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

Abstract

We recently reported that ETAS 50, a standardized extract from the Asparagus officinalis stem, 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.

Antioxidant and Anti-Inflammatory Properties of Anthocyanins Extracted from Oryza sativa L. in Primary Dermal Fibroblasts

“…This study indicated that ANT reduced the lesions induced by 5-FU in the oral mucosa via NF- κ B-mediated biological manipulations [26]. Furthermore, ANT suppressed the H 2 O 2 -induced IL-6 production and NF- κ B activation, which is in agreement with a previous study on normal human dermal fibroblasts exposed to UVB [62]. Our findings are consistent with previous observations in animal and clinical studies, where ANT demonstrated anti-inflammatory effects by inhibiting NF- κ B transactivation and suppressing proinflammatory mediators [48].…”

ETAS®50 Attenuates SARS-CoV-2 Spike Protein-Induced IL-6 and IL-1β Production by Suppressing p44/42 MAPK and Akt Phosphorylation in Murine Primary Macrophages

“…No reuse allowed without permission. [21,[24][25][26][27]. To assess its anti-inflammatory effects, the cells were co-treated with the indicated concentrations of ETAS®50 or dextrin and 100 ng/mL of SARS-CoV-2 spike recombinant protein S1 subunit (Arigo Biolaboratories, Hsinchu City, Taiwan) for 1 to 24 h.…”

“…(0.25, 0.5, 1, or 2 mg/mL) were prepared by directly dissolving each agent in the complete medium, and then the supplemented medium was filter sterilized using a 0.22 μm membrane [21,[24][25][26][27]. To assess its anti-inflammatory effects, the cells were co-treated with the indicated concentrations of ETAS®50 or dextrin and 100 ng/mL of SARS-CoV-2 spike recombinant protein S1 subunit (Arigo Biolaboratories, Hsinchu City, Taiwan) for 1 to 24 h. respectively.…”

“…Moreover, our group previously reported that ETAS®50 attenuates hydrogen peroxideinduced expression of matrix metalloproteinase 9 and pro-inflammatory mediators by suppressing phosphorylation of c-Jun N-terminal kinase (JNK) and nuclear translocation of nuclear factor-κB (NF-κB) p65 subunit, respectively, in murine skin L929 fibroblasts [24,25]. ETAS®50 also attenuated ultraviolet B-induced expression of IL-6 and IL-1β by suppressing the phosphorylation of Akt and nuclear translocation of p65, respectively, in normal human dermal fibroblasts [26,27]. These previous findings suggest that ETAS®50 has the potential to abrogate pro-inflammatory responses by inhibiting TLR4 signaling in S1stimulated macrophages.…”

Standardized Extract of Asparagus officinalis Stem Attenuates SARS-CoV-2 Spike Protein-Induced IL-6 and IL-1β Production by Suppressing p44/42 MAPK and Akt Phosphorylation in Murine Primary Macrophages

“…Moreover, our group previously reported that EAS attenuates hydrogen peroxide-induced expression of matrix metalloproteinase 9 and pro-inflammatory mediators by suppressing phosphorylation of c-Jun N-terminal kinase (JNK) and nuclear translocation of nuclear factor-κB (NF-κB) p65 subunit, respectively, in murine skin L929 fibroblasts [ 24 , 25 ]. EAS also attenuated ultraviolet B-induced expression of IL-6 and IL-1β by suppressing the phosphorylation of Akt and nuclear translocation of p65, respectively, in normal human dermal fibroblasts [ 26 , 27 ]. These previous findings suggest that EAS has the potential to abrogate pro-inflammatory responses by inhibiting TLR4 signaling in S1-stimulated macrophages.…”