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首页> 外文期刊>Cellular & molecular biology letters. >17beta-Estradiol promotes cell proliferation in rat osteoarthritis model chondrocytes via PI3K/Akt pathway.
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17beta-Estradiol promotes cell proliferation in rat osteoarthritis model chondrocytes via PI3K/Akt pathway.

机译：17β-雌二醇通过PI3K / Akt途径促进大鼠骨关节炎模型软骨细胞的细胞增殖。

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摘要

Osteoarthritis (OA) is the most common cause of musculoskeletal pain and disability. The importance of chondrocytes in the pathogenesis of OA is unequivocal. 17beta-estradiol (E2) has a potential protective effect against OA. However, the mechanism of E2 in OA chondrocytes remains unclear. In this study, we investigated the regulative effect of E2 on cell growth and the relationship between E2 and the PI3K/Akt pathway in rat OA model chondrocytes (pretreated with interleukin-1beta). We found that E2 induced chondrocyte proliferation, and increased the expression level of Akt simultaneously, especially the expression level of P-Akt. Furthermore, the inhibition of P-Akt could block chondrocyte proliferation induced by E2. These results suggest that PI3K/Akt activation induced by E2 may be an important factor in the mechanism of E2 in cell proliferation in rat OA model chondrocytes, and help further understanding the role of E2 in OA progression.
机译：骨关节炎（OA）是肌肉骨骼疼痛和残疾的最常见原因。软骨细胞在OA发病机理中的重要性是明确的。 17β-雌二醇（E2）对OA具有潜在的保护作用。但是，OA软骨细胞中E2的机制仍不清楚。在这项研究中，我们研究了E2对大鼠OA模型软骨细胞（用白介素-1β预处理）中细胞生长的调节作用以及E2与PI3K / Akt途径之间的关系。我们发现E2诱导软骨细胞增殖，并同时增加了Akt的表达水平，尤其是P-Akt的表达水平。此外，P-Akt的抑制作用可能会阻止E2诱导的软骨细胞增殖。这些结果表明，E2诱导的PI3K / Akt激活可能是E2在大鼠OA模型软骨细胞细胞增殖机制中的重要因素，并有助于进一步了解E2在OA进展中的作用。

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