目的 探討淫羊藿苷調(diào)控磷脂酰肌醇3激酶（PI3K）/蛋白激酶B（Akt）信號(hào)通路干預(yù)大鼠早期激素性股骨頭壞死的作用機(jī)制。方法 50只SD大鼠隨機(jī)分為對照組、模型組和淫羊藿苷10、20、40mg/kg組，每組10只。除對照組外，其余各組ip脂多糖和im甲潑尼龍制備激素性股骨頭壞死大鼠模型。淫羊藿苷組大鼠分別ig10、20、40mg/kg的淫羊藿苷，對照組、模型組均ig等量生理鹽水，每天1次，連續(xù)6周。采用Micro-CT評估造模是否成功并分析骨密度（BMD）、骨體積密度（BV/TV）、骨表面積密度（BS/TV）、骨小梁厚度（Tb.Th）、骨小梁數(shù)量（Tb.N）、骨小梁分離度（Tb.Sp）；ELISA法檢測血清中血管內(nèi)皮生長因子（VEGF）、一氧化氮（NO）水平；Western blotting法檢測股骨頭PI3K、Akt、磷酸化Akt（p-Akt）蛋白的表達(dá)。結(jié)果 與對照組比較，模型組BMD、Tb.Th、BV/TV、Tb.N、BS/TV、VEGF和NO水平明顯降低，Tb.Sp明顯增高（P＜0.05）；與模型組比較，淫羊藿苷組的BMD、Tb.N、BV/TV、Tb.Th、BS/TV、VEGF和NO水平明顯增高，Tb.Sp明顯降低（P＜0.05）。與對照組比較，模型組PI3K和p-Akt蛋白表達(dá)均減少（P＜0.05）；與模型組比較，淫羊藿苷組PI3K和p-Akt蛋白表達(dá)均增加（P＜0.05）。結(jié)論 淫羊藿苷能夠有效緩解激素性股骨頭壞死的進(jìn)展，其機(jī)制可能與調(diào)節(jié)血清中VEGF、NO水平和增加骨組織中PI3K、Akt、p-Akt蛋白的表達(dá)有關(guān)，從而誘導(dǎo)血管修復(fù)與新生，促進(jìn)骨形成和愈合。

Objective To explore the mechanism of icariin PI3K/Akt signaling pathway in the intervention of early steroid-induced femur head necrosis in rats. Methods Fifty SD rats were randomly divided into control group, model group, icariin 10, 20, 40 mg/kg group, with 10 rats in each group. Except for the control group, the other groups were successively injected with lipopolysaccharide and methylprednisolone by intraperitoneal injection, to prepare the Hormonal necrosis of the femoral head model. Icariin group were given 10, 20, and 40 mg/kg icariin intragastrically, respectively, while control group and model group were given the same amount of normal saline intragastrically, once daily, for 6 weeks. Micro-CT was used to evaluate the success of modeling and to analyze BMD, BV/TV, BS/TV, Tb.Th, Tb.N, and Tb.Sp. ELISA was used to detect the levels of VEGF and NO in serum. Western blotting was used to detect PI3K, Akt, p-Akt protein. Results Compared with the control group, the levels of BMD, Tb.Th, BV/TV, Tb.N, BS/TV, VEGF and NO were significantly decreased in model group, while the levels of Tb.Sp were significantly increased (P<0.05). Compared with model group, the levels of BMD, Tb.N, BV/TV, Tb.Th, BS/TV, VEGF and NO were significantly increased in icariin group, while the levels of Tb.Sp were significantly decreased (P<0.05). Compared with control group, PI3K and P-Akt protein expression in model group were decreased (P<0.05). Compared with model group, PI3K and P-Akt protein expression were increased in icariin group (P<0.05). Conclusion Icariin can effectively alleviate the progression of steroid-induced femoral head necrosis, and its mechanism may be related to regulating the levels of VEGF and NO in serum and increasing the expression of PI3K, Akt and p-Akt in bone tissue, thus inducing vascular repair and regeneration and promoting bone formation and healing.

R285

山東省威海市中醫(yī)藥科技項(xiàng)目（2021N-21）