PMID- 28317089
OWN - NLM
STAT- MEDLINE
DCOM- 20180221
LR  - 20180511
IS  - 1573-675X (Electronic)
IS  - 1360-8185 (Linking)
VI  - 22
IP  - 5
DP  - 2017 May
TI  - EGCG protects against homocysteine-induced human umbilical vein endothelial cells 
      apoptosis by modulating mitochondrial-dependent apoptotic signaling and 
      PI3K/Akt/eNOS signaling pathways.
PG  - 672-680
LID - 10.1007/s10495-017-1360-8 [doi]
AB  - Homocysteine (Hcy) induced vascular endothelial injury leads to the progression 
      of endothelial dysfunction in atherosclerosis. Epigallocatechin gallate (EGCG), a 
      natural dietary antioxidant, has been applied to protect against atherosclerosis. 
      However, the underlying protective mechanism of EGCG has not been clarified. The 
      present study investigated the mechanism of EGCG protected against Hcy-induced 
      human umbilical vein endothelial cells (HUVECs) apoptosis. Methyl thiazolyl 
      tetrazolium assay (MTT), transmission electron microscope, fluorescent staining, 
      flow cytometry, western blot were used in this study. The study has demonstrated 
      that EGCG suppressed Hcy-induced endothelial cell morphological changes and 
      reactive oxygen species (ROS) generation. Moreover, EGCG dose-dependently 
      prevented Hcy-induced HUVECs cytotoxicity and apoptotic biochemical changes such 
      as reducing mitochondrial membrane potential (MMP), decreasing Bcl-2/Bax protein 
      ratio and activating caspase-9 and 3. In addition, EGCG enhanced the protein 
      ratio of p-Akt/Akt, endothelial nitric oxide synthase (eNOS) activation and 
      nitric oxide (NO) formation in injured cells. In conclusion, the present study 
      shows that EGCG prevents Hcy-induced HUVECs apoptosis via modulating 
      mitochondrial apoptotic and PI3K/Akt/eNOS signaling pathways. Furthermore, the 
      results indicate that EGCG is likely to represent a potential therapeutic 
      strategy for atherosclerosis associated with Hyperhomocysteinemia (HHcy).
FAU - Liu, Shumin
AU  - Liu S
AD  - Pharmacology Department, Dalian Medical University, west section 9, south road of 
      Lvshun, 116044, Dalian, China.
FAU - Sun, Zhengwu
AU  - Sun Z
AD  - Pharmacy Department, Dalian Municipal Central Hospital, Dalian, China.
FAU - Chu, Peng
AU  - Chu P
AD  - Pharmacology Department, Dalian Medical University, west section 9, south road of 
      Lvshun, 116044, Dalian, China.
FAU - Li, Hailong
AU  - Li H
AD  - Pharmacology Department, Dalian Medical University, west section 9, south road of 
      Lvshun, 116044, Dalian, China.
FAU - Ahsan, Anil
AU  - Ahsan A
AD  - Pharmacology Department, Dalian Medical University, west section 9, south road of 
      Lvshun, 116044, Dalian, China.
FAU - Zhou, Ziru
AU  - Zhou Z
AD  - Pharmacology Department, Dalian Medical University, west section 9, south road of 
      Lvshun, 116044, Dalian, China.
FAU - Zhang, Zonghui
AU  - Zhang Z
AD  - Pharmacology Department, Dalian Medical University, west section 9, south road of 
      Lvshun, 116044, Dalian, China.
FAU - Sun, Bin
AU  - Sun B
AD  - Pharmacology Department, Dalian Medical University, west section 9, south road of 
      Lvshun, 116044, Dalian, China.
FAU - Wu, Jingjun
AU  - Wu J
AD  - Pharmacology Department, Dalian Medical University, west section 9, south road of 
      Lvshun, 116044, Dalian, China.
FAU - Xi, Yalin
AU  - Xi Y
AD  - Pharmacy Department, Dalian Municipal Central Hospital, Dalian, China.
FAU - Han, Guozhu
AU  - Han G
AD  - Pharmacology Department, Dalian Medical University, west section 9, south road of 
      Lvshun, 116044, Dalian, China.
FAU - Lin, Yuan
AU  - Lin Y
AD  - Pharmacology Department, Dalian Medical University, west section 9, south road of 
      Lvshun, 116044, Dalian, China.
FAU - Peng, Jinyong
AU  - Peng J
AD  - Pharmacology Department, Dalian Medical University, west section 9, south road of 
      Lvshun, 116044, Dalian, China.
FAU - Tang, Zeyao
AU  - Tang Z
AD  - Pharmacology Department, Dalian Medical University, west section 9, south road of 
      Lvshun, 116044, Dalian, China. zeyaotang@163.com.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Apoptosis
JT  - Apoptosis : an international journal on programmed cell death
JID - 9712129
RN  - 0 (Antioxidants)
RN  - 0LVT1QZ0BA (Homocysteine)
RN  - 8R1V1STN48 (Catechin)
RN  - BQM438CTEL (epigallocatechin gallate)
RN  - EC 1.14.13.39 (NOS3 protein, human)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type III)
RN  - EC 2.7.1.- (Phosphatidylinositol 3-Kinases)
RN  - EC 2.7.11.1 (Oncogene Protein v-akt)
SB  - IM
MH  - Antioxidants/*administration & dosage
MH  - Apoptosis/*drug effects
MH  - Atherosclerosis/complications/*diet therapy/genetics/pathology
MH  - Catechin/administration & dosage/*analogs & derivatives
MH  - Homocysteine/toxicity
MH  - Human Umbilical Vein Endothelial Cells/drug effects
MH  - Humans
MH  - Hyperhomocysteinemia/complications/*diet therapy/genetics/pathology
MH  - Mitochondria/drug effects
MH  - Nitric Oxide Synthase Type III/genetics
MH  - Oncogene Protein v-akt/genetics
MH  - Phosphatidylinositol 3-Kinases/genetics
MH  - Signal Transduction/drug effects
OTO - NOTNLM
OT  - Apoptosis
OT  - Epigallocatechin gallate
OT  - Homocysteine
OT  - Protein kinase B
OT  - Reactive oxygen species
EDAT- 2017/03/21 06:00
MHDA- 2018/02/22 06:00
CRDT- 2017/03/21 06:00
PHST- 2017/03/21 06:00 [pubmed]
PHST- 2018/02/22 06:00 [medline]
PHST- 2017/03/21 06:00 [entrez]
AID - 10.1007/s10495-017-1360-8 [pii]
AID - 10.1007/s10495-017-1360-8 [doi]
PST - ppublish
SO  - Apoptosis. 2017 May;22(5):672-680. doi: 10.1007/s10495-017-1360-8.