Абстракт

Objectives: Oxidative stress-induced cellular senescence and mitochondrial dysfunction result in skin aging by increasing ECM levels-degrading proteins such as MMPs, and decreasing collagen synthesis. MMPs also destroy the basement membrane, which is involved in skin elasticity. We evaluated whether skin booster(contains various antioxidant) decreases oxidative stress and mitochondrial dysfunction, eventually increasing skin elasticity in aged animals. Skin booster(AA, NA, coenzymes, glutathione) and sodium hyaluronate improves skin rejuvenation by decreasing oxidative stress and mitochondrial dysfunction Introduction: During the skin aging process, oxidative stress leads to the upregulation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) and its downstream signal pathway of activator protein 1 (AP-1), which eventually increases the levels of extracellular matrix (ECM)-degrading proteins such as collagenase and matrix metalloproteinases (MMPs). We hypothesized that Skin booster(AA,NA) injection could decrease oxidative stress and cellular senescence, which eventually resulted in a reduction in NF-kB/AP-1 and mitochondrial dysfunction in the skin. Materials / method: To determine whether aged animal skin was affected by Skin booster(AA.NA) treatment, 12-month-old aging mice were injected intradermally with RA (100 L/cm2/day) twice every two weeks using a microneedle therapy system (MTS; Derma-Q Gold 0.5 mm, DONGBANG medicare, Seongnam, Republic of Korea). The control was injected with distilled water under the same conditions.To confirm whether the skin elasticity of aged animal skin was changed by skin booster treatment, the skin elasticity of the animal before skin booster(AA,NA) treatment and after 4 weeks was measured. Results: 1.Skin booster decreased oxidative stress in H2O2-Treated Keratinocytes and Aged Animal Skin. 2. Skin booster decreased Mitochondrial Dysfunction and Cellular Senescence in H2O2-Treated Keratinocytes and Aged Skin. 3. Skin booster decreased NF-Kb/AP-1 and MMP1/2/3/9 Expression in Aged Skin. 4. Skin booster increased the Expression of Laminin and Nidogen and the BM Density. 5. Skin booster upregulated the Expression of TGF-B, CTGF, and a-Smooth Muscle Actin (A-SMA) and Collagen Fiber Accumulation in Aged Skin. Conclusion: Our study showed that skin booster(AA,NA) decreased oxidative stress and mtDNA injury, which eventually decreased mitochondrial dysfunction in aged skin. RA also decreased ECM destruction by decreasing the levels of NF-B/AP-1/MMPs and increasing the levels of BM proteins such as nidogen and laminin. RA enhanced the collagen synthesis-related signaling pathway of TGF- and CTGF. These modulations associated with RA treatment led to increased collagen fiber accumulation and skin elasticity in aged skin.