Hsieh Pei-Fang, Yu Cheng-Chia, Chu Pei-Ming, Hsieh Pei-Ling
Department of Urology, E-Da Hospital, Kaohsiung 82445, Taiwan.
Department of Medical Laboratory Science and Biotechnology, Chung-Hwa University of Medical Technology, Tainan 71703, Taiwan.
Antioxidants (Basel). 2021 Sep 12;10(9):1445. doi: 10.3390/antiox10091445.
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.
伤口愈合受损在糖尿病患者中经常发生，给他们带来极大不便。除了长期存在炎症外，氧化应激的积累也与伤口愈合延迟有关。在本研究中，我们测试了毛蕊花糖苷（一种咖啡酰苯乙醇苷）对高糖条件下牙龈上皮细胞活力改善和伤口愈合能力的影响。我们发现毛蕊花糖苷减轻了高糖诱导的细胞毒性和愈合受损，这可能与氧化应激的下调有关。我们的结果表明，毛蕊花糖苷增加了抗氧化酶超氧化物歧化酶（SOD）的活性，降低了氧化应激指标8-羟基脱氧鸟苷（8-OHdG）以及细胞凋亡。此外，毛蕊花糖苷上调了过氧化物酶体增殖物激活受体γ共激活因子1-α（PGC1-α）和核呼吸因子1（NRF1）的表达，并促进了线粒体生物合成，这是通过抑制蛋白激酶C（PKC）/高迁移率族蛋白B1（HMGB1）/晚期糖基化终末产物受体（RAGE）/核因子κB（NFκB）信号传导介导的。同样，我们表明毛蕊花糖苷对氧化应激的抑制作用是通过抑制PKC/HMGB1/RAGE/NFκB激活实现的。此外，我们的数据表明PKC介导的氧化应激可能导致炎症细胞因子白细胞介素-6（IL-6）和白细胞介素-1β（IL-1β）的产生增加。总体而言，我们证明毛蕊花糖苷可能有利于改善糖尿病患者受损的口腔伤口愈合。
