BMP9 inhibits inflammatory response and apoptosis of degenerative nucleus pulposus cells through activating PI3K/Akt signaling pathway

鲁花; 于露; 甄欢欢; 刘汝银; 岳宗进

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BMP9 inhibits inflammatory response and apoptosis of degenerative nucleus pulposus cells through activating PI3K/Akt signaling pathway

更新时间：2026-01-09

- BMP9 inhibits inflammatory response and apoptosis of degenerative nucleus pulposus cells through activating PI3K/Akt signaling pathway
- Journal of Army Medical University Vol. 38, Issue 18, Pages: 2047-2052(2016)
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  CLC： R341;R363.22;R681.53
- Published：2016
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鲁花,于露,甄欢欢,刘汝银,岳宗进.骨形态发生蛋白9激活PI3K/Akt信号通路抑制退变髓核细胞的炎症反应和凋亡[J].陆军军医大学学报(原第三军医大学学报),2016,38(18):2047-2052.

　Lu Hua,Yu Lu,Zhen Huanhuan,Liu Ruyin,Yue Zongjin.BMP9 inhibits inflammatory response and apoptosis of degenerative nucleus pulposus cells through activating PI3K/Akt signaling pathway[J].J Amry Med Univ (J Third Mil Med Univ),2016,38(18):2047-2052.
鲁花,于露,甄欢欢,刘汝银,岳宗进.骨形态发生蛋白9激活PI3K/Akt信号通路抑制退变髓核细胞的炎症反应和凋亡[J].陆军军医大学学报(原第三军医大学学报),2016,38(18):2047-2052. DOI：

　Lu Hua,Yu Lu,Zhen Huanhuan,Liu Ruyin,Yue Zongjin.BMP9 inhibits inflammatory response and apoptosis of degenerative nucleus pulposus cells through activating PI3K/Akt signaling pathway[J].J Amry Med Univ (J Third Mil Med Univ),2016,38(18):2047-2052. DOI：

摘要

目的研究骨形态发生蛋白9（bone morphogenetic protein 9，BMP9）对退变髓核细胞炎症反应和凋亡的影响，并探究其与PI3K/Akt信号通路的关系。方法通过氧糖剥夺（oxygen glucose deprivation，OGD）培养建立退变髓核细胞模型；重组腺相关病毒（adeno-associated virus，AAV）将BMP9转染入人髓核细胞内（human nucleus pulposus cells

HNPCs），实验共分5组：Control组（正常培养的HNPCs）、OGD组（氧糖剥夺模型）、AAV组（氧糖剥夺模型，转染AAV空载体）、AAV-BMP9组（氧糖剥夺模型，转染AAV-BMP9），AAV-BMP9+LY294002组（AAV-BMP9组基础上添加PI3K抑制剂LY294002）。免疫荧光方法检测蛋白聚糖（Aggrecan）和Ⅱ型胶原（type Ⅱ collagen，Col2a1）的表达；Western blot检测p-Akt和p-mTOR的蛋白表达；酶联免疫吸附实验检测细胞培养上清液中TNF-α、IL-1β、IL-6和IL-8的表达；流式细胞术检测细胞的凋亡。结果在氧糖剥夺培养模型中Aggrecan和Col2a1表达明显降低；AAV-BMP9组中p-Akt和p-mTOR的表达明显高于OGD组和AAV组（P0.05）；此外，AAV-BMP9组HNPCs分泌的TNF-α、IL-1β、IL-6和IL-8明显减少，细胞凋亡被显著抑制（P0.05）；LY294002的加入能够显著逆转BMP9的上述效果。结论 BMP9能够抑制退变HNPCs的炎症反应和凋亡，并且这种作用是通过激活PI3K/Akt信号通路实现的。

Abstract

Objective To investigate the effects of bone morphogenetic protein 9 (BMP9) on inflammatory response and apoptosis of degenerative nucleus pulposus cells and to mechanistically explore its association with PI3K/Akt signaling pathway. Methods The degenerative nucleus pulposus cells were generated by oxygen glucose deprivation (OGD) method. BMP9 gene was transinduced into human nucleus pulposus cells (HNPCs) by recombinant adeno-associated virus (AAV) mediated gene transfer. According to the transfection and treatment

HNPCs were divided into 5 groups: Control group (cultured HNPCs without treatment)

OGD group (OGD model)

AAV group (OGD+AAV empty vector)

AAV-BMP9 group (OGD+AAV-BMP9)

and AAV-BMP9+LY294002 group (OGD+AAV-BMP9+PI3K inhibitor LY294002). Immunofluorescence staining was used to detect Aggrecan and type Ⅱ collagen (Col2a1). Western blot were performed to detect the protein expression of p-Akt and p-mTOR. Enzyme linked immunosorbent assay (ELISA) was carried out to measure the levels of TNF-α

IL-1β

IL-6 and IL-8 in the supernatant of medium. Flow cytometry was performed to detect cell apoptosis. Results The expression of Aggrecan and Col2a1 was significantly decreased in OGD model. The protein expression of p-Akt and p-mTOR was higher in AAV-BMP9 group than those in OGD and AAV groups (P0-.05). In addition

the levels of TNF-α

IL-1β

IL-6 and IL-8 were significantly decreased (P0.05) and cell apoptosis was markedly reduced in HNPCs of AAV-BMP9 group. But

LY294002 treatment significantly reversed the above-mentioned effects induced by BMP9 overexpression in degenerative HNPCs. Conclusion BMP9 inhibits the inflammatory response and apoptosis of degenerative HNPCs through activating PI3K/Akt signaling pathway.

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