Suppression of parathyroid hormone production in secondary hyperparathyroidism by RNA interference

继发性甲状旁腺功能亢进（2HPT）是慢性肾脏疾病最重要的并发症之一。透析患者和肾功能衰竭动物模型甲状旁腺中维生素D3受体水平降低。最近的研究表明，功能蛋白可以随着基因转移到甲状旁腺而调整。采用大鼠2HPT模型，研究RNA干扰对甲状旁腺激素（PTH）的抑制作用。四周后血清甲状旁腺素升高至较高水平。随后，将高密度抗甲状旁腺siRNA注射到大鼠甲状旁腺。结果表明，血清甲状旁腺激素浓度被抑制约60%。抑制效果在1 ~ 2周达到峰值，然后有限度地维持。在本研究中，我们认为使用非病毒的胶原细胞给药系统有助于延长药物的有效性。

Secondary hyperparathyroidism(2HPT) is one of the most important complications of chronic kidney disease. Vitamin D3 receptor levels are decreased in the parathyroid glands of dialysis patients and animal models of renal failure. Recent research has shown that the functionality protein can be adjusted with the gene transfer to the parathyroid. We examined the parathyroid hormone(PTH) suppression by the RNA interference using rat 2HPT model. Serum PTH increased to a high level at the posterior when four weeks passed. Afterwards, high density anti-PTH siRNA was injected to rat's parathyroid glands. It was shown that serum PTH concentration was suppressed up to about 60%. The suppression effect was shown the peak on 1-2 weeks, and, then, maintained limitedly. In the present study, it was suggested that using the atelocollagen that was non-viruses drug delivery system contribute to the extension of effectiveness.