Effect of Endomorphins on HUVECs Treated by ox-LDL and Its Related Mechanisms

نویسندگان

  • Juan Zhao
  • Qi Zhang
  • Jing Liu
  • Liming Tian
  • Wenhui Huang
  • Jinxing Quan
  • Jinyang Wang
  • Yanjia Xu
  • Yunfang Wang
  • Ruilan Niu
چکیده

We found in the present study that treatment with ox-LDL decreased the cell viability and the content of nitric oxide (NO) and the activity of nitric oxide synthase (NOS) as well as eNOS mRNA expression, while increasing the mRNA expression and content of endothelin-1 (ET-1) in human umbilical vein endothelial cells (HUVECs). However, endomorphins EM1/EM2 increased the cell viability and the content of NO and the activity of NOS as well as eNOS mRNA expression, while decreasing the mRNA expression and content of ET-1 compared with ox-LDL alone. Meanwhile, the expressions of JNK and p-JNK were enhanced by ox-LDL while being suppressed by EM1/EM2. The results suggested that EM1 and EM2 can correct the endothelial cell dysfunction induced by ox-LDL and the protective effect may be achieved by affecting the JNK pathway.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Rapamycin Inhibits Oxidized Low Density Lipoprotein Uptake in Human Umbilical Vein Endothelial Cells via mTOR/NF-κB/LOX-1 Pathway.

BACKGROUND Lectin-like oxidized low-density lipoprotein-1 (LOX-1) is the major receptor for oxidized low density lipoprotein (ox-LDL) uptake in human umbilical vein endothelial cells (HUVECs). Previously, we found that rapamycin inhibited ox-LDL accumulation in HUVECs, and this effect was related to its role in increasing the activity of autophagy-lysosome pathway. In this study, we determined ...

متن کامل

Compare the Effect of Eicosapentaenoic Acid and Oxidized Low-Density Lipoprotein on the Expression of CD36 and Peroxisome Proliferator-Activated Receptor Gamma

Background: There is evidence that CD36 promotes foam cell formation through internalizing oxidized LDL (ox-LDL) into macrophages therefore, it plays a key role in pathogenesis of atherosclerosis. In addition, CD36 expression seems to be mediated by nuclear receptor peroxisome proliferator-activated receptor gamma (PPAR-γ). The aim of the present study was to evaluate and compare the effect of ...

متن کامل

TLR2 expression doesn't change in ox-LDL mediated inflammation in Human umbilical vein endothelial cells under high glucose culture.

BACKGROUND Inflammatory responses induced by ox-LDL play important roles in atherogenesis, and could be promoted in diabetic patients. Toll-like receptor (TLR)2 is an innate inflammatory receptor, and is enhanced in human umbilical vein endothelial cells (HUVECs) under high glucose conditions. Ox-LDL-TLR2 pathway activation and further inflammation in monocytes are involved in the atheroscleros...

متن کامل

Effects and mechanisms of icariin on atherosclerosis.

PURPOSE Icariin, a flavonoid isolated from the traditional Chinese herbal medicine Epimedium brevicornum Maxim, has been shown to process anti-inflammatory, antioxidative actions and anti-atherosclerosis activity in vivo and in vitro. The purpose of this study was to investigate the effects and mechanisms of icariin on atherosclerosis by human umbilical vein endothelial cells (HUVECs). METHOD...

متن کامل

Allicin prevents oxidized low-density lipoprotein-induced endothelial cell injury by inhibiting apoptosis and oxidative stress pathway.

BACKGROUND Vascular endothelial apoptosis is significantly associated with atherosclerosis and cardiovascular diseases, for which oxidized low-density lipoprotein (ox-LDL) is a major risk factor. Allicin, the primary active ingredient of garlic, has been found to have cardiovascular protective effect by changing the fatty-acid composition, but its effect on ox-LDL-induced vascular endothelial i...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره 2016  شماره 

صفحات  -

تاریخ انتشار 2016