【摘要】：目的:觀察低強度脈沖超聲(LIPUS)對磷酸三鈣(tricalcium phosphate,TCP)磨損顆粒誘導的假體周圍骨細胞(osteocyte)損傷的影響,并探討其可能作用機理。方法:取6~8周齡ICR雄性小鼠30只,隨機分為正常組、模型組和LIPUS治療組,每組10只。模型組和LIPUS治療組小鼠分別于第1、3、5、7、9和第11周向顱頂注射TCP磨損顆粒建立小鼠顱骨溶解模型。正常組小鼠顱頂皮膚僅接受陰性超聲探頭按壓處理,治療組小鼠顱頂皮膚接受LIPUS干預治療3個月,實驗結(jié)束后取顱骨。采用Micro-CT分析各組小鼠顱骨TCP磨損顆粒植入部位周圍溶解情況;應用HE染色比較各組假體周圍骨細胞活性;通過流式細胞術(shù)定量檢測各組假體周圍骨細胞凋亡情況;采用免疫印跡技術(shù)檢測各組假體周圍骨細胞牙本質(zhì)基質(zhì)蛋白(DMP-1)、骨硬化蛋白(SOST)、葡萄糖調(diào)節(jié)蛋白78(GRP78)、肌醇依賴酶1α(IRE1α)、X盒結(jié)合蛋白(XBP1s)、c-Jun氨基末端激酶(JNK)及磷酸化JNK(p-JNK)等蛋白表達水平。結(jié)果:與正常組比較,模型組小鼠假體周圍骨細胞活性明顯降低,細胞凋亡顯著(P0.05),其特征蛋白DMP-1顯著下調(diào),SOST明顯上調(diào),造成DMP-1/SOST增加(P0.05),且內(nèi)質(zhì)網(wǎng)應激通路蛋白GRP78、IRE1α、XBP1s和p-JNK表達水平顯著增加(P0.05)。而LIPUS治療組假體周圍骨細胞損傷及內(nèi)質(zhì)網(wǎng)應激反應顯著減弱,表現(xiàn)為假體周圍骨細胞活性、數(shù)量和DMP-1/SOST明顯增加(P0.05),且IRE1α-XBP1-JNK通路的活化被顯著抑制(P0.05)。結(jié)論:LIPUS可阻止TCP磨損顆粒誘導的假體周圍骨細胞損傷,其作用機制可能與抑制IRE1α-XBP1-JNK信號通路介導的內(nèi)質(zhì)網(wǎng)應激反應密切相關(guān)。
[Abstract]:Aim: to observe the effect of low intensity pulsed ultrasound (LIPUS) on (osteocyte) damage induced by tricalcium phosphate (tricalcium phosphate,TCP) wear particles and to explore its possible mechanism. Methods: thirty ICR male mice aged 6 weeks and 8 weeks were randomly divided into normal group, model group and LIPUS treatment group with 10 mice in each group. The model group and the LIPUS treatment group were injected with TCP wear granule to the top of the cranium at the 1st and 11th week respectively to establish the model of craniolysis in mice. The skullcap skin in the normal group was only treated with negative ultrasound probe and treated with LIPUS intervention for 3 months. The skull was removed after the experiment. Micro-CT was used to analyze the dissolution around the implanted site of TCP wear particles in the skull of each group; HE staining was used to compare the osteocyte activity around the prosthesis in each group; flow cytometry was used to quantitatively detect the apoptosis of bone cells around the prosthesis in each group. The expressions of dentine matrix protein (DMP-1), osteosclerotic protein (SOST), glucose regulatory protein 78 (GRP78), IRE1 偽), X cassette binding protein (XBP1s), c-Jun amino-terminal kinase (JNK) and phosphorylated JNK (p-JNK) were detected by Western blot. Results: compared with the normal group, the osteocyte activity and apoptosis were significantly decreased in the model group (P0.05). The characteristic protein DMP-1 was significantly down-regulated and the SOST was up-regulated in the model group. DMP-1/SOST was increased (P0.05), and the expression levels of GRP78,IRE1 偽, XBP1s and p-JNK in ER stress pathway were significantly increased (P0.05). In LIPUS treatment group, the injury of periprosthetic bone cells and the stress response of endoplasmic reticulum (ER) were significantly decreased, showing that the activity of osteocytes around the prosthesis, the quantity and DMP-1/SOST were significantly increased (P0.05), and the activation of IRE1 偽-XBP1-JNK pathway was significantly inhibited (P0.05). Conclusion: LIPUS can prevent the injury of periprosthetic bone cells induced by TCP wear particles, and its mechanism may be related to the inhibition of endoplasmic reticulum stress mediated by IRE1 偽-XBP1-JNK signaling pathway.
【作者單位】： 紹興文理學院醫(yī)學院;
【基金】：浙江省大學生科學創(chuàng)新活動計劃(2016R428011) 紹興市大學生科技創(chuàng)新項目(紹市教高[2015]138號) 國家級大學生創(chuàng)新創(chuàng)業(yè)訓練計劃項目(201610349010) 浙江省自然科學基金(LY17H060007)
【分類號】：R684

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