Li liver cells and C2C12 skeletal muscle myogenic progenital cells were transiently transfected with expression plasmids for PPAR(PPARα, PPARδ), a luciferase reporter gene construct containing 3 copies of the PPRE from the rat acyl-CoA oxidase gene and β-galactosidase gene. Cells were treated with several concentrated kinds of SSEx1, SSEx2 at the initial time of culture and analyzed PPARα, PPARδ reporter gene activity using spectrophotometer (405 nm). Total RNA was extracted from SSEx1, SSEx2 and measured mRNA levels of mitochondrial MCAD, VLCAD. Representative RT-PCR bands are shown.
Results: 1. SSEx1 increased the expression of PPARα reporter gene activities at 0.1 μg/ml (p<0.01) and 10 μg/ml (p<0.05), SSEx2 at 0.1 μg/ml (p<0.01) and 1 μg/ml (p<0.05) significantly in NMu2Li liver cell lines. 2. SSEx1 increased the expression of PPARα reporter gene activities at 1 μg/ml (p<0.01), SSEx2 at 0.1 μg/ml (p<0.01) significantly in C2C12 skeletal muscle cells. 3. SSEx1, SSEx2 both showed no significant changes of the expression of PPARδ reporter gene activities in C2C12 skeletal muscle cells. 4. SSEx1 increased the modulation of mitochondrial MCAD mRNA expression (p<0.05) significantly in NMu2Li liver cell lines. 5. SSEx1, SSEx2 both increased the modulation of mitochondrial MCAD mRNA expression (p<0.05) significantly in C2C12 skeletal muscle cells.
Conclusions: These results show the SSEx1, SSEx2 can be used as therapeutic agent for metabolic syndrome and it’s molecular mechanisms of PPAR more contribute to the activation of PPARα then PPARδ reporter gene activities and it’s total RNA more contribute to the modulation of mitochondrial MCAD then VLCAD mRNA expression.
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KEYWORD
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Sopungsungi-won(Shufengshunqiyuan) (SSEx1, SSEx2), PPARα, PPARδ, MCAD, VLCAD, metabolic syndrome
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