Glucose deprivation-induced IL-6 expression and release isn't mediated through NF-κB pathway in C2C12 myocytes
【摘要】：正Introduction:IL-6 is a pleiotropic cytokine secreted by many different cells.Skeletal muscle is one of important sources of IL-6,which might have relationship with energy metabolism.In the present research,we explore the effect of glucose deprivation(GD,glucose deprivation results in low intramuscular glycogen status) on skeletal muscle-derived IL-6 expression and release,and its signaling regulation by NF-kB pathway in C2C12 myocytes in vitro.Methods:(1) C2C12 mouse myoblast was differentiated into myotube.(2) Differentiated C2C12 myotubes were replaced with DMEM medium containing 4.5 g/L glucose(glucose control,GC) or DMEM medium not containing glucose(glucose deprivation,GD) for 24 h.IL-6 mRNA level was analyzed by Real-Time PCR.IL-6 protein level in the medium was analyzed by ELISA.(3) 200 nmol/L NF-κB activation inhibitor was added into medium at the condition of glucose deprivation and glucose control.IL-6 protein in the medium was analyzed by ELISA after 24 h treatment.Data are expressed as mean±SD.Results:(1) As compared to glucose control, glucose deprivation was able to enhance IL-6 mRNA expression,and IL-6 mRNA expression was significantly increased by glucose deprivation at 24 h(0.87±0.36 vs 2.80±0.96,P0.05).(2) As compared to glucose control, glucose deprivation was able to enhance protein release,IL-6 protein level in medium was significantly increased in glucose deprivation at 24 h(1285.38±118.62 vs 2617.11±389.20,P0.05).(3) IL-6 protein level in glucose control + NF-κB activation inhibitor decreased compared with glucose control,but had no significantly effect(1285.38±118.62 vs 941.46±7.09,P0.05).IL-6 protein level in glucose deprivation + NF-κB activation inhibitor decreased compared with glucose deprivation,but also had no significantly effect(2617.11±389.20 vs 2139.02±753.52,P0.05). Conclusion:(1) Glucose deprivation was able to enhance skeletal muscle IL-6 mRNA expression.(2) Glucose deprivation was able to enhance skeletal muscle-derived IL-6 protein release.(3) Glucose deprivation-induced IL-6 release isn't primary mediated through NF-κB signal pathway in C2C12 myocytes.