Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Advance glycation end products (AGEs) have been postulated to play an important role in diabetic complications such as atherosclerosis disease. Adhesion and migration of leukocyte to endothelial cells (EC) is one of the early key steps in the pathogenesis. Crocetin is an important ingredient of diet in India and also used in various systems of indigenous medicine. In this study, we investigated effect of crocetin on leukocyte adherence to bovine endothelial cells (BEC) induced by AGEs in vitro and the possible mechanisms involved. BEC were pre-incubated with crocetin (0.01, 0.1, and 1 microM) for 12 h and exposed to AGEs (100 microg/ml). Cells proliferation was determined by MTT; leukocyte-endothelial cell adhesion was assayed by myeloperoxidase methods; intercellular adhesion molecular-1 (ICAM-1) protein expression was studied by immunocytochemistry and mitochondrial membrane potential (MMP) was analyzed by the retention of rhodamine 123 (RH123); furthermore, levels of anion (O(2)(-)), malonicdialdehyde (MDA) in super cells culture and superoxide dismutase (SOD) in cells were also detected, respectively. Results demonstrated that crocetin could inhibit AGE-induced BEC growth suppression and significantly reduce adhesion rate of leukocyte to BEC (P < 0.01 or P < 0.05); ICAM-1 protein was also suppressed (P < 0.05). Furthermore, crocetin could increase activity of SOD (P < 0.05), decrease levels of MDA and O(2)(-) (P < 0.01). In addition, down-regulated MMP was also increased by crocetin (P < 0.01 or P < 0.05). These data revealed crocetin could prevent the adhesion of leukocyte to BEC and down-regulation the expression of ICAM-1, and the possible mechanisms might be related to its antioxidant activity, which is through up-regulation of the activity of antioxidant enzymes and protection for mitochondrion.
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PMID:Crocetin inhibits leukocyte adherence to vascular endothelial cells induced by AGEs. 1652 88

Angiotensin II (Ang II) induces vascular smooth muscle cells (VSMCs) proliferation, which plays an important role in the development and progression of atherosclerosis. Ang II-induced cellular events have been implicated, in part, in the activation of extracellular signal-regulated kinases 1/2 (ERK1/2). Crocetin is a natural carotenoid compound isolated from Gardenia jasminoids Ellis. In the present study, we investigated the effect of crocetin on the Ang II-induced VSMCs proliferation and ERK1/2 activation. 3-[4,5-dimethylthiazol-2-yl]-2,5-dephenyl tetrazolium bromide (MTT) and [3H]thymidine incorporation assay showed that the Ang II-induced VSMCs proliferation was inhibited significantly by crocetin. In-gel kinase assay indicated that Ang II elicited rapid and significant increase of ERK1/2 activity in VSMCs, which was suppressed by crocetin markedly. Western blotting analysis and cell-based enzyme-linked immunosorbent assay (ELISA) demonstrated that crocetin significantly inhibited the phosphorylation and activation of ERK1/2 induced by Ang II. Using the indirect immunofluorescent technique, we also found that crocetin inhibited nuclear translocation of activated ERK1/2 induced by Ang II. These findings suggest that the suppression by crocetin of the Ang II-induced VSMCs proliferation can be attributed, at least in part, to its inhibitory effect on ERK1/2 pathway.
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PMID:ERK1/2 pathway is involved in the inhibitory effect of crocetin on angiotensin II-induced vascular smooth muscle cell proliferation. 1658 Mar 46

Antioxidants have been expected to have potential as antiatherogenic agents. Crocetin is a natural carotenoid antioxidant isolated from Gardenia jasminoids Ellis. Therefore, in the present study, we investigated the inhibitory effect of Crocetin on experimental atherosclerosis in quails. The atherosclerosis model was established by feeding hyperlipidamic diet to quail and Crocetin (25, 50, 100 mg/kg/day) was administered by oral gavage. At the 9th week, serum lipids, malondialdehyde and nitric oxide were measured, and Hematoxylin-Eosin (H&E) stains was used to investigate the histopathological changes of aorta. Results showed that Crocetin could reduce the levels of serum total cholesterol, triglyceride, low density lipoprotein cholesterol and inhibit the formation of aortic plaque. Crocetin could also reduce malondialdehyde and inhibit the descending of nitric oxide in serum. The results suggested that Crocetin could inhibit the formation of atherosclerosis in quails, which might be related to the hypolipidemic effects along with the antioxidative properties of Crocetin.
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PMID:Influence of Crocetin on experimental atherosclerosis in hyperlipidamic-diet quails. 1710 48