Antioxidant cinnamaldehyde attenuates UVB-induced photoaging.
Acrolein
/ analogs & derivatives
Animals
Antioxidants
/ pharmacology
Cell Line
Cinnamomum aromaticum
Collagen Type I
/ metabolism
Collagen Type I, alpha 1 Chain
DNA Damage
/ drug effects
Female
Heme Oxygenase-1
/ metabolism
Humans
Keratinocytes
/ drug effects
MAP Kinase Signaling System
/ drug effects
Malondialdehyde
/ metabolism
Matrix Metalloproteinase 13
/ metabolism
Membrane Proteins
/ metabolism
Mice
Phytotherapy
Plant Extracts
/ pharmacology
Reactive Oxygen Species
/ metabolism
Skin Aging
/ drug effects
Ultraviolet Rays
Antioxidant
Cinnamaldehyde
DNA damage
Photoaging
Reactive oxygen species
Ultraviolet
Journal
Journal of dermatological science
ISSN: 1873-569X
Titre abrégé: J Dermatol Sci
Pays: Netherlands
ID NLM: 9011485
Informations de publication
Date de publication:
Dec 2019
Dec 2019
Historique:
received:
13
05
2019
revised:
07
10
2019
accepted:
01
11
2019
pubmed:
19
11
2019
medline:
19
6
2020
entrez:
19
11
2019
Statut:
ppublish
Résumé
Ultraviolet (UV) irradiation disrupts skin through several deleterious actions, such as induction of reactive oxygen species (ROS), DNA damage, and collagen degradation. Cinnamaldehyde (CIN) is a major constituent of the cinnamon and it possesses potent antioxidative activity; however, it is unclear whether CIN is capable of inhibiting the adverse effects of UVB. To investigate protective effects of CIN against UVB-induced photodamage. HaCaT keratinocytes were pretreated with CIN, irradiated with UVB, and assessed for the ROS production by flow cytometry and for the DNA damage by ELISA. As in vivo mouse model, Hos:HR-1 hairless mice were treated with ointments containing DMSO or CIN and irradiated multiple times with UVB. After 10 weeks of irradiation, wrinkle formation, epidermal thickness, infiltrating cell number, malondialdehyde amount, collagen amount, MAP kinase signaling, and related gene expressions (Hmox1, Col1a1, Mmp1a, and Mmp13) were analyzed. CIN significantly reduced the ROS production and accelerated the repair of DNA damage pyrimidine(6-4)pyrimidone photoproducts in UVB-irradiated human keratinocytes in vitro. In the mouse model, topical application of CIN significantly inhibited wrinkle formation, epidermal hyperplasia, and dermal inflammatory cell infiltration. The antioxidative process was significantly promoted in the CIN-applied site, as evidenced by upregulation of the antioxidative enzyme Hmox1 as well as the reduced accumulation of malondialdehyde. In addition, topical application of CIN normalized the UVB-induced collagen/Col1a1 downregulation and the UVB-induced Mmp13 upregulation, implying the prevention of UVB-induced collagen degradation. CIN and CIN-containing herbal agents may exert potent protective effects against UVB exposure on skin.
Sections du résumé
BACKGROUND
BACKGROUND
Ultraviolet (UV) irradiation disrupts skin through several deleterious actions, such as induction of reactive oxygen species (ROS), DNA damage, and collagen degradation. Cinnamaldehyde (CIN) is a major constituent of the cinnamon and it possesses potent antioxidative activity; however, it is unclear whether CIN is capable of inhibiting the adverse effects of UVB.
OBJECTIVE
OBJECTIVE
To investigate protective effects of CIN against UVB-induced photodamage.
METHODS
METHODS
HaCaT keratinocytes were pretreated with CIN, irradiated with UVB, and assessed for the ROS production by flow cytometry and for the DNA damage by ELISA. As in vivo mouse model, Hos:HR-1 hairless mice were treated with ointments containing DMSO or CIN and irradiated multiple times with UVB. After 10 weeks of irradiation, wrinkle formation, epidermal thickness, infiltrating cell number, malondialdehyde amount, collagen amount, MAP kinase signaling, and related gene expressions (Hmox1, Col1a1, Mmp1a, and Mmp13) were analyzed.
RESULTS
RESULTS
CIN significantly reduced the ROS production and accelerated the repair of DNA damage pyrimidine(6-4)pyrimidone photoproducts in UVB-irradiated human keratinocytes in vitro. In the mouse model, topical application of CIN significantly inhibited wrinkle formation, epidermal hyperplasia, and dermal inflammatory cell infiltration. The antioxidative process was significantly promoted in the CIN-applied site, as evidenced by upregulation of the antioxidative enzyme Hmox1 as well as the reduced accumulation of malondialdehyde. In addition, topical application of CIN normalized the UVB-induced collagen/Col1a1 downregulation and the UVB-induced Mmp13 upregulation, implying the prevention of UVB-induced collagen degradation.
CONCLUSIONS
CONCLUSIONS
CIN and CIN-containing herbal agents may exert potent protective effects against UVB exposure on skin.
Identifiants
pubmed: 31735467
pii: S0923-1811(19)30340-8
doi: 10.1016/j.jdermsci.2019.11.001
pii:
doi:
Substances chimiques
Antioxidants
0
Collagen Type I
0
Collagen Type I, alpha 1 Chain
0
Membrane Proteins
0
Plant Extracts
0
Reactive Oxygen Species
0
Malondialdehyde
4Y8F71G49Q
Acrolein
7864XYD3JJ
Heme Oxygenase-1
EC 1.14.14.18
Hmox1 protein, mouse
EC 1.14.14.18
Matrix Metalloproteinase 13
EC 3.4.24.-
Mmp13 protein, mouse
EC 3.4.24.-
cinnamaldehyde
SR60A3XG0F
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
151-158Informations de copyright
Copyright © 2019 Japanese Society for Investigative Dermatology. Published by Elsevier B.V. All rights reserved.