RGD Reference Report - Liraglutide attenuates atherosclerosis via inhibiting ER-induced macrophage derived microvesicles production in T2DM rats. - Rat Genome Database

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Liraglutide attenuates atherosclerosis via inhibiting ER-induced macrophage derived microvesicles production in T2DM rats.

Authors: Li, Jinjin  Liu, Xiaojuan  Fang, Qianhua  Ding, Min  Li, Chunjun 
Citation: Li J, etal., Diabetol Metab Syndr. 2017 Dec 1;9:94. doi: 10.1186/s13098-017-0289-y. eCollection 2017.
RGD ID: 13792600
Pubmed: PMID:29213335   (View Abstract at PubMed)
PMCID: PMC5710066   (View Article at PubMed Central)
DOI: DOI:10.1186/s13098-017-0289-y   (Journal Full-text)


Background: We investigated the effects of liraglutide on the formation and progression of atherosclerosis in type 2 diabetes mellitus (T2DM) rats.
Methods: Sprague-Dawley rats were divided into control group, diabetes group and liraglutide treated group. The T2DM rats model with atherosclerosis were induced by high fat diet followed small dosage streptozotocin injection. Body weight and blood glucose levels were monitored once a week for 3 months and then the rats were sacrificed.Peripheral blood and aorta tissues were collected for further biochemical and pathological estimation respectively. Moreover, immunohistochemistry staining was used to detect the infiltration of macrophages and cell apoptosis in tissue samples. The amount of microvesicles of atherosclerotic plaques was determined by ELISA. Western blot was applied to detect the protein expressions of CHOP, GRP78 and caspase-3 in tissue samples. The mRNA expressions of SREBP-1c and FAS were detected by RT-PCR.
Results: The rat model of diabetic atherosclerosis was established successfully. Compared with the control group, glucose, triglycerides, total cholesterol, AST, ALT, BUN, fasting insulin and homeostatic model assessment insulin resistance levels in peripheral blood were significantly increased in the diabetes group. While, these indicators in the liraglutide group were significantly lower than that in the diabetes group. Moreover, the atherosclerotic plaques were observed in the rats of diabetes group but not remarkable in the liraglutide group. The ratio between aorta intima and media thickness was significantly greater in the diabetes group than that in the liraglutide group. Compared with the diabetes group, the infiltration and apoptosis of macrophages were milder in the liraglutide group. The expressions of CD68, caspase-3, CHOP and GRP78 in aorta tissue samples were significantly downregulated in the liraglutide group than that in the diabetes group. Furthermore, the microvesicles of aorta tissues in the liraglutide group were significantly decreased than that in the diabetes group. The mRNA expressions of SREBP-1c and FAS were lower in the liraglutide group than that in the diabetes group.
Conclusion: Liraglutide attenuates diabetic atherosclerosis by inhibition of ER stress and subsequent macrophage apoptosis and microvesicles production in T2DM rats.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
CASP3Humanatherosclerosis treatmentISOCasp3 (Rattus norvegicus)associated with type 2 diabetes mellitusRGD 
Casp3Ratatherosclerosis treatmentIEP associated with type 2 diabetes mellitusRGD 
Casp3Mouseatherosclerosis treatmentISOCasp3 (Rattus norvegicus)associated with type 2 diabetes mellitusRGD 
FASHumanatherosclerosis treatmentISOFas (Rattus norvegicus)associated with type 2 diabetes mellitusRGD 
FasRatatherosclerosis treatmentIEP associated with type 2 diabetes mellitusRGD 
FasMouseatherosclerosis treatmentISOFas (Rattus norvegicus)associated with type 2 diabetes mellitusRGD 

Objects Annotated

Genes (Rattus norvegicus)
Casp3  (caspase 3)
Fas  (Fas cell surface death receptor)

Genes (Mus musculus)
Casp3  (caspase 3)
Fas  (Fas cell surface death receptor)

Genes (Homo sapiens)
CASP3  (caspase 3)
FAS  (Fas cell surface death receptor)


Additional Information