Perilla herb oil
(-)-Perillaldehyde/(?)-Perillaaldehyde/1-Cyclohexene-1-carboxaldehyde, 4-isopropenyl-, (S)-(-)-/1-Cyclohexene-1-carboxaldehyde, 4-(1-methylethenyl)-, (S)-/L6UTJ AVH DY1&U1 &&S-(-)- Form/1-Cyclohexene-1-carboxaldehyde, 4-(1-methylethenyl)-, (4S)-/S(-)-Perillaldehyde/(?)-Perillaaldehyde,(S)-p-Mentha-1,8-dien-7-al,(S)-4-Isopropenyl-cyclohexene-1-carboxaldehyde/(S)-p-Mentha-1,8-dien-7-al/(S)-(-)-Perillaldehyde/L-Perillaldehyde/(4S)-4-Isopropenylcyclohex-1-ene-1-carbaldehyde/(-)-4-Isopropenyl-1-cyclohexene-1-carboxaldehyde/Perillaldehyde/L(-)-Perillaldehyde/(S)-4-(prop-1-En-2-yl)cyclohex-1-enecarbaldehyde/(4S)-4-Isopropenyl-1-cyclohexene-1-carbaldehyde
238.0±29.0 °C at 760 mmHg
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For Reference Standard and R&D, Not for Human Use Directly.
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The skin covers the outer surface of the body, so the epidermal keratinocytes within it are susceptible to reactive oxygen species (ROS) generated by environmental pollutants such as benzo(a)pyrene (BaP), a potent activator of aryl hydrocarbon receptor (AHR). Antioxidant activity is generally mediated by the nuclear factor-erythroid 2-related factor-2 (NRF2) and heme oxygenase-1 (HO1) axis in human keratinocytes. Perillaldehyde is the main component of Perilla frutescens, which is a medicinal antioxidant herb traditionally consumed in East Asia. However, the effect of perillaldehyde on the AHR/ROS and/or NRF2/HO1 pathways remains unknown. In human keratinocytes, we found that perillaldehyde (1) inhibited BaP-induced AHR activation and ROS production, (2) inhibited BaP/AHR-mediated release of the CCL2 chemokine, and (3) activated the NRF2/HO1 antioxidant pathway. Perillaldehyde is thus potentially useful for managing inflammatory skin diseases or disorders related to oxidative stress.
Perillaldehyde Inhibits AHR Signaling and Activates NRF2 Antioxidant Pathway in Human Keratinocytes
Yoko Fuyuno 1 , Hiroshi Uchi 1 , Mao Yasumatsu 2 , Saori Morino-Koga 3 , Yuka Tanaka 2 , Chikage Mitoma 1 2 , Masutaka Furue 1 2
2018 Feb 14;
Background: Perillaldehyde is one of the main components in perilla. Previous studies have shown that perillaldehyde exerted an antidepressant effect in mice, some of which is mediated through regulation of the anti-inflammatory system and the monoamine system. The primary objective of this study was to investigate the possible effects of perillaldehyde on the neurotrophic system and to elucidate whether its antidepressant effect requires brain-derived neurotrophic factor (BDNF) signaling.
Methods: Mice were exposed to chronic unpredictable mild stress (CUMS) and orally administrated with perillaldehyde for 4 weeks for behavioral testing.
Results: Perillaldehyde not only reversed the decrease in sucrose preference but also attenuated the increase in feeding latency. In addition, perillaldehyde can attenuate the reduction of CUMS-induced hippocampal BDNF levels. Our further study found that the BDNF receptor tropomyosin receptor kinase B (TrkB) antagonist K252a completely blocked the antidepressant effect of perillaldehyde in mice. Biochemical analysis showed that K252a pretreatment completely prevented the improvement of BDNF, extracellular signal-regulated kinase (ERK) phosphorylation and synaptic protein.
Conclusions: These results indicated that activation of BDNF-ERK signaling in the hippocampus was required, at least in part for the antidepressant effects of perillaldehyde.
Hippocampal BDNF Signaling Is Required for the Antidepressant Effects of Perillaldehyde
Ji-Xiao Zhu 1 , Wei-Qiong Hu 1 , Shu-Qi Dong 2 , Li-Tao Yi 2 , Jin-Xiang Zeng 1 , Min Li 3
Perillaldehyde, a natural monocyclic terpenoid found most abundantly in the herb perilla, has a long history of use as a flavouring ingredient to add spiciness and citrus taste to foods. Previously, it was judged to be safe by several international expert panels. To confirm the safety of flavourings placed on the European Union list of flavourings, perillaldehyde was selected by the European Food Safety Authority as a representative of a subgroup of alicyclic aldehyde flavouring substances to be evaluated for genotoxic potential. Perillaldehyde was tested in a bacterial reverse mutation assay, an in vitro micronucleus assay in human lymphocytes, an HPRT assay in mouse lymphoma cells, and a micronucleus/comet assay in Han Wistar rats. In contrast to previously published results, perillaldehyde induced mutation in Salmonella typhimurium strain TA98 in the absence of metabolic activation. The comet assay was negative for duodenum and weakly positive for liver but only at a hepatotoxic dose of perillaldehyde. All other genotoxicity assays were negative. These data do not provide an indication of any genotoxic potential for perillaldehyde, and they provide the primary basis for recent scientific opinions regarding perillaldehyde genotoxicity announced by several international organizations responsible for safety assessment of food additives and flavourings.
DNA damage; Flavouring agent; Genotoxicity; Perilla aldehyde; Perillaldehyde; p-mentha-1,8-dien-7-al.
Genotoxicity Assessment of the Flavouring Agent, Perillaldehyde
Cheryl A Hobbs 1 , Sean V Taylor 2 , Carol Beevers 3 , Melvyn Lloyd 3 , Rachael Bowen 3 , Lucinda Lillford 3 , Robert Maronpot 4 , Shim-Mo Hayashi 5