Dihydromyricetin Alleviates H9C2 Cell Apoptosis and Autophagy by Regulating CircHIPK3 Expression and PI3K/AKT/mTOR Pathway
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Original Article|Updated:2023-04-27
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Dihydromyricetin Alleviates H9C2 Cell Apoptosis and Autophagy by Regulating CircHIPK3 Expression and PI3K/AKT/mTOR Pathway
Chinese Journal of Integrative MedicineVol. 29, Issue 5, Pages: 434-440(2023)
Affiliations:
1.Key Laboratory for Molecular Genetic Mechanisms and Intervention Research on High Altitude Disease of Tibet Autonomous Region, School of Medicine, Xizang Minzu University, Xianyang, Shaanxi Province (712082), China
2.Key Laboratory of High Altitude Environment and Gene Related to Disease of Tibet Ministry of Education, School of Medicine, Xizang Minzu University, Xianyang, Shaanxi Province(712082), China
3.School of Finance Economics, Xizang Minzu University, Xianyang, Shaanxi Province (712082), China
4.School of Information Engineering, Xizang Minzu University, Xianyang, Shaanxi Province (712082), China
ZHANG Zhi-ying, LIU Chao, WANG Peng-xiang, et al. Dihydromyricetin Alleviates H9C2 Cell Apoptosis and Autophagy by Regulating CircHIPK3 Expression and PI3K/AKT/mTOR Pathway. [J]. Chinese Journal of Integrative Medicine 29(5):434-440(2023)
DOI:
ZHANG Zhi-ying, LIU Chao, WANG Peng-xiang, et al. Dihydromyricetin Alleviates H9C2 Cell Apoptosis and Autophagy by Regulating CircHIPK3 Expression and PI3K/AKT/mTOR Pathway. [J]. Chinese Journal of Integrative Medicine 29(5):434-440(2023) DOI: 10.1007/s11655-022-3687-4.
Dihydromyricetin Alleviates H9C2 Cell Apoptosis and Autophagy by Regulating CircHIPK3 Expression and PI3K/AKT/mTOR Pathway
摘要
Abstract
Objective:
2
To investigate the effect and potential mechanism of dihydromyricetin (Dmy) on H9C2 cell proliferation
apoptosis
and autophagy.
Methods:
2
H9C2 cells were randomly divided into 7 groups
namely control
model
EV (empty pCDH-CMV-MCS-EF1-CopGFP-T2A-Puro vector)
IV (circHIPK3 interference)
Dmy (50 μmol/L)
Dmy+IV
and Dmy+EV groups. Cell proliferation and apoptosis were detected by cell counting kit-8 assay and flow cytometry
respectivley. Western blot was used to evaluate the levels of light chain 3 Ⅱ/Ⅰ (LC3Ⅱ/Ⅰ)
phospho-phosphoinositide 3-kinase (p-PI3K)
protein kinase B (p-AKT)
and phospho-mammalian target of rapamycin (p-mTOR). The level of circHIPK3 was determined using reverse transcriptase polymerase chain reaction. Electron microscopy was used to observe autophagosomes in H9C2 cells.
Results:
2
Compared to H9C2 cells
the expression of circHIPK in H9C2 hypoxia model cells increased significantly (
P
<
0.05). Compared to the control group
the cell apoptosis and autophagosomes increased
cell proliferation rate decreased significantly
and the expression of LC3Ⅱ/Ⅰ significantly increased (all
P
<
0.05). Compared to the model group
the rate of apoptosis and autophagosomes in IV
Dmy
and Dmy+IV group decreased
the cell proliferation rate increased
and the expression of LC3Ⅱ/Ⅰ decreased significantly (all
P
<
0.05). Compared to the control group
the expressions of p-PI3K
p-AKT
and p-mTOR in the model group significantly reduced (
P
<
0.05)
whereas after treatment with Dmy and sh-circHIPK3
the above situation was reversed (
P
<
0.05).
Conclusion:
2
Dmy plays a protective role in H9C2 cells by inhibiting circHIPK expression and cell apoptosis and autophagy
and the mechanism may be related to PI3K/AKT/mTOR pathway.
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