| BackgroundDiabetic peripheral neuropathy is one of the most common and complicated complication of type2diabetes. About70%to80%of patients occur to different damage of sensory and motor nerve function, which can affect the quality of life of patients. Currently the pathogensis of diabetic peripheral neuropathy has not been fully elucidated, the possible mechanism is the result of the combine effects of many factors, which results from not only metabolic factors but also vascular factors, such as oxidative stress, metabolic abnormalities of polyol pathway, accumulation of advanced glycationend products. At present time there is not yet efficient treatment to therapy diabetic peripheral neuropathy, therefore how to effectively curb the occurrence of this disease becomes the hot pot.Lipin family which is produced by the gene LPIN expression has physiological effect not only on regulating lipid metabolism; but also on maintaining normal fatty storage. Lipin family includes at least three members lipin-1, lipin-2, lipin-3. Lipin-1plays dual roles in lipid metabolisms. On one hand lipin-1acts as an Mg2+-dependent phosphatidate type-1(PAP-1), catalyzing a key step in the synthesis of glycerolipids, on the other hand it also acts as a transcriptional coactivator through its direct interaction with peroxisome proliferator-activated receptor (PPAR) γ coactivator-1α (PGC-1α) and PPAR α, catalyzing the gene expression of fatty synthesis and consume. Lipin-1deficiency can decrease the activity of nerve fat pad of epineurium and PAP activity of Schwann cells. Therefore synthesis of phosphatidic acid reduces, which will affect the synthesis of myelin sheath of peripheral nerves, and make nerve conduction velocity slow. Accumulation of phosphatidic acid can stimulate the MEK-Erk bypass pathway to emit abnormal signal, which can increase the degradation and apoptosis of Schwann cells and peripheral neuropathy. Nerve growth factor is one of the growth factors family that discovered earlier than others. It is very essential for neurotransmitter synthesis、the enzyme of protein phosphorylation and methylation, maintaining of neurons normal function and process of repair after injury. Study demonstrate that peripheral nerve repair dysfunction is respectively related to NGF deficiency, synthesis and expression of receptors decrease.ObjectiveTo observe the effect of the high concentration of glucose on rat Schwann cells in vitro, and explore the possible mechanism. To observe the expression level of lipin-1and NGF protein.MethodsRSC96cells were cultured in vitro divided into normal control group(25mmol/L) and high glucose group(100mmol/L). The proliferation and apoptosis of Schwann cell were respectively detected by MTT and flow cytometry. The expression of lipin-1, nerve growth factor were detected by western blotting; and the expression of lipin-1were further tested by immuno fluorescence under the high concentration of glucose. Statistical software SPSS18.0was used for data analysis. All the measurement data was expressed as x±s deviation. The difference was statistically significant if P<<0.05.Result1. MTT assay:Compared with normal control group, the proliferation of RSC96Schwann cells were inhibited by high glucose, the difference was significant between the two group (P<0.05).2. Flow cytometry include:Compared with the late apoptosis rate of RSC96Schwann cells in normal control group (1.56±0.72)%, the rate increased significantly in high glucose group (12.4±0.65)%, the difference in the two groups was significant (P<0.05).3. The expression of lipin-1and NGF in Schwann cells cultured in high glucose medium were reduced detected by western-blotting (P<0.05), and the expression of lipin-1was further detected by flow cytometry(P<0.05).ConclusionThe high concentration of glucose decreased the proliferation of Schwann cells. |
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