PMID- 28802718
OWN - NLM
STAT- MEDLINE
DCOM- 20180601
LR  - 20180601
IS  - 1879-0712 (Electronic)
IS  - 0014-2999 (Linking)
VI  - 814
DP  - 2017 Nov 5
TI  - Curcumin ameliorates cardiac dysfunction induced by mechanical trauma.
PG  - 73-80
LID - S0014-2999(17)30502-2 [pii]
LID - 10.1016/j.ejphar.2017.07.048 [doi]
AB  - Curcumin, a phytochemical component derived from turmeric (Carcuma longa), has 
      been extensively investigated because of its anti-inflammatory and anti-oxidative 
      properties. Inflammation and oxidative stress play critical roles in 
      posttraumatic cardiomyocyte apoptosis, which contributes to secondary cardiac 
      dysfunction. This research was designed to identify the protective effect of 
      curcumin on posttraumatic cardiac dysfunction and investigate its underlying 
      mechanism. Noble-Collip drum was used to prepare a mechanical trauma (MT) model 
      of rats, and the hemodynamic responses of traumatized rats were observed by 
      ventricular intubation 12h after trauma. Myocardial apoptosis was determined 
      through terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) 
      staining and caspase-3 activity assay. Tumor necrosis factor-alpha (TNF-alpha) and 
      reactive oxygen species (ROS) generated by monocytes and myocardial cells were 
      identified through enzyme-linked immunosorbent assay (ELISA), and the 
      intracellular alteration of Ca(2+) in cardiomyocytes was examined through 
      confocal microscopy. In vivo, curcumin effectively ameliorated MT-induced 
      secondary cardiac dysfunction and significantly decreased the apoptotic indices 
      of the traumatized myocardial cells. In vitro, curcumin inhibited TNF-alpha 
      production by monocytes and reduced the circulating TNF-alpha levels. With curcumin 
      pretreatment, ROS production and Ca(2+) overload in H9c2 cells were attenuated 
      when these cells were incubated with traumatic plasma. Therefore, curcumin can 
      effectively ameliorate MT-induced cardiac dysfunction mainly by inhibiting 
      systemic inflammatory responses and by weakening oxidative stress reaction and 
      Ca(2+) overload in cardiomyocytes.
CI  - Copyright (c) 2017 Elsevier B.V. All rights reserved.
FAU - Li, Xintao
AU  - Li X
AD  - Department of Physiology, Dalian Medical University, Dalian, Liaoning 116044, 
      China.
FAU - Cao, Tingting
AU  - Cao T
AD  - Department of Physiology, Dalian Medical University, Dalian, Liaoning 116044, 
      China.
FAU - Ma, Shuo
AU  - Ma S
AD  - Department of Physiology, Dalian Medical University, Dalian, Liaoning 116044, 
      China.
FAU - Jing, Zehao
AU  - Jing Z
AD  - Department of Physiology, Dalian Medical University, Dalian, Liaoning 116044, 
      China.
FAU - Bi, Yue
AU  - Bi Y
AD  - Department of Physiology, Dalian Medical University, Dalian, Liaoning 116044, 
      China.
FAU - Zhou, Jicheng
AU  - Zhou J
AD  - Department of Physiology, Dalian Medical University, Dalian, Liaoning 116044, 
      China.
FAU - Chen, Chong
AU  - Chen C
AD  - Department of Physiology, Dalian Medical University, Dalian, Liaoning 116044, 
      China.
FAU - Yu, Deqin
AU  - Yu D
AD  - Department of Physiology, Dalian Medical University, Dalian, Liaoning 116044, 
      China.
FAU - Zhu, Liang
AU  - Zhu L
AD  - Department of Physiology, Dalian Medical University, Dalian, Liaoning 116044, 
      China. Electronic address: zhuliang0210@sina.com.
FAU - Li, Shuzhuang
AU  - Li S
AD  - Department of Physiology, Dalian Medical University, Dalian, Liaoning 116044, 
      China. Electronic address: shuzhuangli@126.com.
LA  - eng
PT  - Journal Article
DEP - 20170810
PL  - Netherlands
TA  - Eur J Pharmacol
JT  - European journal of pharmacology
JID - 1254354
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 3.4.22.- (Caspase 3)
RN  - IT942ZTH98 (Curcumin)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Animals
MH  - Apoptosis/drug effects
MH  - Calcium/metabolism
MH  - Caspase 3/metabolism
MH  - Cell Line
MH  - Curcumin/*pharmacology
MH  - Heart/*drug effects/*physiopathology
MH  - Hemodynamics/drug effects
MH  - Male
MH  - *Mechanical Phenomena
MH  - Myocytes, Cardiac/drug effects/metabolism/pathology
MH  - Oxidative Stress/drug effects
MH  - Rats
MH  - Reactive Oxygen Species/metabolism
MH  - Time Factors
MH  - Tumor Necrosis Factor-alpha/blood
OTO - NOTNLM
OT  - Apoptosis
OT  - Cardiac dysfunction
OT  - Curcumin
OT  - Curcumin (PubChem CID: 969516)
OT  - Mechanical trauma
OT  - Reactive oxygen species
EDAT- 2017/08/15 06:00
MHDA- 2018/06/02 06:00
CRDT- 2017/08/14 06:00
PHST- 2017/04/29 00:00 [received]
PHST- 2017/07/27 00:00 [revised]
PHST- 2017/07/28 00:00 [accepted]
PHST- 2017/08/15 06:00 [pubmed]
PHST- 2018/06/02 06:00 [medline]
PHST- 2017/08/14 06:00 [entrez]
AID - S0014-2999(17)30502-2 [pii]
AID - 10.1016/j.ejphar.2017.07.048 [doi]
PST - ppublish
SO  - Eur J Pharmacol. 2017 Nov 5;814:73-80. doi: 10.1016/j.ejphar.2017.07.048. Epub 
      2017 Aug 10.