A Study On Relevant Changes Of HMGB1 Transfection By Vitiligo Melanocytes Under Oxidative Stress

Vitiligo is a kind of frequently-occurring disease,which is difficult to treat.The incidence of vitiligo is about 2%,showing an upward trend year by year.The disease often occurs in the head and other exposed areas,which is harmful to the physical and mental health of patients.At present,the pathogenesis of epidermal melanocyte damage in vitiligo is not completely clear.In recent years,a great deal of evidence has shown this.For genetic susceptibility,oxidative stress may be a triggering factor,triggering melanocyte apoptosis,inducing specific immune response to autoantigens,and further destroying melanocyte.Antioxidant capacity was significantly reduced,melanocyte apoptosis was prone to oxidative attack,and further autoimmune response might be induced,suggesting that oxidative stress was the direct factor of melanocyte apoptosis.In order to verify the above hypothesis,PIG1(normal human vitiligo melanocyte line)and PIG3v(vitiligo melanocyte line)cell lines were used as the main research objects in this study.The abnormal changes of "Danger Signals" in and out of cells induced by oxidative stress were detected and analyzed.It was revealed that under oxidative stress,after inducing melanocyte apoptosis,"Danger S" in cells.The specific molecular mechanism and effect of ignals and HMGB1 on melanocyte apoptosis.Apoptotic analysis showed that PIG3 v was more damaged than PIG1 under oxidative stress,but the number of damaged cells in the two cell lines after overexpression of HMGB1 was relatively reduced,and the trend was similar.Overexpression of PIG3V resulted in more damaged cells than overexpression of PIG1.This phenomenon indicates that PIG3V is more vulnerable to damage than PIG1 because of its structural or functional defects.Overexpression of HMGB1 in cells can improve the anti-oxidative effect of anti-oxidative stress damage to melanocytes.Therefore,in this study,we found that the expression of NF-kBP65 phosphorylation activity in HMGB1 overexpressed melanocytes was increased compared with that in control cells,which played an inflammatory role in the balance mechanism.The balance of oxidative stress in cells was determined by a variety of complex molecular mechanisms.Therefore,the increase of the expression of NF-kBP65 phosphorylation was accompanied by changes in other molecular weights.A new balance is not enough to destroy the existing balance of antioxidant stress in cells.Overexpression of HMGB1 melanocyte NRF2,IKBalpha and pIKbalpha increased significantly compared with the control group,while Keap1 expression decreased compared with the control group.This indicates that overexpression of HMGB1 in cells plays an important role in activating ERK/Nrf2 signaling pathway and effectively improves the resistance of melanocyte to oxidative stress injury.Therefore,the complexity of antioxidant stress balance and the theory of intermolecular interaction balance are further validated.In conclusion,PIG3V has structural or functional deficiencies,and its resistance to antioxidant stress is relatively poor;overexpression of HMGB1 can improve the antioxidant stress ability of cells;overexpression of HMGB1 can activate ERK/Nrf2 signaling pathway and play an important role in effectively improving the resistance of melanocytes to antioxidant stress injury.