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Long-pulse gastric electrical stimulation protects interstitial cells of Cajal in diabetic rats via IGF-1 signaling pathway

机译:长脉冲胃电刺激通过IGF-1信号通路保护糖尿病大鼠Cajal间质细胞

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摘要

AIM: To investigate the effects of different parameters of gastric electrical stimulation (GES) on interstitial cells of Cajal (ICCs) and changes in the insulin-like growth factor 1 (IGF-1) signal pathway in streptozotocin-induced diabetic rats.METHODS: Male rats were randomized into control, diabetic (DM), diabetic with sham GES (DM + SGES), diabetic with GES1 (5.5 cpm, 100 ms, 4 mA) (DM + GES1), diabetic with GES2 (5.5 cpm, 300 ms, 4 mA) (DM + GES2) and diabetic with GES3 (5.5 cpm, 550 ms, 2 mA) (DM + GES3) groups. The expression levels of c-kit, M-SCF and IGF-1 receptors were evaluated in the gastric antrum using Western blot analysis. The distribution of ICCs was observed using immunolabeling for c-kit, while smooth muscle cells and IGF-1 receptors were identified using α-SMA and IGF-1R antibodies. Serum level of IGF-1 was tested using enzyme-linked immunosorbent assay.RESULTS: Gastric emptying was delayed in the DM group but improved in all GES groups, especially in the GES2 group. The expression levels of c-kit, M-SCF and IGF-1R were decreased in the DM group but increased in all GES groups. More ICCs (c-kit+) and smooth muscle cells (α-SMA+/IGF-1R+) were observed in all GES groups than in the DM group. The average level of IGF-1 in the DM group was markedly decreased, but it was up-regulated in all GES groups, especially in the GES2 group.CONCLUSION: The results suggest that long-pulse GES promotes the regeneration of ICCs. The IGF-1 signaling pathway might be involved in the mechanism underlying this process, which results in improved gastric emptying.
机译:目的:研究不同参数的胃电刺激(GES)对链脲佐菌素诱导的糖尿病大鼠Cajal间质细胞(ICCs)的影响以及胰岛素样生长因子1(IGF-1)信号通路的变化。将雄性大鼠随机分为对照组,糖尿病(DM),假GES(DM + SGES)糖尿病,GES1(5.5 cpm,100 ms,4 mA)(DM + GES1)糖尿病,GES2(5.5 cpm,300 ms)糖尿病,4 mA)(DM + GES2)和糖尿病与GES3(5.5 cpm,550 ms,2 mA)(DM + GES3)组。使用蛋白质印迹分析评估了胃窦中c-kit,M-SCF和IGF-1受体的表达水平。使用c-kit免疫标记观察了ICC的分布,同时使用α-SMA和IGF-1R抗体鉴定了平滑肌细胞和IGF-1受体。结果:DM组胃排空有所延迟,但所有GES组,尤其是GES2组的胃排空有所延迟。 DM组c-kit,M-SCF和IGF-1R的表达水平降低,而所有GES组均升高。在所有GES组中观察到更多的ICC(c-kit + )和平滑肌细胞(α-SMA + / IGF-1R + )。比DM组中的要多。 DM组的IGF-1平均水平明显降低,但在所有GES组,特别是GES2组中均升高。结论:长脉冲GES促进了ICCs的再生。 IGF-1信号通路可能参与了该过程的潜在机制,从而改善了胃排空。

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