التفاصيل البيبلوغرافية
| العنوان: |
Atorvastatin inhibits endoplasmic reticulum stress through AMPK signaling pathway in atherosclerosis in mice. |
| المؤلفون: |
Xiong, Wangqiong, Fei, Minzhong, Wu, Chuntao, Wang, Wei, Luo, Rong, Shen, Liping, Zhang, Zheng |
| المصدر: |
Experimental & Therapeutic Medicine; Mar2020, Vol. 19 Issue 3, p2266-2272, 7p |
| مصطلحات موضوعية: |
ENDOPLASMIC reticulum, ATORVASTATIN, WESTERN immunoblotting, IMMUNOSTAINING, UMBILICAL veins |
| مستخلص: |
Effect of atorvastatin inhibition of endoplasmic reticulum stress and amelioration of atherosclerosis through AMPK pathway were studied. Eight-week-old male apolipoprotein E-deficient (ApoE−/−) mice were fed with high-fat diet for 2 weeks and randomly divided into two groups: Atorvastatin treatment group was given atorvastatin (5 mg/kg/day) injection for a total of 6 weeks; control group was given the same dose of PBS through intraperitoneal injection for a total of 6 weeks. H&E staining was used to detect plaque size; immunohistochemical staining was used to detect T cells, macrophages and phospho-protein kinase-like ER kinase (phospho-PERK) in localized plaques. Proteins were extracted from mouse thoracic and abdominal aortic tissues. Western blot analysis was used to detect the protein expression levels of endoplasmic reticulum stress-related molecules phospho-eukaryotic initiation factor-2α (p-eIF2α), eukaryotic initiation factor (eIF2a), and sliced x-box binding protein 1 (sXBP-1). Cultured human umbilical vein endothelial cells (HUVECs), induced endoplasmic reticulum stress with human oxidized low density lipoprotein (ox-LDL), were treated with atorvastatin, AMPK agonist 5-amino-4-imidazolecarboxamide riboside-I-β-D-ribofuranoside (AICAR) and AMPK-DN that expressed a dominant-negative mutant of AMPK. Western blot analysis was used to test the expression levels of endoplasmic reticulum stress-related molecules p-elF2a and sXBP-1. The area of aortic plaques in atorvastatin group was obviously decreased, and the infiltrations of CD3+ T cells and macrophages in the localized plaques were reduced. The endoplasmic reticulum stress-related proteins sXBP-1 and p-eIF2a were significantly reduced. The results of immunohistochemistry also showed a significant decrease in the level of phospho-PERK (p-PERK) in atorvastatin group. The results in ox-LDL-induced HUVECs showed that atorvastatin inhibited ox-LDL-induced endoplasmic reticulum stress, and the AMPK agonist AICAR also had the same effect, which was offset by DN-AMPK treatment. Atorvastatin inhibits ER stress both in vitro and in vivo and this protective effect is mediated by AMPK activation. [ABSTRACT FROM AUTHOR] |
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| قاعدة البيانات: |
Complementary Index |
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