【摘要】：[目的]本實驗主要探討流體剪切力與ERK5信號通路在成骨細胞增殖反應(yīng)中的作用關(guān)系,為確立骨組織中的機械應(yīng)力傳導機制提供依據(jù)。 [方法]通過對體外培養(yǎng)的成骨細胞施加相同強度不同時間的流體剪切力,結(jié)合EKR5阻斷劑,應(yīng)用MTT和免疫熒光標記的方法檢測成骨細胞的增殖活性,分析ERK5信號通路介導的流體剪切力對成骨細胞的增殖的影響。 [結(jié)果]在相同強度(12dyn/cm2)、不同時間的流體剪切力作用下,比較靜置對照組,短時間內(nèi)的流體剪切力(t≤1h)促進成骨細胞增殖的作用明顯(P0.05),細胞生長曲線前移,CylinD1與CDK4表達量顯著增高(P0.05)；但在1.5h、2h卻明顯表現(xiàn)出抑制增殖的作用(P0.05)；而相同時間FSS作用下,利用ERK5阻斷劑BIX02188阻斷ERK5信號通路后,成骨細胞的增殖反應(yīng)受到抑制CylinD1與CDK4的表達量隨之降低,與對照組比較表現(xiàn)出顯著差異(P0.05),且CylinD1與CDK4的表達呈正相關(guān)關(guān)系(r=0.55,P0.05)。 [結(jié)論]正常生理環(huán)境中,ERK5信號通路存在且參與成骨細胞的正常增殖活動。12dyne/cm2的FSS刺激可以通過ERK5-CylinD1-CDK4信號傳導通路起到調(diào)節(jié)成骨細胞增殖活動的作用,短時間(t≤60min)持續(xù)FSS刺激可通過ERK5-CylinD1-CDK4信號傳導通路正性調(diào)節(jié)細胞周期,促進成骨細胞增殖；而長時間(t60min)FSS刺激則會抑制ERK5的磷酸化,通過ERK5-CylinD1-CDK4信號傳導通路調(diào)控細胞周期調(diào)控因子起到抑制細胞增殖的作用。
[Abstract]:[objective] to investigate the relationship between fluid shear stress and ERK5 signaling pathway in osteoblast proliferation, and to provide a basis for establishing the mechanism of mechanical stress conduction in bone tissue. [methods] the proliferation activity of osteoblasts was detected by MTT and immunofluorescence labeling by applying fluid shear force of the same strength and different time to the osteoblasts cultured in vitro, combined with EKR5 blocker. To investigate the effect of fluid shear stress mediated by ERK5 signaling pathway on the proliferation of osteoblasts. [results] under the same strength (12dyn/cm2) and different time of fluid shear stress, the static control group was compared. The effect of fluid shear stress (t 鈮，

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