An extract of Hypericum perforatum induces wound healing through inhibitions of Ca2+ mobilizations, mitochondrial oxidative stress and cell death in epithelial cells: Involvement of TRPM2 channels

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BIOCELL, vol.43, no.4, pp.271-283, 2019 (SCI-Expanded) identifier identifier

  • Publication Type: Article / Article
  • Volume: 43 Issue: 4
  • Publication Date: 2019
  • Doi Number: 10.32604/biocell.2019.08333
  • Journal Name: BIOCELL
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.271-283
  • Süleyman Demirel University Affiliated: Yes


The wound is induced by several mechanical and metabolic factors. In the etiology of the wound recovery, excessive oxidative stress, calcium ion (Ca2+) influx, and apoptosis have important roles. Ca2+-permeable TRPM2 channel is activated by oxidative stress. Protective roles of Hypericum perforatum extract (HP) on the mechanical nerve injury-induced apoptosis and oxidative toxicity through regulation of TRPM2 in the experimental animals were recently reported. The potential protective roles in HP treatment were evaluated on the TRPM2-mediated cellular oxidative toxicity in the renal epithelium (MPK) cells. The cells were divided into three groups as control, wound, and wound + HP treatment (75 mu M for 72 h). Wound diameters were more importantly decreased in the wound+HP group than in the wound group. In addition, the results of laser confocal microscopy analyses indicated protective roles of HP and TRPM2 antagonists (N-(p-Amylcinnamoyl) anthranilic acid and 2-aminoethyl diphenylborinate) against the wound-induced increase of Ca2+ influx and mitochondrial ROS production. The wound-induced increase of early (annexin V-FITC) apoptosis and late (propidium iodide) apoptosis were also decreased in the cells by the HP treatment. In conclusion, HP treatment acted protective effects against wound-mediated oxidative cell toxicity and apoptosis through TRPM2 inhibition. These effects may be attributed to their potent antioxidant effect.