The bibenzyl derivatives of Dendrobium officinale prevent UV-B irradiation induced photoaging via SIRT3

Ding-Kang Chen,Liu Yang,Jiang-Miao Hu,Hui-Yan Shao

doi:10.1007/s13659-022-00323-6

Abstract

Dendrobium officinale is a valuable medicinal herb that is widely used in traditional Chinese medicine. The chemical constituents of D. officinale have attracted much attention and a large number of compounds have been reported including many bibenzyl derivatives. 13 bibenzyl derivatives from D. officinale were sent for molecular docking, surface plasmon resonance (SPR) assay and after detection of Mn-SOD and SIRT3 activities in or not in HaCaT cells, it was concluded that bibenzyl derivatives did not directly activate Mn-SOD but promoted SIRT3 proteins. In addition, HaCaT cells were irradiated with UV-B to induce an oxidative stress model in vitro to further verify the effect of bibenzyl derivatives. The results show that bibenzyl derivatives could directly bind to SIRT3, enhance the deacetylation and then activate Mn-SOD, so as to protect UV-B induced skin photoaging.Graphical

Highlights

Skin photoaging is mainly caused by long-term contact with ultraviolet (UV)-A (400–320 nm) and UV-B (320– 280 nm) radiation in sunlight, resulting in skin morphological changes [1]
2.1 Bibenzyl derivatives binds to SIRT3 protein SIRT3 is a major mitochondrial NAD+ dependent deacetylase, which plays an important role in regulating mitochondrial metabolism and energy production, and is related to the beneficial effects of exercise and caloric restriction
Molecular docking study of SIRT3 protein against 13 bibenzyl derivatives in D. officinale was carried out using receptor based molecular docking by Maestro 11.9

Summary

Introduction

Skin photoaging is mainly caused by long-term contact with ultraviolet (UV)-A (400–320 nm) and UV-B (320– 280 nm) radiation in sunlight, resulting in skin morphological changes [1]. Manganese superoxide dismutase (Mn-SOD) is a major superoxide anion scavenging enzyme in the mitochondrial matrix [5] It reduces mitochondrial oxidative stress by converting superoxide anion into hydrogen peroxide. Deacetylation at K68 and K122 sites enhances the Mn-SOD activity, so reduces the damage caused by oxidative stress [8, 9]. These results suggest that the deacetylation activity of SIRT3 plays an important role in maintaining redox homeostasis

Results

Discussion

Conclusion