Role of "Sirt1-autophagy" on hypoxia-induced apoptosis in mice cementoblasts

Tan Xi

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Role of "Sirt1-autophagy" on hypoxia-induced apoptosis in mice cementoblasts

更新时间：2023-04-16

- Role of "Sirt1-autophagy" on hypoxia-induced apoptosis in mice cementoblasts
- Journal of Chongqing Medical University Vol. 48, Issue 1, Pages: 24-29(2023)
- 作者机构：
  
  重庆医科大学附属口腔医学院、口腔疾病与生物医学重庆市重点实验室、重庆市高校市级口腔生物医学工程重点实验室,重庆,401147
- 作者简介：
- 基金信息：
- DOI：
  CLC： R783.3
- Revised：2020-03-05，
  
  Accepted：18 March 2020，
  
  Published：2023
- 稿件说明：
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Tan Xi. Role of "Sirt1-autophagy" on hypoxia-induced apoptosis in mice cementoblasts[J]. Journal of chongqing medical university, 2023, 48(1): 24-29.
DOI：

Tan Xi. Role of "Sirt1-autophagy" on hypoxia-induced apoptosis in mice cementoblasts[J]. Journal of chongqing medical university, 2023, 48(1): 24-29. DOI：

摘要

目的：初步研究“Sirt1-自噬”在低氧诱导小鼠成牙骨质细胞OCCM-30凋亡中的作用。方法：体外培养小鼠成牙骨质细胞，随机分为对照组、低氧组、低氧+Sirt1激活剂白藜芦醇组、低氧+自噬抑制剂3-MA组、低氧+白藜芦醇+Sirt1抑制剂ex527组、低氧+白藜芦醇+3-MA组，MDC染色观察自噬溶酶体变化；LC3 Ⅱ免疫荧光检测自噬体变化；透射电镜观察自噬体；Western blot检测Sirt1、LC3Ⅱ、p62等蛋白表达；流式细胞仪检测细胞凋亡情况；不同组间结果数据采用单因素方差分析，组间采用LSD-t分析。结果：低氧组较对照组自噬溶酶体含量（P=0.000）及自噬体数量（P=0.000）明显增加，LC3Ⅱ蛋白表达明显增加（P=0.001），p62蛋白表达明显减少（P=0.000），细胞凋亡率增加（P=0.000）；低氧+白藜芦醇组较低氧组自噬溶酶体（P=0.019）及自噬体数量（P=0.000）、LC3 Ⅱ蛋白表达（P=0.049）、Sirt1蛋白表达（P=0.000）明显增加，p62蛋白表达明显减少（P=0.000），细胞凋亡率减少（P=0.021）；低氧+白藜芦醇+ex527组较低氧+白藜芦醇组自噬溶酶体（P=0.000）及自噬体数量（P=0.000）、LC3 Ⅱ蛋白表达（P=0.000）、Sirt1蛋白表达（P=0.000）明显减少，p62蛋白表达明显增加（P=0.000），细胞凋亡率增加（P=0.000）；低氧+白藜芦醇+3-MA组较低氧+白藜芦醇组自噬溶酶体（P=0.000）及自噬体数量（P=0.000）、LC3 Ⅱ蛋白表达明显减少（P=0.000），p62蛋白表达明显增加（P=0.000），细胞凋亡率增加（P=0.000），Sirt1蛋白表达减少（P=0.146），差异无统计学意义。结论：自噬相关分子可能是低氧环境下Sirt1的下游作用分子，自噬在低氧诱导小鼠成牙骨质细胞（OCCM-30）凋亡中起保护作用。

Abstract

Objective: To investigate the role of "Sirt1-autophagy" on the hypoxia-induced apoptosis in OCCM-30 cementoblasts of mouse. Methods: OCCM-30 cells were cultured in vitro and were randomly divided into the control group

the hypoxia group

the hy-poxia + resveratrol group

the hypoxia + 3-MA group

the hypoxia + resveratrol + ex527 group and the hypoxia + resveratrol + 3-MA group. Changes of autophagy lysosomes in each group were observed by MDC staining and changes of autophagosome light chain Ⅱ (LC3 Ⅱ) were detected by immunofluorescence assay. The expression of Sirt1

LC3 Ⅱ and p62 proteins was detected by Western blot. Cell apoptosis was detected by flow cytometry. Results of different groups were analyzed by one-way ANOVA and different groups were analyzed by LSD-t. Results: Compared with the control group

the content of autophagy lysosomes (P=0.000) and the number of autophagosomes (P=0.000) in the hypoxia group were significantly increased

the expression of LC3 Ⅱ (P=0.001) protein was signifi-cantly increased

the expression of p62 protein was significantly decreased (P=0.000)

and the apoptosis rate was increased (P=0.000). Compared with the hypoxia group

the number of autophagy lysosomes (P=0.019) and autophagosomes (P=0.000)

and the expression of LC3 Ⅱ protein (P=0.000) and Sirt1 protein (P=0.049

P=0.000) in the hypoxia + resveratrol group were significantly increased

the expression of p62 protein (P=0.000) was signifi-cantly decreased

and the apoptosis rate was decreased (P=0.021). Compared with the hypoxia + resveratrol group

the number of autophagy lysosomes (P=0.000) and autophagosomes (P=0.000)

and the expression of LC3 Ⅱ (P=0.000) and Sirt1 (P=0.000) in the hypoxia + resveratrol + ex527 group were sig-nificantly decreased

the expression of p62 protein (P=0.000) was significantly increased

and the apoptosis rate was increased (P=0.000). Compared with the hypoxia + resveratrol group

the num-ber of autophagy lysosomes (P=0.000) and autophagosomes (P=0.000)

and the expression of LC3 Ⅱ (P=0.000) protein expression in the hypoxia + resveratrol + 3-MA group were significantly decreased

the expression of p62 protein (P=0.000) was increased

the apoptosis rate was increased (P=0.000)

and the expression of Sirt1 protein (P=0.146) was decreased

with no statistically significant difference. Conclusion: Autophagy-related molecules may be downstream acting molecules of Sirt1 in the hypoxic environment and autophagy plays a protective role in hypoxia-induced apoptosis of OCCM-30.

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