Abstract
Endomorphins (EMs) have a very important bridge-function in cardiovascular, endocrinological, and neurological systems. This study is to investigate the effects of EMs on the synthesis and secretion of vasoactive substances induced by advanced glycation end products in primary cultured human umbilical vein endothelial cells (HUVECs). Firstly, HUVECs were stimulated with AGEs-bovine serum albumin (AGEs-BSA), bovine serum albumin (BSA), or both AGEs-BSA and EMs together, respectively. Then, HUVEC survival rate was calculated by MTT assay, the levels of NO, endothelial nitric oxide synthase (eNOS), and inducible nitric oxide synthase (iNOS) were detected by colorimetric analysis, and the contents of endothelin-1 (ET-1) were detected by ELISA. The mRNA levels of eNOS and ET-1 were measured by RT-PCR. The expression of p38 mitogen-activated protein kinase (p38 MAPK) was detected by immunofluorescence assay. The results showed that the mRNA expression and secretion of eNOS were significantly enhanced after incubation with EMs compared to those with AGEs-BSA, while the secretion of NO and iNOS, mRNA expression, and secretion of ET-1 had opposite changes. The fluorescence intensity of p38MAPK in nuclear was decreased after pretreatment with EMs compared to incubation with AGEs-BSA. Conclusion. The present study suggests that EMs have certain protection effect on AGEs-BSA-induced injury in HUVEC.
Highlights
Overwhelming evidence proved that the formation and accumulation of advanced glycation end products (AGEs) progress in a normal aging process and at an accelerated rate under diabetes [1, 2]; an increase in the steady-state levels of highly reactive dicarbonylic compounds may lead to the formation of AGEs, while an increase in the generation of AGEs can be partly explained by the process of non-enzymatic glycosylation of proteins
Whereas pretreatment with EM1 and EM2 (10 μM, 1 μM, 0.1 μM, 10 nM) significantly increased the cells viability compared to AGEs-bovine serum albumin (BSA) group, the function was obvious at 24 h, 48 h compared to 6 h (P < 0.005 versus P < 0.05), and high concentration was more obvious than low concentration, which indicated that EMs can attenuate the reduction of cell viability by AGEs-BSA in a time- and concentration-dependent manner (Figure 2)
These results indicated that EM1 inhibited the nitric oxide (NO) production in a concentrationdependent manner in human umbilical vein endothelial cells (HUVECs) stimulated by AGEs-BSA
Summary
Overwhelming evidence proved that the formation and accumulation of advanced glycation end products (AGEs) progress in a normal aging process and at an accelerated rate under diabetes [1, 2]; an increase in the steady-state levels of highly reactive dicarbonylic compounds may lead to the formation of AGEs, while an increase in the generation of AGEs can be partly explained by the process of non-enzymatic glycosylation of proteins. These proteins appear to contribute to diverse cellular functions, such as the specific recognition and degradation of AGEs-modified proteins [3]. Preventing the endothelial cell from AGE-triggered injury may improve diabetes-associated vascular complications
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