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Study Of The Mechanism On The Increase Of Reactive Oxygen Species In Pathological Scars

Posted on:2007-04-03Degree:DoctorType:Dissertation
Country:ChinaCandidate:W R LiFull Text:PDF
GTID:1104360185494574Subject:Surgery
Abstract/Summary:PDF Full Text Request
Objective: To determine the mechanism and significance on an increase in the level of reactive oxygen species in pathological scars.Methods: We obtained tissues samples from normal skin(n = 8), hypertrpphic scars(n = 10) and keloids(n = 10) and detected spectrophotometrically biomarkers in the above-mentioned tissues: the contents of MDA and Hyp, the activities of XO, SOD, CAT, GPX and T-AOC. The expressions and locations of SOD-1 and XO were evaluated by immunohistochemistric staining. And semi quantitative RT-PCR was used to observe the expression changes of SOD-1 and SOD-3mRNA. Normal skin tissues acted as controls.Results: Compared with normal skin tissues, the contents of MDA and Hyp were significantly higer in pathological scars(P<0.05). And there was a positive correlation between the contents of MDA and Hyp(r=0.5530,P<0.05). XO and SOD activity were higher, CAT activity was decreased remarkably in pathological scars than that in normal skin tissues(P<0.05). And the activity ratios of CAT/CuZn — SOD and GPX/CuZn — SOD were obviously reduced(P<0.05). However, no significantly differences were observed in the decrease of T-AOC and activity of GPX. The immunohistochemistric staining results showed a remarkable increase of XO and SOD-1 protein expression respectively in keratinocytes and fibroblasts, and positive expression of XO and SOD-1 protein in vascular endothelial cell among the three groups. Semi quantitative RT-PCR showed that SOD-1mRNA expression in pathological scars was higher than that in normal skin tissues(P<0.05), but here was no significantly difference in S0D-3mRNA expression. Differences in...
Keywords/Search Tags:Hypertrpphic scar, Keloid, Malonaldehyde, Hydroxyproline, Total antioxidant capacity, Xanthine oxidase, Antioxidase
PDF Full Text Request
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