Effect of Tumor Necrosis Factor-α on Resistin Expression in 3T3-L1 Adipocytes and Its Mechanism
- Author:
Zaigang YANG
1
;
Muxun ZHANG
;
Lijun XU
;
Jianhua ZHANG
;
Hongwei WANG
Author Information
1. Tongji Hospital, Tongji Medical College, HuazhongUniversity of Science and Technology
- Keywords:
tumor necrosis factor-α;
resistin;
3T3-L1 adipocyte;
mechanism
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2005;25(2):121-123,130
- CountryChina
- Language:Chinese
-
Abstract:
In order to investigate the effect of tumor necrosis factor-α (TNFα) on resistin expression in 3T3-L1 adipocytes, and further explore its mechanisms, the differentiated 3T3-L1 adipocytes were incubated with 0, 1, 10, 100 ng/mL TNFα respectively for 24 h, and then the expression of resistin was determined. The differentiated 3T3-L1 adipocytes were incubated with 100 ng/mL TNFα for 3, 6, 24 h respectively, and then the expression of resistin mRNA was analyzed.3T3-L1 adipocytes were induced to differentiate into mature adipocytes. The cells were randomly divided into 4 groups for culture. In the control group, no drugs were added. Cells of TNFα group were treated with 100 ng/mL TNFα. In Ro-31-8220 group, 5μmol/L protein kinase C inhibitor Ro-31-8220 was added. With TNFα+Ro-31-8220 group, 100 ng/mL TNFα were added 1 h after the addition of 5 μmol/L Ro-31-8220. All adipocytes were cultured for 24 h. Reverse transcriptionpolymerase chain reaction (RT-PCR) and Western blotting were employed to detect the expression of resistin gene. Our results showed that resistin protein and mRNA in 3T3-L1 adipocytes were inhibited by TNFα at different concentrations (P＜0.01), and the inhibitory effect increased with the concentration (P＜0.01). At the same concentrations, the inhibitory effect increased with time (P ＜0.01). Ro-31-8220 could inhibit its expression and the inhibitive effect remained unchanged with addition of TNFα(P＞0.05). It was concluded that TNFα could inhibit the expression of resistin in 3T3-L1 adipocytes. The mechanism may be that the expression of resistin is partly controlled by protein kinase C signal conduction pathway.
