PMID- 28713489
OWN - NLM
STAT- MEDLINE
DCOM- 20180409
LR  - 20181113
IS  - 1942-0994 (Electronic)
IS  - 1942-0900 (Print)
IS  - 1942-0994 (Linking)
VI  - 2017
DP  - 2017
TI  - The Inhibitory Effect of WenxinKeli on H9C2 Cardiomyocytes Hypertrophy Induced by 
      Angiotensin II through Regulating Autophagy Activity.
PG  - 7042872
LID - 10.1155/2017/7042872 [doi]
LID - 7042872
AB  - OBJECTIVES: We investigated the role of cardiomyocyte autophagy and its 
      regulatory mechanisms by WenxinKeli (WXKL) in cells subjected to hypertrophy. 
      METHODS: H9C2 cardiomyocytes were divided into 8 groups. Cytoskeletal proteins as 
      well as endogenously expressed autophagy marker proteins were studied by confocal 
      imaging. Western blotting was used to assess the levels of light chain-3 (LC3) 
      and mechanistic target of rapamycin (mTOR). The cell viability assay was used to 
      detect the content of ATP. Flow cytometry was used to detect apoptotic 
      cardiomyocytes. RESULTS: (1) Compared with the control group, the length and 
      width of cells in the Angiotensin II (AngII) group were significantly increased, 
      while those in the 3-methyladenine (3-MA) and the WXKL groups were decreased. (2) 
      Compared with AngII group, the expression of LC3 II/I protein in the 3-MA and 
      WXKL groups was downregulated, while the expression of mTOR protein was 
      upregulated. (3) Compared with the AngII group, the cardiomyocytes in the WXKL 
      group showed increased ATP and decreased apoptosis rate and number of 
      autophagosome. CONCLUSIONS: We propose a novel role of WXKL as a likely inhibitor 
      of cardiac hypertrophy by regulation of pathological autophagy.
FAU - Li, Jie
AU  - Li J
AUID- ORCID: 0000-0002-7598-6391
AD  - Guang'anmen Hospital, Chinese Academy of Chinese Medical Sciences, Beijing 
      100053, China.
AD  - Key Laboratory of Chinese Internal Medicine of the Ministry of Education, 
      Dongzhimen Hospital Affiliated to Beijing University of Chinese Medicine, Beijing 
      100700, China.
FAU - Li, Yang
AU  - Li Y
AD  - Department of Cardiology, General Hospital of People's Liberation Army, Beijing 
      100853, China.
FAU - Zhang, Ying
AU  - Zhang Y
AUID- ORCID: 0000-0002-2543-8602
AD  - Xuan Wu TCM Hospital, Beijing 100053, China.
FAU - Hu, Dan
AU  - Hu D
AD  - Masonic Medical Research Laboratory, Utica, NY 13501, USA.
FAU - Gao, Yonghong
AU  - Gao Y
AD  - Key Laboratory of Chinese Internal Medicine of the Ministry of Education, 
      Dongzhimen Hospital Affiliated to Beijing University of Chinese Medicine, Beijing 
      100700, China.
FAU - Shang, Hongcai
AU  - Shang H
AUID- ORCID: 0000-0001-6628-354X
AD  - Key Laboratory of Chinese Internal Medicine of the Ministry of Education, 
      Dongzhimen Hospital Affiliated to Beijing University of Chinese Medicine, Beijing 
      100700, China.
FAU - Xing, Yanwei
AU  - Xing Y
AUID- ORCID: 0000-0002-1392-9738
AD  - Guang'anmen Hospital, Chinese Academy of Chinese Medical Sciences, Beijing 
      100053, China.
LA  - eng
PT  - Journal Article
DEP - 20170620
PL  - United States
TA  - Oxid Med Cell Longev
JT  - Oxidative medicine and cellular longevity
JID - 101479826
RN  - 11128-99-7 (Angiotensin II)
SB  - IM
MH  - Angiotensin II/pharmacology/*therapeutic use
MH  - Animals
MH  - Autophagy/*drug effects
MH  - Cardiomegaly/metabolism
MH  - Heart Failure/*drug therapy/mortality/pathology
MH  - Humans
MH  - Medicine, Chinese Traditional/*methods
MH  - Myocytes, Cardiac/*drug effects
MH  - Rats
PMC - PMC5496123
EDAT- 2017/07/18 06:00
MHDA- 2018/04/10 06:00
PMCR- 2017/06/20
CRDT- 2017/07/18 06:00
PHST- 2017/03/13 00:00 [received]
PHST- 2017/05/02 00:00 [accepted]
PHST- 2017/07/18 06:00 [entrez]
PHST- 2017/07/18 06:00 [pubmed]
PHST- 2018/04/10 06:00 [medline]
PHST- 2017/06/20 00:00 [pmc-release]
AID - 10.1155/2017/7042872 [doi]
PST - ppublish
SO  - Oxid Med Cell Longev. 2017;2017:7042872. doi: 10.1155/2017/7042872. Epub 2017 Jun 
      20.