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Diabetologia：抑制前列腺素D2-GPR44 /DP2轴可提高人胰岛的生存和功能

2020-07-28 MedSci原创 MedSci原创

人胰岛；生存；功能
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炎症信号和前列腺素合成增加在糖尿病的发展过程中发挥重要作用。

炎症信号和前列腺素合成增加在糖尿病的发展过程中发挥重要作用。前列腺素D2 (PGD2)受体GPR44/DP2在人胰岛中高表达，通路的激活将导致胰岛素分泌受损。在慢性高血糖情况下，GPR44活化对胰岛功能和生存率的作用尚不清楚。在本研究中，我们使用选择性GPR44拮抗剂(AZ8154)在移植了人胰岛的糖尿病小鼠体内和体外研究了GPR44对胰岛的抑制作用。

将人胰岛暴露于PGD2或促炎细胞因子，观察抑制GPR44对胰岛存活率的影响。此外，我们还研究了高浓度葡萄糖(HG)和IL-1抑制的人胰岛中GPR44抑制的分子机制。小鼠移植后第10天和第15天进行IVGTT。研究结束后，对移植的人胰岛中的代谢变量、循环中的促炎细胞因子和肝细胞生长因子(HGF)进行分析。

PGD2或促炎细胞因子诱导人胰岛细胞凋亡，而GPR44抑制则逆转了这一作用。GPR44抑制拮抗了由HG和IL-1蛋白诱导的胰岛葡萄糖刺激的胰岛素分泌减少。与此同时，akt -糖原合酶激酶3的激活，forkhead o -1的磷酸化和失活，以及胰腺和十二指肠homeobox-1和HGF的上调。向移植有少量人胰岛的糖尿病小鼠施用GPR44拮抗剂长达17天，导致IVGTT期间空腹血糖降低，血糖波动降低。 与媒介物组相比，在第4天和整个治疗期间，人C肽水平的提高支持了改善的葡萄糖调节。GPR44抑制可降低血浆TNF-α水平和生长调节的癌基因-α/趋化因子（C-X-C基序）配体1，并增加人胰岛中的HGF水平。

在炎症和高血糖应激下，抑制人胰岛的GPR44有可能改善胰岛的功能和存活率。这可能意味着移植后胰岛的存活率更高。

原始出处：

Shadab Abadpour, Björn Tyrberg,Inhibition of the prostaglandin D2–GPR44/DP2 axis improves human islet survival and function

 

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    2021-05-12 zhouqu_8

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    2021-03-22 ms9608593228839890

    #DIA#

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    2021-06-08 makuansheng

    #前列腺素#

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    2020-12-23 baoya

    #胰岛#

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    2021-02-27 ms5439512287675881

    #BET#

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