Efficacy of Camellia japonica fruit shell extract on hair loss
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Presented by: Jiyoung You
Background: Hair loss is not a fatal disease to life, but it causes psychological stress including intense emotional suffering. Nutritional deficiency, hormonal imbalance, dyeing, and oxidative stress is associated with hair loss. Currently, mitigation of hair loss is being studied in various targets, such as proliferation of dermal papilla cells (DPCs), reduction of dihydrotestosterone (DHT) production, and reduction of oxidative stress. DPCs, composed of mesenchymal fibroblast, controls and maintains the hair cycle. So, proliferation of DPCs lead to hair follicle development and hair growth. Wnt/β-catenin pathways play an important role in proliferation of DPCs. DHT induce early hair regression and hair miniaturization through inhibition of the Wnt/β-catenin signaling in DPCs. Oxidative stress is known to induce premature senescence and secretion of hair follicle inhibitory factors in DPCs.
Camellia japonica belongs to the camellia genus in azalea order and is an evergreen tree that grows naturally in Korea, Japan, and China. C. japonica contains active compounds such as polyphenol, vitamin E, saponin, triterpenoids, and various fatty acids which exert antioxidant, antimicrobial, wound healing, anti-pollution, and anti-inflammatory activity. C. japonica fruit shell (CJFS) is discarded after seed collection for obtaining oil, and its biological activity remains to be elucidated. In this study we investigated the effect of C. japonica fruit shell extract (CJFSE) on hair loss alleviation by measuring proliferation of DPCs, production of DHT, and reduction of oxidative stress.
Materials and Methods: The dried fruit shells of Camellia japonica from Jeju Island were extracted with EtOH. Cell viability and proliferation were identified through MTT and Ki67 staining in Human follicle dermal papilla cells (HFDPCs) respectively, and Dkk-1 secreted from HFDPCs was measured by ELISA. Activity of 5α-reductase was analyzed by HPLC, and to confirm reduction of oxidation stress, DPPH assay and senescence model induced by H2O2 were used. SA-β-gal activity was measured via fluorescence microscopy and FACS analysis. Spheroid culture was conducted on the ultra-low attachment plate, and the size of spheroids was measured using the ImageJ system.
Results: In proliferation of DPCs, we found that CJFSE increase the proliferation of HFDPCs and Ki67 expression which is indicator of hair growth. And we confirmed that secretion of Dkk-1, a negative regulator of Wnt signaling, was reduced by CJFSE. In addition, a spheroid culture of HFDPCs was conducted to confirm the effect of CJFSE on the volume of the hair shaft, and we observed that CJFSE increases the spheroid size. These data suggest that CJFSE may increase DPC proliferation by inhibition of Dkk-1. CJFSE inhibited the conversion of testosterone to DHT in rat liver microsomes model and prevented DHT-induced decrease of viability in HFDPCs. Oxidative stress causes HFDPC senescence, which contribute to hair loss. Accordingly, we investigated whether CJFSE has antioxidant capacity, and can inhibit cellular senescence induced by oxidative stress. CJFSE showed DPPH scavenging activity and attenuated β-gal activity induced by H2O2 in HFDPCs. These findings indicate that CJFSE can mitigate hair loss induced by of DHT through inhibition of 5α-reductase activity and inhibit the oxidative stress induced cellular senescence through radical scavenging activity. To clarify the detail mechanism of CJFSE on hair growth, further study needs to be performed.
Conclusion: CJFSE increased the proliferation and spheroid size of HFDPCs as well as suppressed DHT production and mitigated its negative effect on HFDPC viability. Furthermore, CJFSE showed antioxidant activity and attenuated oxidative stress induced cellular senescence in HFDPCs. Taken together, these results suggest that CJFSE can be effectively used for hair growth or hair loss relief as a natural product.
Camellia japonica belongs to the camellia genus in azalea order and is an evergreen tree that grows naturally in Korea, Japan, and China. C. japonica contains active compounds such as polyphenol, vitamin E, saponin, triterpenoids, and various fatty acids which exert antioxidant, antimicrobial, wound healing, anti-pollution, and anti-inflammatory activity. C. japonica fruit shell (CJFS) is discarded after seed collection for obtaining oil, and its biological activity remains to be elucidated. In this study we investigated the effect of C. japonica fruit shell extract (CJFSE) on hair loss alleviation by measuring proliferation of DPCs, production of DHT, and reduction of oxidative stress.
Materials and Methods: The dried fruit shells of Camellia japonica from Jeju Island were extracted with EtOH. Cell viability and proliferation were identified through MTT and Ki67 staining in Human follicle dermal papilla cells (HFDPCs) respectively, and Dkk-1 secreted from HFDPCs was measured by ELISA. Activity of 5α-reductase was analyzed by HPLC, and to confirm reduction of oxidation stress, DPPH assay and senescence model induced by H2O2 were used. SA-β-gal activity was measured via fluorescence microscopy and FACS analysis. Spheroid culture was conducted on the ultra-low attachment plate, and the size of spheroids was measured using the ImageJ system.
Results: In proliferation of DPCs, we found that CJFSE increase the proliferation of HFDPCs and Ki67 expression which is indicator of hair growth. And we confirmed that secretion of Dkk-1, a negative regulator of Wnt signaling, was reduced by CJFSE. In addition, a spheroid culture of HFDPCs was conducted to confirm the effect of CJFSE on the volume of the hair shaft, and we observed that CJFSE increases the spheroid size. These data suggest that CJFSE may increase DPC proliferation by inhibition of Dkk-1. CJFSE inhibited the conversion of testosterone to DHT in rat liver microsomes model and prevented DHT-induced decrease of viability in HFDPCs. Oxidative stress causes HFDPC senescence, which contribute to hair loss. Accordingly, we investigated whether CJFSE has antioxidant capacity, and can inhibit cellular senescence induced by oxidative stress. CJFSE showed DPPH scavenging activity and attenuated β-gal activity induced by H2O2 in HFDPCs. These findings indicate that CJFSE can mitigate hair loss induced by of DHT through inhibition of 5α-reductase activity and inhibit the oxidative stress induced cellular senescence through radical scavenging activity. To clarify the detail mechanism of CJFSE on hair growth, further study needs to be performed.
Conclusion: CJFSE increased the proliferation and spheroid size of HFDPCs as well as suppressed DHT production and mitigated its negative effect on HFDPC viability. Furthermore, CJFSE showed antioxidant activity and attenuated oxidative stress induced cellular senescence in HFDPCs. Taken together, these results suggest that CJFSE can be effectively used for hair growth or hair loss relief as a natural product.