Downregulation of mi R-146a, cyclooxygenase-2 and advanced glycation end-products in simvastatin-treated older patients with hyperlipidemia.

Autor:	Yang, Zhou Xin, Wang, Ya Zhen, Jia, Bing Bing, Mao, Gen Xiang, Lv, Yuan Dong, Wang, Guo Fu, Yu, Hong
Předmět:	DRUG therapy for hyperlipidemia SIMVASTATIN ALKALINE phosphatase BIOCHEMISTRY BLOOD testing C-reactive protein CHOLESTEROL ENZYME-linked immunosorbent assay GENE expression INTERLEUKIN-1 LACTATE dehydrogenase NONSTEROIDAL anti-inflammatory agents POLYMERASE chain reaction TUMOR necrosis factors CYCLOOXYGENASE 2 ALANINE aminotransferase ADVANCED glycation end-products OLD age THERAPEUTICS
Zdroj:	Geriatrics & Gerontology International; Mar2016, Vol. 16 Issue 3, p322-328, 7p
Abstrakt:	Aim Hyperlipidemia is a disease with abnormally elevated levels of lipids/lipoproteins in the blood, and it is regarded as an important risk factor for cardiovascular and cerebrovascular diseases. Statins have been found to prevent vascular diseases by reducing low-density lipoprotein cholesterol and regulation of immune responses. Here, we aim to study the expression change of immune-related microRNA and genes in older patients with hyperlipidemia after treatment with simvastatin. Methods A total of 25 older male patients with hyperlipidemia were included in the study and received simvastatin treatment (20 mg/day). Clinical characteristics of these patients were examined, including lipoprotein cholesterol, high-sensitivity C-reactive protein, blood routine and biochemical characters. We tested mi R-146a, interleukin-1-receptor-associated kinase 1, tumor necrosis factor-receptor-associated factor 6 and cyclooxygenase-2 level by real-time polymerase chain reaction, and expressions of advanced glycation end-products, p53 and p21 were analyzed by enzyme-linked immunosorbent assay. Results Simvastatin treatment effectively reduced total cholesterol and low-density lipoprotein cholesterol, but had little effect on high-density lipoprotein cholesterol. High-sensitivity C-reactive protein was slightly reduced. Expression of cyclooxygenase-2 and advanced glycation end-products were significantly reduced. Furthermore, simvastatin effectively reduced the expression of p53 and p21. Significantly downregulated mi R-146a, and an obvious reduction of interleukin-1-receptor-associated kinase 1were also detected, whereas tumor necrosis factor-receptor-associated factor 6 remained unchanged. Besides, there was a significant reduction of alanine transaminase, aspertate aminotransferase, alkaline phosphatase and lactate dehydrogenase. Conclusion Simvastatin treatment could inhibit inflammation and senescence-associated genes in older patients with hyperlipidemia, suggesting its application in inflammatory and age-related diseases. Geriatr Gerontol Int 2015; ●●: ●●-●●. [ABSTRACT FROM AUTHOR]
Databáze:	Complementary Index
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