PMID- 29289557
OWN - NLM
STAT- MEDLINE
DCOM- 20181211
LR  - 20210208
IS  - 1872-6216 (Electronic)
IS  - 0047-6374 (Linking)
VI  - 175
DP  - 2018 Oct
TI  - Salidroside attenuates endothelial cellular senescence via decreasing the 
      expression of inflammatory cytokines and increasing the expression of SIRT3.
PG  - 1-6
LID - S0047-6374(17)30163-X [pii]
LID - 10.1016/j.mad.2017.12.005 [doi]
AB  - OBJECTIVE: Endothelial cellular senescence is an important contributor to the 
      endothelial dysfunction and atherosclerosis. Our previous studies suggested that 
      salidroside (SAL) can alleviate atherosclerosis and protect endothelial cells 
      against oxidative stress induced damage. However, the effect and mechanism of SAL 
      on endothelial cellular senescence is still unclear. Here, we investigated the 
      underlying mechanisms of SAL on preventing endothelial cellular premature 
      senescence. METHODS AND RESULTS: We established a hyperhomocysteinemia 
      (HHcy)mouse model via high methionine diet (HMD) to explore the protective effect 
      of SAL. According to our results, the HMD elevated the concentration of serum 
      homocysteine. HHcy induced the collagen deposition and the up-regulation of 
      senescence markers, i.e. p16(INK4A) and p21(CIP1), in intima-medial of aorta. In 
      addition, SAL also inhibited the expression of CD68 and intercellular adhesion 
      molecule 1 (ICAM1) in aorta. In senescent human umbilical vein endothelial cells 
      (HUVECs) induced by H(2)O(2), SAL treatment alleviated the expression of 
      p16(INK4A) and p21(CIP1) and reduced the activity of senescence-associated 
      (SA)-beta-gal. CONCLUSION: our data suggested that SAL decreased the expression of 
      inflammatory cytokines and up-regulated the expression of SIRT3, which might be 
      the underlying mechanism of SAL on preventing endothelial cells from premature 
      senescence.
CI  - Copyright (c) 2018 Elsevier B.V. All rights reserved.
FAU - Xing, Sha-Sha
AU  - Xing SS
AD  - Clinical Drug Trial Center, Affiliated Hospital of Chengdu University, Chengdu 
      University, Chengdu, Sichuan, 610081, PR China.
FAU - Li, Jian
AU  - Li J
AD  - Department of Basic Medicine, Chengdu University School of Medicine, Chengdu, 
      Sichuan, 610106, PR China.
FAU - Chen, Lin
AU  - Chen L
AD  - Department of Urology, Affiliated Hospital of Chengdu University, Chengdu, 
      Sichuan, 610081, PR China.
FAU - Yang, Ya-Fei
AU  - Yang YF
AD  - Department of Urology, Affiliated Hospital of Chengdu University, Chengdu, 
      Sichuan, 610081, PR China.
FAU - He, Ping-Lin
AU  - He PL
AD  - Department of Urology, Affiliated Hospital of Chengdu University, Chengdu, 
      Sichuan, 610081, PR China.
FAU - Li, Jun
AU  - Li J
AD  - Clinical Drug Trial Center, Affiliated Hospital of Chengdu University, Chengdu 
      University, Chengdu, Sichuan, 610081, PR China; Department of General Surgery, 
      Affiliated Hospital of Chengdu University, Chengdu University, Chengdu, Sichuan, 
      610081, PR China. Electronic address: junl_paper@sina.com.
FAU - Yang, Jin
AU  - Yang J
AD  - Clinical Drug Trial Center, Affiliated Hospital of Chengdu University, Chengdu 
      University, Chengdu, Sichuan, 610081, PR China; Department of Urology, Affiliated 
      Hospital of Chengdu University, Chengdu, Sichuan, 610081, PR China. Electronic 
      address: dr.jinyang@163.com.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20171228
PL  - Ireland
TA  - Mech Ageing Dev
JT  - Mechanisms of ageing and development
JID - 0347227
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (CDKN2A protein, human)
RN  - 0 (Cdkn1a protein, mouse)
RN  - 0 (Cdkn2a protein, mouse)
RN  - 0 (Cyclin-Dependent Kinase Inhibitor p16)
RN  - 0 (Cyclin-Dependent Kinase Inhibitor p21)
RN  - 0 (Cytokines)
RN  - 0 (Glucosides)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Phenols)
RN  - 0 (Sirt3 protein, mouse)
RN  - 9007-34-5 (Collagen)
RN  - EC 3.2.1.23 (beta-Galactosidase)
RN  - EC 3.5.1.- (SIRT3 protein, human)
RN  - EC 3.5.1.- (Sirtuin 3)
RN  - M983H6N1S9 (rhodioloside)
SB  - IM
MH  - Animals
MH  - Anti-Inflammatory Agents/*pharmacology
MH  - Aorta/*drug effects/enzymology/pathology
MH  - Cells, Cultured
MH  - Cellular Senescence/*drug effects
MH  - Collagen/metabolism
MH  - Cyclin-Dependent Kinase Inhibitor p16/metabolism
MH  - Cyclin-Dependent Kinase Inhibitor p21/metabolism
MH  - Cytokines/*metabolism
MH  - Disease Models, Animal
MH  - Glucosides/*pharmacology
MH  - Human Umbilical Vein Endothelial Cells/*drug effects/enzymology/pathology
MH  - Humans
MH  - Hyperhomocysteinemia/*drug therapy/enzymology/pathology
MH  - Inflammation Mediators/*metabolism
MH  - Male
MH  - Mice, Inbred BALB C
MH  - Phenols/*pharmacology
MH  - Sirtuin 3/*metabolism
MH  - Up-Regulation
MH  - Vascular Remodeling/drug effects
MH  - beta-Galactosidase/metabolism
OTO - NOTNLM
OT  - Endothelial cellular senescence
OT  - Inflammatory cytokines
OT  - SIRT3
OT  - Salidroside
EDAT- 2018/01/01 06:00
MHDA- 2018/12/12 06:00
CRDT- 2018/01/01 06:00
PHST- 2017/06/15 00:00 [received]
PHST- 2017/12/26 00:00 [revised]
PHST- 2017/12/27 00:00 [accepted]
PHST- 2018/01/01 06:00 [pubmed]
PHST- 2018/12/12 06:00 [medline]
PHST- 2018/01/01 06:00 [entrez]
AID - S0047-6374(17)30163-X [pii]
AID - 10.1016/j.mad.2017.12.005 [doi]
PST - ppublish
SO  - Mech Ageing Dev. 2018 Oct;175:1-6. doi: 10.1016/j.mad.2017.12.005. Epub 2017 Dec 
      28.