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Arctiin blocks hydrogen peroxide-induced senescence and cell death though microRNA expression changes in human dermal papilla cells.

Bae S, Lim KM, Cha HJ, An IS, Lee JP, Lee KS, Lee GT, Lee KK, Jung HJ, Ahn KJ, An S - Biol. Res. (2014)

Bottom Line: In the present study, we found that arctiin exerts anti-oxidative effects on human hair dermal papilla cells (HHDPCs).The results showed that arctiin pretreatment significantly inhibited the H2O2-induced reduction in cell viability.This effect was confirmed by senescence associated-beta galactosidase (SA-β-gal) assay results; we found that arctiin pretreatment impaired H2O2-induced senescence in HHDPCs.

View Article: PubMed Central - PubMed

Affiliation: Korea Institute for Skin and Clinical Sciences, Konkuk University, 120 Neungdong-ro, Gwangjin-gu, Seoul, 143-701, Republic of Korea. sbae@konkuk.ac.kr.

ABSTRACT

Background: Accumulating evidence indicates that reactive oxygen species (ROS) are an important etiological factor for the induction of dermal papilla cell senescence and hair loss, which is also known alopecia. Arctiin is an active lignin isolated from Arctium lappa and has anti-inflammation, anti-microbial, and anti-carcinogenic effects. In the present study, we found that arctiin exerts anti-oxidative effects on human hair dermal papilla cells (HHDPCs).

Results: To better understand the mechanism, we analyzed the level of hydrogen peroxide (H2O2)-induced cytotoxicity, cell death, ROS production and senescence after arctiin pretreatment of HHDPCs. The results showed that arctiin pretreatment significantly inhibited the H2O2-induced reduction in cell viability. Moreover, H2O2-induced sub-G1 phase accumulation and G2 cell cycle arrest were also downregulated by arctiin pretreatment. Interestingly, the increase in intracellular ROS mediated by H2O2 was drastically decreased in HHDPCs cultured in the presence of arctiin. This effect was confirmed by senescence associated-beta galactosidase (SA-β-gal) assay results; we found that arctiin pretreatment impaired H2O2-induced senescence in HHDPCs. Using microRNA (miRNA) microarray and bioinformatic analysis, we showed that this anti-oxidative effect of arctiin in HHDPCs was related with mitogen-activated protein kinase (MAPK) and Wnt signaling pathways.

Conclusions: Taken together, our data suggest that arctiin has a protective effect on ROS-induced cell dysfunction in HHDPCs and may therefore be useful for alopecia prevention and treatment strategies.

No MeSH data available.


Analysis of intracellular ROS levels with DCF-DA assays. (A) HHDPCs were pre-treated with DMSO or arctiin (20 μM) followed by H2O2 (750 μM) prior to flow cytometry. (B) The graph indicates the mean value of M1-phase (DCF-DA-stained) cells from three independent experiments. *p < 0.05 compared with H2O2-treated HHDPCs.
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Fig3: Analysis of intracellular ROS levels with DCF-DA assays. (A) HHDPCs were pre-treated with DMSO or arctiin (20 μM) followed by H2O2 (750 μM) prior to flow cytometry. (B) The graph indicates the mean value of M1-phase (DCF-DA-stained) cells from three independent experiments. *p < 0.05 compared with H2O2-treated HHDPCs.

Mentions: ROS generation mediated by H2O2 is characterized by increases in cell death and cell cycle arrest in several cell lines [1]. To determine whether arctiin pretreatment inhibits H2O2-mediated ROS generation, we performed DCF-DA analyses to assess intracellular ROS production in HHDPCs. As shown in Figure 3A, arctiin did not alter intracellular ROS levels in untreated control cells, but it significantly abolished the H2O2-induced increase in intracellular ROS generation. Cells treated with 750 μM H2O2 showed a 45.77% accumulation of M phase (DCF-positive) cells as compared with untreated control cells (Figure 3B). However, pretreatment with 20 μM arctiin, led to reduction of 29.77% of cells in the M phase as compared with H2O2-treated cells (Figure 3B). These results suggest that H2O2-mediated ROS production in HHDPCs is inhibited by arctiin.Figure 3


Arctiin blocks hydrogen peroxide-induced senescence and cell death though microRNA expression changes in human dermal papilla cells.

Bae S, Lim KM, Cha HJ, An IS, Lee JP, Lee KS, Lee GT, Lee KK, Jung HJ, Ahn KJ, An S - Biol. Res. (2014)

Analysis of intracellular ROS levels with DCF-DA assays. (A) HHDPCs were pre-treated with DMSO or arctiin (20 μM) followed by H2O2 (750 μM) prior to flow cytometry. (B) The graph indicates the mean value of M1-phase (DCF-DA-stained) cells from three independent experiments. *p < 0.05 compared with H2O2-treated HHDPCs.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4196076&req=5

Fig3: Analysis of intracellular ROS levels with DCF-DA assays. (A) HHDPCs were pre-treated with DMSO or arctiin (20 μM) followed by H2O2 (750 μM) prior to flow cytometry. (B) The graph indicates the mean value of M1-phase (DCF-DA-stained) cells from three independent experiments. *p < 0.05 compared with H2O2-treated HHDPCs.
Mentions: ROS generation mediated by H2O2 is characterized by increases in cell death and cell cycle arrest in several cell lines [1]. To determine whether arctiin pretreatment inhibits H2O2-mediated ROS generation, we performed DCF-DA analyses to assess intracellular ROS production in HHDPCs. As shown in Figure 3A, arctiin did not alter intracellular ROS levels in untreated control cells, but it significantly abolished the H2O2-induced increase in intracellular ROS generation. Cells treated with 750 μM H2O2 showed a 45.77% accumulation of M phase (DCF-positive) cells as compared with untreated control cells (Figure 3B). However, pretreatment with 20 μM arctiin, led to reduction of 29.77% of cells in the M phase as compared with H2O2-treated cells (Figure 3B). These results suggest that H2O2-mediated ROS production in HHDPCs is inhibited by arctiin.Figure 3

Bottom Line: In the present study, we found that arctiin exerts anti-oxidative effects on human hair dermal papilla cells (HHDPCs).The results showed that arctiin pretreatment significantly inhibited the H2O2-induced reduction in cell viability.This effect was confirmed by senescence associated-beta galactosidase (SA-β-gal) assay results; we found that arctiin pretreatment impaired H2O2-induced senescence in HHDPCs.

View Article: PubMed Central - PubMed

Affiliation: Korea Institute for Skin and Clinical Sciences, Konkuk University, 120 Neungdong-ro, Gwangjin-gu, Seoul, 143-701, Republic of Korea. sbae@konkuk.ac.kr.

ABSTRACT

Background: Accumulating evidence indicates that reactive oxygen species (ROS) are an important etiological factor for the induction of dermal papilla cell senescence and hair loss, which is also known alopecia. Arctiin is an active lignin isolated from Arctium lappa and has anti-inflammation, anti-microbial, and anti-carcinogenic effects. In the present study, we found that arctiin exerts anti-oxidative effects on human hair dermal papilla cells (HHDPCs).

Results: To better understand the mechanism, we analyzed the level of hydrogen peroxide (H2O2)-induced cytotoxicity, cell death, ROS production and senescence after arctiin pretreatment of HHDPCs. The results showed that arctiin pretreatment significantly inhibited the H2O2-induced reduction in cell viability. Moreover, H2O2-induced sub-G1 phase accumulation and G2 cell cycle arrest were also downregulated by arctiin pretreatment. Interestingly, the increase in intracellular ROS mediated by H2O2 was drastically decreased in HHDPCs cultured in the presence of arctiin. This effect was confirmed by senescence associated-beta galactosidase (SA-β-gal) assay results; we found that arctiin pretreatment impaired H2O2-induced senescence in HHDPCs. Using microRNA (miRNA) microarray and bioinformatic analysis, we showed that this anti-oxidative effect of arctiin in HHDPCs was related with mitogen-activated protein kinase (MAPK) and Wnt signaling pathways.

Conclusions: Taken together, our data suggest that arctiin has a protective effect on ROS-induced cell dysfunction in HHDPCs and may therefore be useful for alopecia prevention and treatment strategies.

No MeSH data available.