Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.24.23 (MMP)
 4,246 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Foot ulceration is a major cause of morbidity in patients with diabetes, and abnormal peripheral neuropathy often results in hospitalization. Up-regulation of matrix metalloproteinases and down-regulation of tissue inhibitor of metalloproteinase 1 are noted to be distinctive biological functions of diabetic dermal fibroblasts. The aim of this study was to evaluate the biological effects of modified retinoids on diabetic fibroblasts. Myricetin, a natural compound, balances the TIMP1/MMP ratio and oxidative stress in diabetic fibroblasts. Our results indicate that myricetin significantly ameliorates the effects of diabetes on dermal fibroblasts. In addition, we found that the oxidative stress imbalance induced by a high glucose concentration plays an important role in the changes to dermal fibroblasts that occur in diabetes. Our findings support the hypothesis that myricetin has the potential to repair faulty skin function arising from diabetes.
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PMID:Myricetin, a potent natural agent for treatment of diabetic skin damage by modulating TIMP/MMPs balance and oxidative stress. 2776 36

Canine osteosarcoma is an aggressive primary bone tumor that shows metastasis to distal regions and is associated with a high mortality rate. However, the pathophysiological mechanisms of canine osteosarcoma are not well characterized. In addition, development of prognostic factors and novel therapeutic agents is necessary to efficiently treat osteosarcoma. Therefore, we studied the effects of myricetin, an antioxidant found in berries, nuts, teas, wine, and vegetables, on apoptosis and signal transduction in the canine osteosarcoma cell lines, D-17 and DSN. Results of the present study demonstrated that treatment with myricetin decreased cell proliferation and DNA replication, while it increased apoptotic DNA fragmentation in D-17 and DSN cells. In addition, it increased generation of ROS, lipid peroxidation, and depolarization of MMP in both D-17 and DSN cells. Myricetin treatment activated phosphorylation of AKT, p70S6K, ERK1/2, JNK, and p90RSK in canine osteosarcoma cells. Moreover, inhibition of PI3K and MAPK using LY294002, U0126, or SP600125, in addition to myricetin treatment, effectively suppressed cell proliferation compared to treatment with myricetin or each inhibitor alone. Therefore, we concluded that myricetin may be a potentially effective and less toxic therapeutic agent to prevent and control progression of canine osteosarcoma.
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PMID:Myricetin treatment induces apoptosis in canine osteosarcoma cells by inducing DNA fragmentation, disrupting redox homeostasis, and mediating loss of mitochondrial membrane potential. 2966 65