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논문 기본 정보

자료유형
학술저널
저자정보
김다혜 (동의대학교) 최영현 (동의대학교)
저널정보
한국식품영양과학회 한국식품영양과학회지 한국식품영양과학회지 제53권 제11호
발행연도
2024.11
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1,143 - 1,152 (10page)

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Oxidative stress influences the onset and progression of chronic diseases in various organs, including the skin. Betulinic acid, a member of the naturally occurring lupine-type pentacyclic triterpene family, has broad pharmacological potential, including antioxidant activity. However, the molecular mechanisms by which it can protect against oxidative damage in human keratinocytes have not been investigated thoroughly. Therefore, this study aimed to evaluate whether betulinic acid could protect against oxidative stress-mediated cellular damage mimicked by hydrogen peroxide (H₂O₂) in human keratinocyte HaCaT cells. The results demonstrated that betulinic acid suppressed H₂O₂-induced cytotoxicity while suppressing generation of reactive oxygen species. Betulinic acid also significantly inhibited H₂O₂-induced autophagy, which was associated with the down-regulation of the expression of key autophagy inducers. In addition, betulinic acid maintained mitochondrial homeostasis by reducing cytochrome c release from mitochondria to the cytosol and the loss of mitochondrial membrane potential in H₂O₂-treated cells. Moreover, in the presence of betulinic acid, the H₂O₂ㄹ-induced increase in the Bcl-2 associated X protein/B-cell lymphoma-2 (Bax/Bcl-2) expression ratio, caspase-3 activity, and cleavage of poly (ADP-ribose) polymerase were effectively attenuated, thereby offsetting the induction of apoptosis. Furthermore, betulinic acid pretreatment significantly abolished H2O2-induced endoplasmic reticulum (ER) stress by suppressing ER stress-regulating proteins and cytosolic calcium (Ca<sup>2+</sup>) overload. Therefore, our results demon- strated that betulinic acid could protect against mitochondrial impairment and Ca<sup>2+</sup>-mediated ER stress by minimizing oxidative stress, thereby inhibiting H₂O₂-induced cellular injury in HaCaT keratinocytes.

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