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Qiliqiangxin Rescues Mouse Cardiac Function by Regulating AGTR1/TRPV1-Mediated Autophagy in STZ-Induced Diabetes Mellitus
- 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.
- Subjects :
- Qiliqiangxin
AGTR1
TRPV1
Autophagy
Diabetes
Physiology
QP1-981
Biochemistry
QD415-436
Subjects
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