Isomenthone protects human dermal fibroblasts from TNF-α-induced death possibly by preventing activation of JNK and p38 MAPK

2012 ◽  
Vol 50 (10) ◽  
pp. 3514-3520 ◽  
Author(s):  
Eunsun Jung ◽  
Sangyo Byun ◽  
Seungbeom Kim ◽  
Moohan Kim ◽  
Deokhoon Park ◽  
...  
Keyword(s):  
P38 Mapk ◽  
Dermal Fibroblasts ◽  
Human Dermal Fibroblasts ◽  
Tnf Α

scholarly journals Efficacy of Alpinumisoflavone Isolated from Maclura tricuspidata Fruit in Tumor Necrosis Factor-α-Induced Damage of Human Dermal Fibroblasts

Antioxidants ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 514
Author(s):  
Sullim Lee ◽  
Giang Do Hoang ◽  
Daeyoung Kim ◽  
Ho Sueb Song ◽  
Sungyoul Choi ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Dermal Fibroblasts ◽  
The Body ◽  
Hazardous Substances ◽  
Human Dermal Fibroblasts ◽  
Cutaneous Lesions ◽  
Matrix Metalloproteinase 1 ◽  
Tnf Α ◽  
Necrosis Factor

The skin is an important organ in the human body that protects the body from environmentally hazardous substances. Reactive oxygen species (ROS) cause inflammatory reactions and degradation of the extracellular matrix leading to skin aging and various cutaneous lesions. This study evaluated the potential of isoflavones isolated from Maclura tricuspidata fruit to prevent TNF-α-induced skin inflammation in normal human dermal fibroblasts (HDFs). It focused on alpinumisoflavone (AIF) that suppressed the accumulation of ROS and nitric oxide (NO) in tumor necrosis factor-alpha (TNF-α)-treated HDFs. AIF inhibited the TNF-α-induced increase in matrix metalloproteinase-1, decreased procollagen I α1, and suppressed pro-inflammatory mediators and pro-inflammatory cytokines, including NO synthase, cyclooxygenase-2, interleukin (IL)-1β, IL-6, and IL-8 that trigger inflammatory responses. AIF inhibited nuclear factor-κB and activating protein 1 mitogen-activated protein kinases that were increased by TNF-α stimulation. These results suggest that AIF may protect skin from aging and various cutaneous lesions.

Up-regulation of ICAM-1 expression on human dermal fibroblasts by IFN β in the presence of TNF-α

FEBS Letters ◽  
1995 ◽  
Vol 363 (1-2) ◽  
pp. 141-144 ◽  
Author(s):  
Takashi Horikoshi ◽  
Kyori Ezoe ◽  
Hidemi Nakagawa ◽  
Hiroaki Eguchi ◽  
Niro Hanada ◽  
...  
Keyword(s):  
Dermal Fibroblasts ◽  
Human Dermal Fibroblasts ◽  
Tnf Α

scholarly journals Primary Ciliogenesis by 2-Isopropylmalic Acid Prevents PM2.5-Induced Inflammatory Response and MMP-1 Activation in Human Dermal Fibroblasts and a 3-D-Skin Model

2021 ◽  
Vol 22 (20) ◽  
pp. 10941
Author(s):  
Ji-Eun Bae ◽  
Daejin Min ◽  
Ji Yeon Choi ◽  
Hyunjung Choi ◽  
Joon Bum Kim ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Primary Cilia ◽  
Dermal Fibroblasts ◽  
Oxygen Species ◽  
Human Dermal Fibroblasts ◽  
Skin Model ◽  
Skin Cells ◽  
Tnf Α ◽  
Stress Kinase ◽  
Pro Inflammatory Cytokines

Particulate matters (PMs) increase oxidative stress and inflammatory response in different tissues. PMs disrupt the formation of primary cilia in various skin cells, including keratinocytes and melanocytes. In this study, we found that 2-isopropylmalic acid (2-IPMA) promoted primary ciliogenesis and restored the PM2.5-induced dysgenesis of primary cilia in dermal fibroblasts. Moreover, 2-IPMA inhibited the generation of excessive reactive oxygen species and the activation of stress kinase in PM2.5-treated dermal fibroblasts. Further, 2-IPMA inhibited the production of pro-inflammatory cytokines, including IL-6 and TNF-α, which were upregulated by PM2.5. However, the inhibition of primary ciliogenesis by IFT88 depletion reversed the downregulated cytokines by 2-IPMA. Moreover, we found that PM2.5 treatment increased the MMP-1 expression in dermal fibroblasts and a human 3-D-skin model. The reduced MMP-1 expression by 2-IPMA was further reversed by IFT88 depletion in PM2.5-treated dermal fibroblasts. These findings suggest that 2-IPMA ameliorates PM2.5-induced inflammation by promoting primary ciliogenesis in dermal fibroblasts.

scholarly journals Alnus Sibirica Extracts Suppress the Expression of Inflammatory Cytokines Induced by Lipopolysaccharides, Tumor Necrosis Factor-α, and Interferon-γ in Human Dermal Fibroblasts

Molecules ◽  
2019 ◽  
Vol 24 (16) ◽  
pp. 2883 ◽  
Author(s):  
Jeongyoon Choi ◽  
Sunghee Moon ◽  
Hyemi Bae ◽  
Young-Won Kim ◽  
Donghee Lee ◽  
...  
Keyword(s):  
Immune Responses ◽  
Interferon Γ ◽  
Dermal Fibroblasts ◽  
Raw264.7 Cells ◽  
Human Dermal Fibroblasts ◽  
Inflammatory Reactions ◽  
Tnf Α ◽  
Inflammatory Processes ◽  
Factor Α ◽  
Oxidative Effects

The effects of Alnus sibirica (AS) extracts on cytokine expression induced by inflammatory stimulants were examined in human dermal fibroblasts (HDFs) and RAW264.7 cells. The anti-oxidative effect and effect on cell viability of AS extracts were evaluated, and four extracts with the highest anti-oxidative effects were selected. HDFs and RAW264.7 cells were treated with inflammatory stimulants, and the expression of cytokines involved in acute (IL-6 and IL-10) and chronic (IL-18) inflammation, the initiation of the immune response (IL-33), and non-specific immune responses (IL-1β, IL-8, and TNF-α) were determined using a reverse-transcription polymerase chain reaction. LPS increased the expression of all the cytokines, except for IL-18; however, AS extracts, particularly AS2 and AS4, reduced this increase, and TNF-α treatment markedly increased the expression of cytokines related to non-specific immune responses. IFN-γ treatment induced no significant changes, except for increased IL-33 expression in HDFs. AS extracts inhibited the increase in the expression of IL-33 and other cytokines in HDFs. Thus, the exposure of HDFs and RAW264.7 cells to inflammatory stimulants increased the expression of cytokines related to all the inflammatory processes. HDFs are involved not only in simple tissue regeneration but also in inflammatory reactions in the skin. AS2 and AS4 may offer effective therapy for related conditions.

scholarly journals ETAS®50 Attenuates Ultraviolet-B-Induced Interleukin-6 Expression by Suppressing Akt Phosphorylation in Normal Human Dermal Fibroblasts

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Ken Shirato ◽  
Tomoko Koda ◽  
Jun Takanari ◽  
Junetsu Ogasawara ◽  
Takuya Sakurai ◽  
...  
Keyword(s):  
P38 Mapk ◽  
Dermal Fibroblasts ◽  
Ultraviolet B ◽  
Asparagus Officinalis ◽  
Mrna Levels ◽  
Human Dermal Fibroblasts ◽  
Akt Phosphorylation ◽  
Normal Human ◽  
Anti Inflammatory ◽  
Normal Human Dermal Fibroblasts

We recently reported that ETAS 50, a standardized extract from theAsparagus officinalisstem, exerted anti-inflammatory effects on ultraviolet-B- (UV-B-) irradiated normal human dermal fibroblasts (NHDFs) by inhibiting nuclear factor-κB p65 nuclear import and the resulting interleukin-1β(IL-1β) expression. To further elucidate the antiphotoaging potency of ETAS 50, we examined the anti-inflammatory effects on UV-B-irradiated NHDFs by focusing on the stress-activated mitogen-activated protein kinase (MAPK) and Akt signaling pathways. NHDFs were treated with 1 mg/mL of ETAS 50 or dextrin (vehicle control) after UV-B irradiation (20 mJ/cm2) for different time periods. Phosphorylation levels of c-Jun N-terminal kinase (JNK), p38 MAPK, and Akt were analyzed by western blotting. IL-6 mRNA levels were analyzed by real-time polymerase chain reaction. UV-B-irradiated NHDFs showed increased phosphorylation levels of JNK, p38 MAPK, and Akt, as well as increased mRNA levels of IL-6. ETAS 50 treatment after UV-B irradiation suppressed the increased phosphorylation levels of Akt without affecting those of JNK and p38 MAPK. ETAS 50 as well as Akt inhibitor Perifosine repressed UV-B irradiation-induced IL-6 mRNA expression. These results suggest that ETAS 50 treatment represses UV-B irradiation-induced IL-6 expression by suppressing Akt phosphorylation. The present findings demonstrate the potential of ETAS 50 to prevent photoaging by attenuating UV-B irradiation-induced proinflammatory responses in skin fibroblasts.

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