FOLLOWUS
1.Department of Cardiology, the Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou (510630), China
2.Department of Cardiology, the Eighth Affiliated Hospital of Sun Yat-Sen University, Shenzhen, Guangdong Province (518033), China
3.Department of Cardiology, the First Affiliated Hospital of Henan University, Kaifeng, Henan Province (475001), China
4.Department of Nutrition and Food Science, Texas A&M University, College Station, TX (77843), United States of America
5.Institute of Integrated Traditional Chinese and Western Medicine, Sun Yat-Sen University, Guangzhou (510630), China
Prof. QIAN Xiao-xian, E-mail: qianxx@mail.sysu.edu.cn
纸质出版日期:2021-05-01,
网络出版日期:2020-01-09,
录用日期:2019-08-21
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Shi-ye KE, Shu-jie YU, Ding-hui LIU, 等. Ginsenoside Rb1 Protects Human Umbilical Vein Endothelial Cells against High Glucose-Induced Mitochondria-Related Apoptosis through Activating SIRT3 Signalling Pathway*[J]. Chinese Journal of Integrative Medicine, 2021,27(5):336-344.
Shi-ye KE, Shu-jie YU, Ding-hui LIU, et al. Ginsenoside Rb1 Protects Human Umbilical Vein Endothelial Cells against High Glucose-Induced Mitochondria-Related Apoptosis through Activating SIRT3 Signalling Pathway*[J]. Chinese Journal of Integrative Medicine, 2021,27(5):336-344.
Shi-ye KE, Shu-jie YU, Ding-hui LIU, 等. Ginsenoside Rb1 Protects Human Umbilical Vein Endothelial Cells against High Glucose-Induced Mitochondria-Related Apoptosis through Activating SIRT3 Signalling Pathway*[J]. Chinese Journal of Integrative Medicine, 2021,27(5):336-344. DOI: 10.1007/s11655-020-3478-8.
Shi-ye KE, Shu-jie YU, Ding-hui LIU, et al. Ginsenoside Rb1 Protects Human Umbilical Vein Endothelial Cells against High Glucose-Induced Mitochondria-Related Apoptosis through Activating SIRT3 Signalling Pathway*[J]. Chinese Journal of Integrative Medicine, 2021,27(5):336-344. DOI: 10.1007/s11655-020-3478-8.
Objective:
2
To investigate whether ginsenoside Rb1 (Rb1) can protect human umbilical vein endothelial cells (HUVECs) against high glucose-induced apoptosis and examine the underlying mechanism.
Methods:
2
HUVECs were divided into 5 groups: control group (5.5 mmol/L glucose)
high glucose (HG
40 mmol/L) treatment group
Rb1 (50 μmol/L) treatment group
Rb1 plus HG treatment group
and Rb1 and 3-(
1
H-1
2
3-triazol-4-yl) pyridine (3-TYP
16 μmol/L) plus HG treatment group. Cell viability was evaluated by cell counting kit-8 assay. Mitochondrial and intracellular reactive oxygen species were detected by MitoSox Red mitochondrial superoxide indicator and dichloro-dihydro-fluorescein diacetate assay
respectively. Annexin V/propidium iodide staining and fluorescent dye staining were used to measure the apoptosis and the mitochondrial membrane potential of HUVECs
respectively. The protein expressions of apoptosis-related proteins [Bcl-2
Bax
cleaved caspase-3 and cytochrome c (Cyt-c)]
mitochondrial biogenesis-related proteins [proliferator-activated receptor gamma coactivator 1-alpha
nuclear respiratory factor-1 and mitochondrial transcription factor A)]
acetylation levels of forkhead box O3a and SOD2
and sirtuin-3 (SIRT3) signalling pathway were measured by immunoblotting and immunoprecipitation.
Results:
2
Rb1 ameliorated survival in cells in which apoptosis was induced by high glucose (
P
<
0.05 or
P
<
0.01). Upon the addition of Rb1
mitochondrial and intracellular reactive oxygen species generation and malondialdehyde levels were decreased (
P
<
0.01)
while the activities of antioxidant enzymes were increased (
P
<
0.05 or
P
<
0.01). Rb1 preserved the mitochondrial membrane potential and reduced the release of Cyt-c from the mitochondria into the cytosol (
P
<
0.01). In addition
Rb1 upregulated mitochondrial biogenesis-associated proteins (
P
<
0.01). Notably
the cytoprotective effects of Rb1 were correlated with SIRT3 signalling pathway activation (
P
<
0.01). The effect of Rb1 against high glucose-induced mitochondria-related apoptosis was restrained by 3-TYP (
P
<
0.05 or
P
<
0.01).
Conclusion:
2
Rb1 could protect HUVECs from high glucose-induced apoptosis by promoting mitochondrial function and suppressing oxidative stress through the SIRT3 signalling pathway.
ginsenoside Rb1high glucosehuman umbilical vein endothelial cellsapoptosismitochondriaSIRT3 signalling pathway
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