Aster koraiensis extract improves impaired skin wound healing during hyperglycemia

Diabetes mellitus (DM) is one of the most common diseases found across the world. Aster koraiensis extract (AKE) has a protective effect on diabetic complications such as diabetic retinopathy. However, the effects of AKE on hyperglycemia-linked impairment of wound healing during DM have not been elu...

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Veröffentlicht in:Integrative medicine research 2018, 7(4), 25, pp.351-357
Hauptverfasser: Hyun, Soo-Wang, Kim, Junghyun, Jo, Kyuhyung, Kim, Jin Sook, Kim, Chan-Sik
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Sprache:eng
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Zusammenfassung:Diabetes mellitus (DM) is one of the most common diseases found across the world. Aster koraiensis extract (AKE) has a protective effect on diabetic complications such as diabetic retinopathy. However, the effects of AKE on hyperglycemia-linked impairment of wound healing during DM have not been elucidated. In this study, we investigated the effects of AKE on delayed wound healing induced by DM. DM was induced by intraperitoneal administration of streptozotocin (STZ; 75mg/kg) to Sprague Dawley (SD) rats. Next, a wound was induced on the back of rats after administration of STZ. Further, AKE was prepared using an alcoholic extraction of A. koraiensis and orally administered daily for 18 days. Wound healing was evaluated using an in vitro migration assay and measuring the wound area in vivo. Skin tissue thickness was evaluated using hematoxylin and eosin staining. Matrix metalloprotease (MMP) activity and expression were detected using zymography and immunohistochemistry. AKE administration improved the delayed migration of keratinocytes in hyperglycemic animals. It also attenuated an increase in keratinocyte MMP-2/9 activity induced by hyperglycemia. AKE protected against DM-induced impaired wound healing in rats and prevented the degradation of skin tissue induced by DM. In addition, AKE attenuated DM-induced increase in MMP-2/9 expression in skin tissue. In conclusion, AKE may promote wound healing by re-epithelization via promotion of keratinocyte migration and by attenuating the disruption of the skin tissue layer via MMP-2/9 inhibition during hyperglycemia.
ISSN:2213-4220
2213-4239
DOI:10.1016/j.imr.2018.09.001