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收稿:2016-12-14,
纸质出版:2017-08-30
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顾业芸, 周启程, 公欣华, 等. 二氢山奈酚衍生物调控AMPK/PGC-1α通路抑制棕榈酸诱导的C2C12成肌分化细胞脂质沉积[J]. 第三军医大学学报, 2017,39(16):1606-1611.
Yeyun GU, Qicheng ZHOU, Xinhua GONG, et al. Dihydrokaempferol derivatives inhibit palmitic acid-induced lipid deposition in C2C12 myotubes through AMPK/PGC-1α pathway[J]. Journal of Third Military Medical University, 2017, 39(16): 1606-1611.
顾业芸, 周启程, 公欣华, 等. 二氢山奈酚衍生物调控AMPK/PGC-1α通路抑制棕榈酸诱导的C2C12成肌分化细胞脂质沉积[J]. 第三军医大学学报, 2017,39(16):1606-1611. DOI: 10.16016/j.1000-5404.201612097.
Yeyun GU, Qicheng ZHOU, Xinhua GONG, et al. Dihydrokaempferol derivatives inhibit palmitic acid-induced lipid deposition in C2C12 myotubes through AMPK/PGC-1α pathway[J]. Journal of Third Military Medical University, 2017, 39(16): 1606-1611. DOI: 10.16016/j.1000-5404.201612097.
Objective
2
To determine the effects of 4 derivatives from dihydrokaempferol on lipid deposition in C2C12 myotubes (C2C12-MD cells) and investigate the underlying mechanisms.
Methods
2
Mouse C2C12 myoblasts were differentiated into myotubes and then treated by palmitic acid (PA) alone or in combination with 4 derivatives of dihydrokaempferol (kaempferol
dihydromyricetin
myricetin and quercetin) respectively. Lipid deposition was evaluated by oil red O staining and triglyceride (TG) content measurement. Glucose uptake was measured by using 2-NBDG fluorescent probe. The protein levels of AMP-activated protein kinase (AMPK)
phosphorylated AMPK (p-AMPK) and peroxisome proliferator activator receptor gamma coactivator-1alpha (PGC-1α) were detected by Western blotting.
Results
2
PA induced more lipid deposition
significantly increased TG content
and significantly decreased glucose uptake under insulin stimul
ation as well as the protein levels of p-AMPK and PGC-1α in C2C12 myotubes (
P
<
0.05). Kaempferol treatment had no significant effects on these changes induced by PA. However
the other 3 derivatives markedly inhibited these changes induced by PA
and dihydromyricetin showed a stronger inhibitory effect (
P
<
0.05). Moreover
AMPK inhibitor compound C could significantly reverse the inhibitory effect of dihydromyricetin (
P
<
0.05).
Conclusion
2
Three derivatives of dihydrokaempferol (dihydromyricetin
myricetin and quercetin) inhibit PA-induced lipid deposition in C2C12-MD cells through AMPK/PGC-1α signaling pathway
and thereby improve insulin resistance.
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