Topical Application of Propolis Enhances Cutaneous Wound Healing by Promoting TGFBeta/ Smad-Mediated Collagen Production in a Streptozotocin-Induced Type I Diabetic Mouse Model

Journal Article

Garraudg, Wael N. Hozzein, Gamal Badrc Ahmad A. Al Ghamdi Ayat Sayed Noori S. Al-Wailif Olivier . 2015

• المجلة \ الصحيفة: Cellular Physiology and Biochemistry
• رقم العدد: 3
• رقم الإصدار السنوي: 37
• الصفحات: 940-954

مستخلص المنشور

Diabetic wounds represent an added burden for diabetic patients and health care
providers worldwide as they have low healing potential and residual ulceration due to
associated neuropathy and vasculopathy [1]. Wound healing consists of overlapping but
coordinated processes, including homeostasis, inflammation, granulation tissue formation
and tissue remodeling [2]. An array of cytokines, growth factors, immune and inflammatory
mediators, as well as their associated signaling cascades, are involved in tissue regeneration
and wound closure [3]. In diabetes, both the cellular and extracellular milieus are abnormal,
showing prolonged inflammatory and immune responses, impaired growth factor
production, decreased angiogenesis and the production of atypical extracellular components
and remodeling matrix metalloproteinases (MMPs) [4, 5].
The pro-inflammatory cytokines IL-1β, IL-6 and TNF-α are primarily released by immune
cells early during the wound healing process (inflammatory stage) and act as effectors for
keratinocytes and fibroblasts to stimulate tissue deposition and epithelialization [6, 7].
Persistent inflammation has been directly linked to delayed healing and wound chronicity [5].
Indeed, high levels of these cytokines are found in diabetic ulcers and have been associated
with scarring events, which is the end result of fibroblast apoptosis and extracellular matrix
(ECM) degradation [8].