Abstract
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.
Highlights
Diabetic foot ulceration is a common and serious complication of diabetes that leads to 38,500 amputations each year [1]
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
We examined the effects of myricetin on procollagen I and III expression levels using enzyme-linked immunosorbent assay (ELISA) as these proteins are considered crucial to diabetic ulceration recovery in the clinic [16]
Summary
Diabetic foot ulceration is a common and serious complication of diabetes that leads to 38,500 amputations each year [1]. It has been shown that reduced procollagen synthesis and increased levels of connective tissuedegrading matrix metalloproteinases (MMPs) are important factors in the early diagnosis of diabetic foot ulceration [2,3,4,5]. Pustovrh et al [7] found that in addition to regulating the TIMP1/MMP ratio, cellular oxidative stress affects MMP activities. González developed a relationship model of MMP activity and oxidative stress in diabetic rats, in which oxidative stress was shown to be involved in the developmental pathways of diabetic dermal fibroblasts [7]. It was found that high glucose levels in diabetic fibroblasts may be capable of inducing oxidative stress and mitochondrial dysfunction in neurons [8]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
