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Apelin-13 promotes expression of pyroptosis related protein in aortic cells in diabetic mice through eNOS/NO pathway

Authors :
WANG Yang-jia, ZHANG Jia, LI Bin, ZENG Xiang-jun
Source :
Jichu yixue yu linchuang, Vol 40, Iss 2, Pp 155-160 (2020)
Publication Year :
2020
Publisher :
Institute of Basic Medical Sciences and Peking Union Medical College Hospital, Chinese Academy of Medical Sciences / Peking Union Medical College., 2020.

Abstract

Objective To observe the effects and mechanisms of Apelin-13 on expression of pyroptosis related proteins in aorta of diabetic mice. Methods C57/BL mice of eight weeks old were used as control group;kkAy mice of eight weeks old were used as type 2 diabetic models;osmotic pumps were used to treat kkAy mice with apelin-13 at a rate of 30 μg/(kg·d),and L-NAME(eNOS inhibitor) was injected intraperitoneally at a dose of 10 mg/(kg·d) to kkAy mice. Blood was collected for detection of Hb1Ac. The aortae were harvested and fixed. Morphological changes were observed with HE staining. Expression of eNOS,NLRP3,caspase-1 and gasdermin D were measured with immunohistochemical staining. Results Compared to the control group, the level of eNOS in the aorta of diabetic mice was significantly higher than that in control mice (P<0.05),the levels of NLRP3,caspase-1 and gasdermin D were also higher than that in control mice. After apelin-13 treatment,the expressions of eNOS,NLRP3,caspase-1 and gasdermin D were further increased (P<0.05). After L-NAME and apelin-13 treatment, the expressions of eNOS, NLRP3,caspase-1 and gasdermin D were reduced as compared to apelin-13 treatment alone(P<0.05). Conclusions Apelin-13 may promote the expression of pyroptosis related protein in aortic cells by increasing eNOS/NO pathway,which would induce structural and functional damage in diabetic arteries.

Details

Language :
Chinese
ISSN :
10016325
Volume :
40
Issue :
2
Database :
Directory of Open Access Journals
Journal :
Jichu yixue yu linchuang
Publication Type :
Academic Journal
Accession number :
edsdoj.3e1553edddc94bda9c067ca76280c5de
Document Type :
article