PMID- 34456712
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20210831
IS  - 1663-9812 (Print)
IS  - 1663-9812 (Electronic)
IS  - 1663-9812 (Linking)
VI  - 12
DP  - 2021
TI  - Curcumin Nanoparticles Attenuate Lipotoxic Injury in Cardiomyocytes Through 
      Autophagy and Endoplasmic Reticulum Stress Signaling Pathways.
PG  - 571482
LID - 10.3389/fphar.2021.571482 [doi]
LID - 571482
AB  - Although curcumin (CUR) has many advantages, its hydrophobicity and instability 
      limit its application. In this study, the anti-lipotoxic injury activity of 
      CUR-loaded nanoparticles (CUR-NPs) and the corresponding mechanism were examined 
      in palmitate (PA)-treated cardiomyocytes. An amphiphilic copolymer was selected 
      as the vehicle material, and CUR-NPs with suitable sizes were prepared under 
      optimized conditions. Cellular uptake was examined by confocal laser scanning 
      microscopy, and cell proliferation inhibition rate was measured using the 
      3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetra bromide (MTT) assay. The terminal 
      deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay was 
      used to detect cell apoptosis. The protein expression was detected by western 
      blot. Exposure to PA reduces the proliferation of cardiomyocytes, but this effect 
      was strongly reversed by CUR-NPs. In addition, our data showed that CUR-NPs 
      strongly inhibited cell apoptosis in PA-treated cardiomyocytes. Furthermore, 
      CUR-NPs remarkably increased the expression of LC3-II, as well as inhibited the 
      expression of p-PERK, p-eIF2alpha, and ATF4 in PA-treated cardiomyocytes. Salubrinal 
      (an eIF2alpha inhibitor) blocked the protective effect of CUR-NPs against PA-induced 
      cardiomyocyte injury. Our results suggested that CUR-NPs can activated the 
      autophagy pathway and protect myocardial cells from apoptosis, and these effects 
      may be mediated by the eIF2alpha-related endoplasmic reticulum stress signaling 
      pathway.
CI  - Copyright (c) 2021 Gu, Xia, Chen and Li.
FAU - Gu, Yue
AU  - Gu Y
AD  - Department of Reparatory and Critical Care Medicine, The First Affiliated 
      Hospital of Jilin University, Changchun, China.
FAU - Xia, Huan
AU  - Xia H
AD  - Department of Reparatory and Critical Care Medicine, The First Affiliated 
      Hospital of Jilin University, Changchun, China.
FAU - Chen, Xiao
AU  - Chen X
AD  - Hubei Province Key Laboratory on Cardiovascular, Cerebrovascular, and Metabolic 
      Disorders, Hubei University of Science and Technology, Xianning, China.
FAU - Li, Jing
AU  - Li J
AD  - Medical College, Huzhou University, Huzhou, China.
LA  - eng
PT  - Journal Article
DEP - 20210311
PL  - Switzerland
TA  - Front Pharmacol
JT  - Frontiers in pharmacology
JID - 101548923
PMC - PMC8386169
OTO - NOTNLM
OT  - autophagy
OT  - cardiomyocyte
OT  - curcumin
OT  - endoplasmic reticulum stress
OT  - nanoparticles
COIS- The authors declare that the research was conducted in the absence of any 
      commercial or financial relationships that could be construed as a potential 
      conflict of interest.
EDAT- 2021/08/31 06:00
MHDA- 2021/08/31 06:01
PMCR- 2021/03/11
CRDT- 2021/08/30 05:48
PHST- 2020/06/16 00:00 [received]
PHST- 2021/01/12 00:00 [accepted]
PHST- 2021/08/30 05:48 [entrez]
PHST- 2021/08/31 06:00 [pubmed]
PHST- 2021/08/31 06:01 [medline]
PHST- 2021/03/11 00:00 [pmc-release]
AID - 571482 [pii]
AID - 10.3389/fphar.2021.571482 [doi]
PST - epublish
SO  - Front Pharmacol. 2021 Mar 11;12:571482. doi: 10.3389/fphar.2021.571482. 
      eCollection 2021.