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Qiliqiangxin Rescues Mouse Cardiac Function by Regulating AGTR1/TRPV1-Mediated Autophagy in STZ-Induced Diabetes Mellitus

Authors :
Jing Tong
Yan Lai
Yi-An Yao
Xue-Jun Wang
Yu-Shuang Shi
Han-Jin Hou
Jian-Yun Gu
Fei Chen
Xue-Bo Liu
Source :
Cellular Physiology and Biochemistry, Vol 47, Iss 4, Pp 1365-1376 (2018)
Publication Year :
2018
Publisher :
Cell Physiol Biochem Press GmbH & Co KG, 2018.

Abstract

Background/Aims: To explore the potential role of qiliqiangxin (QLQX) A traditional Chinese medicine and the involvement of angiotensin II receptor type 1 (AGTR1) and transient receptor potential vanilloid 1 (TRPV1) in diabetic mouse cardiac function. Methods: Intragastric QLQX was administered for 5 weeks after streptozotocin (STZ) treatment. Additionally, Intraperitoneal injections of angiotensin II (Ang II) or intragastric losartan (Los) were administered to assess the activities of AGTR1 and TRPV1. Two-dimensional echocardiography and tissue histopathology were used to assess cardiac function Western blot was used to detect the autophagic biomarkers Such as light chain 3 P62 and lysosomal-associated membrane protein 2 And transmission electron microscopy was used to count the number of autophagosomes. Results: Decreased expression of TRPV1 and autophagic hallmarks and reduced numbers of autophagolysosomes as well as increased expression of angiotensin converting enzyme 1 and AGTR1 were observed in diabetic hearts. Blocking AGTR1 with Los mimicked the QLQX-mediated improvements in cardiac function Alleviated myocardial fibrosis and enabled autophagy Whereas Ang II abolished the beneficial effects of QLQX in wild type diabetic mice but not in TRPV1-/- diabetic mice. Conclusions: QLQX may improve diabetic cardiac function by regulating AGTR1/ TRPV1-mediated autophagy in STZ-induced diabetic mice.

Details

Language :
English
ISSN :
10158987 and 14219778
Volume :
47
Issue :
4
Database :
Directory of Open Access Journals
Journal :
Cellular Physiology and Biochemistry
Publication Type :
Academic Journal
Accession number :
edsdoj.33ca489b5ed439992a75f25cf4419d1
Document Type :
article
Full Text :
https://doi.org/10.1159/000490822