Ecdysone (α-ecdysone) is a steroidal molting hormone that exists in insects and plants and activates mineralocorticoid receptor (MR), leading to glomerular diseases[1]. Ecdysone is also an essential regulator of developmental transitions, including molting and metamorphosis in insects[2].
Ecdysone (0.1, 1, 5, and 10μM for 24h) significantly downregulated the key proteins of the TLR-pathways such as TLR-4, MYD88, IKK-α and IKK-ϒ in RAW 264.7 cells. These proteins were associated with inflammation. Therefore, ecdysone could suppress the TLR pathway to protect cells from inflammation[3].
Ecdysone treatment (6µg/g/d) resulted in evident mesangial deposition of fibronectin and significant reduction in the expression of podocyte-specific molecules such as synaptophysin in male C57BL/6 mice. These phenomena indicated that ecdysone treatment caused glomerulosclerosis and podocyte injury[4].
References:
[1]. Lu M, Wang P, Ge Y, Dworkin L, Brem A, Liu Z, et al. Activation of mineralocorticoid receptor by ecdysone, an adaptogenic and anabolic ecdysteroid, promotes glomerular injury and proteinuria involving overactive GSK3beta pathway signaling. Sci Rep. 2018;8(1):12225. Epub 20180815. doi: 10.1038/s41598-018-29483-7. PubMed PMID: 30111886.
[2]. Xu T, Jiang X, Denton D, Kumar S. Ecdysone controlled cell and tissue deletion. Cell Death Differ. 2020;27(1):1-14. Epub 20191119. doi: 10.1038/s41418-019-0456-9. PubMed PMID: 31745213.
[3].Bhardwaj M, Mamadalieva NZ, Chauhan AK, Kang SC. alpha-Ecdysone suppresses inflammatory responses via the Nrf2 pathway in lipopolysaccharide-stimulated RAW 264.7 cells. Int Immunopharmacol. 2019;73:405-13. Epub 20190529. doi:10.1016/j.intimp.2019.05.038. PubMed PMID: 31152978.
[4]. Lu M, Wang P, Zhou S, Flickinger B, Malhotra D, Ge Y, et al. Ecdysone Elicits Chronic Renal Impairment via Mineralocorticoid-Like Pathogenic Activities. Cell Physiol Biochem. 2018;49(4):1633-45. Epub 20180918. doi: 10.1159/000493499. PubMed PMID: 30227391.
蜕皮激素（α-蜕皮激素）是一种存在于昆虫和植物中的类固醇蜕皮激素，可激活盐皮质激素受体（MR），从而导致肾小球疾病[1]。蜕皮激素也是昆虫发育转变的重要调节因子，包括蜕皮和变态[2]。
蜕皮激素（0.1、1、5和10μM，持续24小时）在RAW 264.7细胞中显著下调TLR通路的关键蛋白，例如TLR-4、MYD88、IKK-α和IKK-ϒ。这些蛋白与炎症发生有关。因此，蜕皮激素可以抑制TLR通路，从而保护细胞免受炎症影响[3]。
蜕皮激素治疗（6μg/g/d）会导致雄性 C57BL/6 小鼠的纤连蛋白在系膜处明显沉积以及足细胞特异性分子（例如突触素）的表达显著减少。这些现象表明，蜕皮激素治疗会造成肾小球硬化和足细胞损伤[4]。