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• W1982608265 abstract "Background: In addition to vasculopathy and poor wound healing, ischemia-reperfusion injury (IRI) is increasingly recognized as a factor that contributes to complications such as chronic wounds in diabetic patients. Recent work in our lab and others has shown that the endogenous signaling molecule hydrogen sulfide (HS) can mitigate IRI in a number of euglycemic animal models. However, in the setting of diabetes, in which tissues are known to be even more sensitive to the deleterious effects of IRI, there is a paucity of data regarding the cytoprotective effects of HS. Materials and Methods: Six 8-week-old male C57/BL6 mice were rendered diabetic via one intraperitoneal injection of 200 mg/kg streptozotocin. Hyperglycemia was confirmed by blood glucose readings of greater than 300 mg/uL on two consecutive days. After a total of four weeks in a diabetic state, mice were randomized to 2 groups (no HS and 10μM intravenous HS delivered 20 minutes prior to ischemia) and then subjected to 3 hours of tourniquet-induced hindlimb ischemia followed by 3 hours of reperfusion. At this time, the animal was sacrificed and the gastrocnemius and soleus muscles were harvested bilaterally. The tissue was processed for histology, and paraffin sections were stained with hematoxylin and eosin in order to determine architectural integrity, and subjected to a TUNEL assay in order to determine the apoptotic index (AI) for each group. Values are reported as mean AI±SE, and a student's t-test was performed comparing the two groups. Statistical significance was set at p<0.05. Results: Upon histologic examination, ischemic tissue from the limbs of non-treated diabetic mice subjected to ischemia-reperfusion displayed major architectural changes compared to ischemic tissue from the non-ischemic controls, manifesting as extracellular edema and intracellular vacuolization. Conversely, ischemic tissue from diabetic mice that had been treated with HS showed minimal structural change. The AI of ischemic tissue from mice that had been treated with HS (4.1% ± 1.1%) was significantly reduced compared to that of non-treated mice (10.6% ± 2.0%; p=0.014). There was no appreciable amount of apoptosis in the control limbs from either the non-treated or HS-treated mice (0.4% ± 0.4% and 0.4% ± 0.3%, respectively; p=0.736). Conclusions: These are the first data to demonstrate that micromolar HS significantly reduces IRI-related muscle damage and apoptosis in the hindlimb muscle of diabetic mice. In addition to its documented utility in mitigating IRI in euglycemic animal models, HS has the potential to be an important adjunct to the surgical treatment of IRI-related conditions in diabetic patients. These findings are especially relevant given the large proportion of patients with diabetes within the cohort of patients requiring lower extremity revascularization." @default.
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• W1982608265 date "2010-02-01" @default.
• W1982608265 modified "2023-09-27" @default.
• W1982608265 title "Sweet Protection: Hydrogen Sulfide Significantly Ameliorates Lower Extremity Ischemia-Reperfusion Injury in Diabetic Mice" @default.
• W1982608265 doi "https://doi.org/10.1016/j.jss.2009.11.516" @default.
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