Abstract
Impaired wound healing often occurs in patients with diabetes and causes great inconvenience to them. Aside from the presence of prolonged inflammation, the accumulation of oxidative stress is also implicated in the delayed wound healing. In the present study, we tested the effect of verbascoside, a caffeoyl phenylethanoid glycoside, on the improvement of cell viability and wound healing capacity of gingival epithelial cells under high glucose condition. We showed that verbascoside attenuated the high glucose-induced cytotoxicity and impaired healing, which may be associated with the downregulation of oxidative stress. Our results demonstrated that verbascoside increased the activity of the antioxidant enzyme SOD and reduced the oxidative stress indicator, 8-OHdG, as well as apoptosis. Moreover, verbascoside upregulated the PGC1-α and NRF1 expression and promoted mitochondrial biogenesis, which was mediated by suppression of PKC/HMGB1/RAGE/NFκB signaling. Likewise, we showed the inhibitory effect of verbascoside on oxidative stress was via repression of PKC/HMGB1/RAGE/NFκB activation. Also, our data suggested that the PKC-mediated oxidative stress may lead to the elevated production of inflammatory cytokines, IL-6 and IL-1β. Collectively, we demonstrated that verbascoside may be beneficial to ameliorate impaired oral wound healing for diabetic patients.
Highlights
Diabetes mellitus is a multifaceted metabolic disorder that represents a major concern globally
Since HMGB1 can be phosphorylated by protein kinase C (PKC) for secretion [16], we aimed to investigate the effect of verbascosides on the expression of PKC/HMGB1/receptor for advanced glycation end products (RAGE)/nuclear factor-κB (NF-κB) signaling and if verbascosides treatment improved the compromised wound repair of gingival cells under high glucose condition through suppression of oxidative stress and inflammation
Epithelial cells migrate and proliferate at the injured site during the healing process, and we showed that these capacities of epithelial cells were inhibited under the high glucose condition (Figure 1D)
Summary
Diabetes mellitus is a multifaceted metabolic disorder that represents a major concern globally. A significant amount of health expenditure due to diabetes becomes a disease burden to be reckoned with. Diabetes and its complications, such as macrovascular and microvascular diseases, constitute major causes of morbidity and mortality [2]. This chronic inflammatory disease affects the cardiovascular system, but it causes dysregulation of wound healing, including in the oral tissues [3]. Diabetes has been known to be a risk factor of periodontitis, which is characterized by the destruction of the supporting structures of the teeth [4]. It has been indicated that diminished cell proliferation and migration, the elevation of proinflammatory cytokines, and reduced formation of new connective tissue and bone were
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