Effect of lncRNA SNHG16 targeting miR-182-5p on hypoxia/reoxygenation-induced cardiomyocyte apoptosis

GUAN Zhen-hua; CHEN Yun-xiao; LI Jie; LUO Hong-yu; SHI Wei-lin; WANG Wei; LIU Sha-sha

doi:10.11659/jjssx.12E025028

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Effect of lncRNA SNHG16 targeting miR-182-5p on hypoxia/reoxygenation-induced cardiomyocyte apoptosis

Basic Research | 更新时间：2026-06-16

- Effect of lncRNA SNHG16 targeting miR-182-5p on hypoxia/reoxygenation-induced cardiomyocyte apoptosis
- JOURNAL OF REGIONAL ANATOMY AND OPERATIVE SURGERY Vol. 35, Issue 6, Pages: 497-504(2026)
- 作者机构：
  
  1.保定市第一中心医院心内科，河北保定 071000
  2.保定市第一中心医院心脏重症医学科，河北保定 071000
  3.邯郸市第一医院老年医学二科，河北邯郸 056000
  4.邢台市中心医院心脏康复科，河北邢台 054000
  5.保定市第一中心医院检验三科，河北保定 071000
  6.保定市第一中心医院心血管内五科，河北保定 071000
- 作者简介：
- 基金信息：
- DOI：10.11659/jjssx.12E025028
  CLC： R542.2+2
- Received：04 December 2025，
  
  Published：25 June 2026
- 稿件说明：
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关振华,陈云肖,李洁等.lncRNA SNHG16靶向调控miR-182-5p对缺氧/复氧诱导的心肌细胞凋亡的影响[J].局解手术学杂志,2026,35(06):497-504.

GUAN Zhen-hua,CHEN Yun-xiao,LI Jie,et al.Effect of lncRNA SNHG16 targeting miR-182-5p on hypoxia/reoxygenation-induced cardiomyocyte apoptosis[J].JOURNAL OF REGIONAL ANATOMY AND OPERATIVE SURGERY,2026,35(06):497-504.
关振华,陈云肖,李洁等.lncRNA SNHG16靶向调控miR-182-5p对缺氧/复氧诱导的心肌细胞凋亡的影响[J].局解手术学杂志,2026,35(06):497-504. DOI： 10.11659/jjssx.12E025028.

GUAN Zhen-hua,CHEN Yun-xiao,LI Jie,et al.Effect of lncRNA SNHG16 targeting miR-182-5p on hypoxia/reoxygenation-induced cardiomyocyte apoptosis[J].JOURNAL OF REGIONAL ANATOMY AND OPERATIVE SURGERY,2026,35(06):497-504. DOI： 10.11659/jjssx.12E025028.

摘要

目的

探讨lncRNA SNHG16对缺氧/复氧（H/R）诱导的心肌细胞凋亡的影响及对miR-182-5p的调控作用。

方法

将细胞分为对照组（正常培养）、模型组（H/R诱导）、si-NC组、si-SNHG16组、si-SNHG16+anti-NC组、si-SNHG16+anti-miR-182-5p组，除对照组与模型组以外，其余各组细胞均在H/R诱导后转染相应质粒。Edu实验检测细胞增殖；流式细胞术及AO/EB染色检测细胞凋亡；ELISA检测细胞心肌损伤、炎症反应及氧化应激相关因子水平；DCFDA荧光探针法检测细胞活性氧（ROS）生成量；Western blot检测凋亡相关蛋白表达；qRT-PCR检测各组细胞lncRNA SNHG16、miR-182-5p水平；双荧光素酶报告基因实验及RNA pull-down实验检测lncRNA SNHG16与miR-182-5p的靶向关系。

结果

与对照组比较，模型组细胞Edu阳性率、SOD活性、miR-182-5p水平降低（

0.05），细胞凋亡率、凋亡细胞占比、乳酸脱氢酶（LDH）、肌酸激酶（CK）、白细胞介素（IL）-6、IL-1β、肿瘤坏死因子-α（TNF-α）、ROS、丙二醛（MDA）、lncRNA SNHG16及裂解型胱天蛋白酶-3（C-Caspase-3）、B细胞淋巴瘤-2相关X蛋白（Bax

）/B细胞淋巴瘤-2（Bcl-2）表达水平升高（

0.05）；与si-NC组比较，si-SNHG16组细胞Edu阳性率、超氧化物歧化酶（SOD）活性、miR-182-5p水平升高（

0.05），细胞凋亡率、凋亡细胞占比、LDH、CK、IL-6、IL-1β、TNF-α、ROS、MDA、lncRNA SNHG16及C-Caspase-3、Bax/Bcl-2表达水平降低（

0.05）；与si-SNHG16+anti-NC组比较，si-SNHG16+anti-miR-182-5p组细胞Edu阳性率、SOD活性、miR-182-5p水平降低（

0.05），细胞凋亡率、凋亡细胞占比、LDH、CK、IL-6、IL-1β、TNF-α、ROS、MDA及C-Caspase-3、Bax/Bcl-2表达水平升高（

0.05）。RNA pull-down实验发现lncRNA SNHG16与miR-182-5p之间存在相互作用；与WT-SNHG16和miR-NC共转染的心肌细胞相比，WT-SNHG16和miR-182-5p mimics共转染的心肌细胞相对荧光素酶活性降低（

0.05）。

结论

沉默lncRNA SNHG16可通过上调miR-182-5p减少H/R诱导的心肌细胞凋亡。

Abstract

Objective

To explore the effect of lncRNA SNHG16 on cardiomyocyte apoptosis induced by hypoxia/reoxygenation （H/R） and its regulatory role on miR-182-5p.

Methods

The cells were divided into the control group （normal culture），the model group （induced by H/R），the si-NC group，the si-SNHG16 group，the si-SNHG16+anti-NC group，and the si-SNHG16+anti-miR-182-5p group. Except for the control group and the model group，the cells in the other groups were transfected with the corresponding plasmids after H/R induction. Edu assay was used to detect the cell proliferation. Flow cytometry and AO/EB staining were used to detect the cell apoptosis. ELISA was used to detect the levels of myocardial injury，inflammatory response and oxidative stress-related factors in cells. DCFDA fluorescence probe method was used to detect the production of reactive oxygen species （ROS） in cells. Western blot was used to detect the expression of apoptosis-related proteins. qRT-PCR was used to detect the levels of lncRNA SNHG16 and miR-182-5p in each group of cells. Dual-luciferase reporter gene assay and RNA pull-down assay was used to detect the targeting relationship between lncRNA SNHG16 and miR-182-5p.

Results

Compared with the control group，the Edu positive rate，SOD activity and miR-182-5p level in the model group decreased （

0.05），the apoptosis rate，the proportion of apoptotic cells，the levels of lactate dehydrogenase（LDH），creatine kinase（CK），interleukin （IL）-6，IL-1β，tumor necrosis factor-alpha（TNF-α），ROS，malondialdehyde（MDA），lncRNA SNHG16，and the expressions of cleaved caspase-3（C-Caspase-3） and B-cell lymphoma-2-associated X protein（Bax）/B-cell lymphoma-2（Bcl-2） ratio increased （

0.05）. Compared with the si-NC group，the Edu positive rate，superoxide dismutase（SOD） activity and miR-182-5p level in the si-SNHG16 group increased （

0.05），the apoptosis rate，the proportion of apoptotic cells，the levels of LDH，CK，IL-6，IL-1β，TNF-α，ROS，MDA，lncRNA SNHG16，and the expressions of C-Caspase-3 and Bax/Bcl-2 ratio decreased （

0.05）. Compared with the si-SNHG16+anti-NC group，the Edu positive rate，SOD activity and miR-182-5p level in the si-SNHG16+anti-miR-182-5p group decreased （

0.05），the apoptosis rate，the proportion of apoptotic cells，the levels of LDH，CK，IL-6，IL-1β，TNF-α，ROS，MDA，and the expressions of C-Caspase-3 and Bax/Bcl-2 ratio increased （

0.05）. The RNA pull-down experiment revealed that there was an interaction between lncRNA SNHG16 and miR-182-5p. Compared with the cardiomyocytes co-transfected with WT-SNHG16 and miR-NC，the cardiomyocytes co-transfected with WT-SNHG16 and miR-182-5p mimics showed a relative decrease in luciferase activity （

0.05）.

Conclusion

Silencing lncRNA SNHG16 can reduce H/R-induced cardiomyocyte apoptosis by upregulating miR-182-5p.

关键词

Keywords

references

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