• KOL
    • Oxidative Stress
    • Apigenin Attenuates...
    • Apigenin attenuates dopamine-induced apoptosis in melanocytes via oxidative stress-related p38, c-Jun NH2-terminal kinase and Akt signaling: Influence Statistics

      Expert Impact

      Concepts for whichthey havehas direct influence:Oxidative stress,Akt apigenin,Protective effects,Protective effects apigenin,Apigenin attenuates,Apigenin apoptosis,Melanocytes oxidative,Cjun nh2terminal kinase.

      Key People For Oxidative Stress

      Top KOLs in the world
      #1
      Halliwell Halliwell
      oxidative damage lipid peroxidation hydrogen peroxide
      #2
      Irwin Fridovich
      superoxide dismutase escherichia coli xanthine oxidase
      #3
      Helmut Helmut
      singlet oxygen oxidative stress lipid peroxidation
      #4
      Bruce N Ames
      salmonella typhimurium dna damage oxidative stress
      #5
      Earl Reece Stadtman
      glutamine synthetase escherichia coli protein oxidation
      #6
      Kunio Kunio
      lipid peroxides amino acid hydrogen bonding

      Apigenin attenuates dopamine-induced apoptosis in melanocytes via oxidative stress-related p38, c-Jun NH2-terminal kinase and Akt signaling

      Abstract

      BACKGROUND: Accumulating evidence suggests that the occurrence of oxidative stress leads to melanocyte degeneration in vitiligo. Elevated level of dopamine (DA), an initiator of oxidative stress, reportedly is found in patients with vitiligo and induces melanocyte death in vitro. DA-treated melanocytes have been used as a model to search for antioxidants for treating vitiligo.

      OBJECTIVE: We investigated the protective effects of apigenin against DA-induced apoptosis in melanocytes and the molecular mechanism underlying those effects.

      METHODS: Melanocytes with or without pretreatment with apigenin were exposed to DA. Then cell viabilities were measured by MTT assay. Cellular reactive oxygen species (ROS) levels and the percentage of apoptotic cells were detected by flow cytometry analysis. Activation of caspase 3, poly(ADP-ribose) polymerase (PARP) and oxidative stress-related signaling, including p38, c-Jun NH2-terminal kinase (JNK) and Akt, were assessed by Western blotting.

      RESULTS: Apigenin attenuated DA-induced apoptotic cell death, relieved ROS accumulation and activated caspase 3 and PARP, suggesting the protective effects of apigenin against DA-induced oxidative stress and apoptosis in melanocytes. Moreover, DA induced phosphorylation of p38, JNK and Akt, while inhibitors of p38, JNK and Akt significantly decreased DA-induced apoptosis. However, pretreatment with apigenin significantly inhibited DA-triggered activation of p38, JNK and Akt, suggesting the involvement of p38, JNK and Akt in the protective effects of apigenin against DA-induced cytotoxicity.

      CONCLUSION: These results suggest that apigenin attenuates dopamine-induced apoptosis in melanocytes via oxidative stress-related p38, JNK and Akt signaling and therefore could be a potential agent in treating vitiligo.

      Sign-in to see all concepts, it's free!

       

    Download on the App StoreGet it on Google Play

    Copyright © 2023 Key Opinion Leaders, LLC.