Pollen Typhae total flavones inhibit expression of interleukin-6 in C2C12 skeletal muscle cells cultured with palmitate
- Author:
Shaoying LOU
;
Yi LIU
;
Weihua CHEN
;
Jian YING
;
Yanming HE
;
Wenjian WANG
- Publication Type:Journal Article
- From:
Journal of Integrative Medicine
2008;6(5):488-92
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE: To observe the effects of Pollen Typhae total flavones (PTF) on expression of interleukin-6 (IL-6) mRNA and protein secretion in C2C12 cell strain of skeletal muscle cells cultured with palmitate, and to explore the mechanism of PTF in relieving insulin resistance (IR). METHODS: The IR of C2C12 cells was induced by co-culturing with palmitate. The C2C12 cells were divided into normal control group, untreated group, PDTC (a nuclear factor-kappaB inhibitor) treated group, rosiglitazone (ROS)-treated group, ROS+ PDTC-treated group, PTF-treated group and PTF+PDTC-treated group. Sixteen hours after culture, the transportation rate of glucose was observed by (3)H-deoxyglucose uptake method; IL-6 mRNA expression in C2C12 cells was assayed by real time polymerase chain reaction (Real-time PCR), and level of IL-6 protein secretion in culture supernatant was detected by enzyme linked immunosorbent assay. RESULTS: Compared with the normal control group, the transportation rate of glucose of cells in untreated group was decreased 30.43% after 16-hour palmitate culture, and was increased 32.39% in the PTF-treated group. Compared with the untreated group, the levels of IL-6 mRNA expression in cells and IL-6 protein secretion in supernatant were significantly decreased in the PTF-treated group (P<0.05). The levels of IL-6 mRNA expression in cells and IL-6 protein secretion in supernatant were increased in PTF+PDTC-treated group as compared with PFT-treated group (P<0.05). CONCLUSION: PTF can inhibit the IL-6 mRNA expression and IL-6 protein secretion via nuclear factor-kappaB pathway in C2C12 skeletal muscle cells, which may be one of its mechanisms in relieving inflammation conditions and insulin resistance in C2C12 skeletal muscle cells.
