@Article{biocell.2019.08333,
AUTHOR = {Fuat USLUSOY, Mustafa NAZIROĞLU},
TITLE = {An extract of <i>Hypericum perforatum</i> induces wound healing through inhibitions of Ca<sup>2+</sup> mobilizations, mitochondrial oxidative stress and cell death in epithelial cells: Involvement of TRPM2 channels},
JOURNAL = {BIOCELL},
VOLUME = {43},
YEAR = {2019},
NUMBER = {4},
PAGES = {271--283},
URL = {http://www.techscience.com/biocell/v43n4/38127},
ISSN = {1667-5746},
ABSTRACT = {The wound is induced by several mechanical and metabolic factors. In the etiology of the wound recovery,
excessive oxidative stress, calcium ion (Ca<sup>2+</sup>) influx, and apoptosis have important roles. Ca<sup>2+</sup>-permeable TRPM2 channel is activated by oxidative stress. Protective roles of <i>Hypericum perforatum</i> 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 µM 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 Ca<sup>2+</sup> 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.},
DOI = {10.32604/biocell.2019.08333}
}