香菇多糖
罗格列酮
蛋白激酶B
化学
过氧化物酶体增殖物激活受体
信使核糖核酸
PI3K/AKT/mTOR通路
内分泌学
内科学
信号转导
分子生物学
受体
生物
生物化学
医学
基因
多糖
作者
D G Li,J L Li,Daqing Sun,Xiaodan Sun,Q Liu
出处
期刊:Genetics and Molecular Research
[Genetics and Molecular Research]
日期:2015-01-01
卷期号:14 (3): 8084-8090
被引量:6
标识
DOI:10.4238/2015.july.17.17
摘要
We investigated the mechanism of the effect of lentinan on 3T3-L1 fat cell formation by inhibiting the peroxisome proliferator-activated receptor gamma (PPARγ)/protein kinase B (AKT) signaling pathway. 3T3-L1 fat cells were treated with 80 mM lentinan with or without the PPARγ activator, 100 mM rosiglitazone for 24 h. Reverse transcription-polymerase chain reaction was applied to detect PPARγ and AKT mRNA expression levels. Western blotting was used to detect AKT protein expression level. Compared with the control group, 80 mM lentinan increased PPARγ mRNA expression and downregulated AKT mRNA expression. After treatment with rosiglitazone, PPARγ mRNA expression increased by 78% (P < 0.05), while AKT mRNA expression decreased by 71% (P < 0.05). Lentinan treatment decreased AKT protein expression by 33%, and AKT protein expression in the lentinan and rosiglitazone co-treatment group was reduced by 28% compared with the lentinan treatment group. We found that 80 mM lentinan increased PPARγ mRNA expression and reduced AKT mRNA. Combination treatment with rosiglitazone increased this effect. This suggests that lentinan can depress 3T3-L1 fat cell formation by inhibiting the PPARγ/AKT signaling pathway.
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