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通过观察温肾固疏方对去卵巢骨质疏松(PMOP)大鼠的骨密度及对白细胞介素-1β、肿瘤坏死因子-α、白细胞介素-6的血清含量和转化生长因子-β骨组织表达的影响,探讨其治疗骨质疏松的可能作用机制。将48只SPF级雌性SD大鼠分为6组:假手术组、模型组、雌激素组、温肾固疏方高、中、低剂量组。造模4周后开始给药,连续给药12周,酶联免疫法(ELISA)检测外周血清白细胞介素-1β(IL-1β)、肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)含量;q RT-PCR法检测骨组织转化生长因子-β(TGF-β)m RNA含量。与假手术组相比较,去势模型组大鼠骨密度(BMD)、TGF-β mRNA显著降低(p<0.05),而IL-1β、TNF-α、IL-6均显著升高(p<0.01),符合绝经后骨质疏松症改变;干预治疗后,与模型组比较,温肾固疏方高、中剂量组椎骨BMD显著升高(p<0.05),IL-1β、TNF-α、IL-6显著减少(p<0.05),温肾固疏方高剂量组TGF-β mRNA显著增加(p<0.05)。温肾固疏方治疗骨质疏松的作用机制可能与其下调IL-1β、TNF-α、IL-6等促炎细胞因子的表达,抑制骨吸收;同时上调TGF-β等抑炎细胞因子的表达,促进骨形成有关。
By observing the effect of Wenshen GuZhu Recipe on bone mineral density and serum levels of interleukin-1β, tumor necrosis factor-α and interleukin-6 in ovariectomized rats with osteoporosis (PMOP) and transforming growth factor-β The impact of tissue expression, to explore its possible mechanism of treatment of osteoporosis. Forty-eight SPF female SD rats were divided into 6 groups: sham-operation group, model group, estrogen group, high, medium and low dose groups of Wenshenzushuang. After 4 weeks of treatment, the rats were dosed for 12 weeks, and the levels of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), interleukin -6 (IL-6) were detected by flow cytometry. The content of transforming growth factor-β (TGF-β) m RNA in bone tissue was detected by q RT-PCR. Compared with the sham group, the BMD and TGF-β mRNA in the castration group were significantly decreased (p <0.05), while the levels of IL-1β, TNF-α and IL-6 in the castration group were significantly increased (p < 0.01), which was in line with the changes of postmenopausal osteoporosis. Compared with the model group, the BMD of vertebrae in high-dose and middle-dose groups of Wenshen GuZhu Recipe was significantly increased (p <0.05) IL-6 significantly decreased (p <0.05), and the expression of TGF-β mRNA increased significantly in high-dose group (p <0.05). The mechanism of action of Wenshen Guashu Recipe in treating osteoporosis may be related to down-regulating the expression of IL-1β, TNF-α, IL-6 and other proinflammatory cytokines and inhibiting bone resorption; meanwhile, up-regulating the expression of anti-inflammatory cytokines such as TGF- , Promote bone formation.