Park Ju Ho1, Jang Jun Sung2, Kim Ki Cheon1, Hong Jin Tae3. 1. College of Pharmacy and Medical Research Center, Chungbuk National University, 194-31 Osongsaengmyeong 1-ro, Osong-eup, Heungduk-gu, Cheongju, Chungbuk 361-951, Republic of Korea; INIST ST CO., LTD., 500, Sinnae-ro, Geumwang-eup, Eumseong-gun, Chungcheongbuk-do 27644, Republic of Korea. 2. College of Pharmacy and Medical Research Center, Chungbuk National University, 194-31 Osongsaengmyeong 1-ro, Osong-eup, Heungduk-gu, Cheongju, Chungbuk 361-951, Republic of Korea. 3. College of Pharmacy and Medical Research Center, Chungbuk National University, 194-31 Osongsaengmyeong 1-ro, Osong-eup, Heungduk-gu, Cheongju, Chungbuk 361-951, Republic of Korea. Electronic address: jinthong@chungbuk.ac.kr.
Abstract
BACKGROUND: Centella asiatica phytosome (CA phytosome) has potent antioxidant and anti-inflammatory properties. However, its anti-dermatitic effect has not yet been reported. PURPOSE: We investigated the effects of CA phytosome on inflammatory reponses by macrophages in an atopic dermatitis (AD) mouse model. STUDY DESIGN: The effects of CA phytosome on atopic dermatitis were examined by using phthalic anhydride (PA)-induced AD mouse model and RAW 264.7 murine macrophages. METHODS: An AD-like lesion was induced by a topical application of 5% phthalic anhydride (PA) to the dorsal skin or ear of HR-1 mice. After AD induction, 100 µl (20 µl/cm2) of 0.2% and 0.4% CA phytosome was spread on the dorsal skin and ear of the mice three times a week for four weeks. We evaluated histopathological changes and changes in protein expression by Western blotting for iNOS and COX-2; NF-κB activity was determined by EMSA. We also measured TNF-α, IL-1β, and IgE concentration in the blood of AD mice by ELISA. RESULTS: Histological analysis showed that CA phytosome inhibited infiltration of inflammatory cells. CA phytosome treatment inhibited the expression of iNOS and COX-2, activity of NF-κB, and release of TNF-α, IL-1β, and IgE. In addition, CA phytosome (5, 10, and 20 µg/ml) potently inhibited LPS (1 µg/ml)-induced NO production as well as iNOS and COX-2 expression in RAW 264.7 macrophage. Furthermore, CA phytosome inhibited LPS-induced DNA binding activities of NF-κB, and this was associated with the discontinuation of IκBα degradation and subsequent decreases in the translocation of p65 and p50 into the nucleus. CONCLUSION: From our data, CA phytosome application, which operates via NF-κB signaling inhibition, seems to be a promising AD treatment. Herein, we investigated the effects of Centella asiatica phytosome (CA phytosome) on inflammatory responses by macrophages in an atopic dermatitis (AD) mouse model. An AD-like lesion was induced by the topical application of 5% phthalic anhydride (PA) to the dorsal skin or ear of HR-1 mice. After AD induction, 100 µl (20 µl/cm2) of 0.2% and 0.4% CA phytosome was spread on the dorsal skin and ear of the mice three times a week for four weeks. We evaluated dermatitis severity, histopathological changes, and changes in protein expression by Western blotting for iNOS and COX-2; NF-κB activity was determined by gel electromobility shift assay (EMSA). We also measured TNF-α, IL-1β, and IgE concentration in the blood of AD mice by enzyme-linked immunosorbent assay (ELISA). CA phytosome attenuated the development of PA-induced AD. Histological analysis showed that CA phytosome inhibited hyperkeratosis, proliferation of mast cells, and infiltration of inflammatory cells. Furthermore, CA phytosome treatment inhibited the expression of iNOS and COX-2, activity of NF-κB, and release of TNF-α, IL-1β, and IgE. In addition, CA phytosome (5, 10, and 20 µg/ml) potently inhibited lipopolysaccharide (LPS) (1 µg/ml)-induced NO production as well as iNOS and COX-2 expression in RAW 264.7 macrophage cells. Furthermore, CA phytosome inhibited LPS-induced DNA binding activities of NF-κB, and this was associated with the discontinuation of IκBα degradation and subsequent decreases in the translocation of p65 and p50 into the nucleus. From our data, CA phytosome application, which operates via NF-κB signaling inhibition, seems to be a promising AD treatment.
BACKGROUND:Centella asiatica phytosome (CA phytosome) has potent antioxidant and anti-inflammatory properties. However, its anti-dermatitic effect has not yet been reported. PURPOSE: We investigated the effects of CA phytosome on inflammatory reponses by macrophages in an atopic dermatitis (AD) mouse model. STUDY DESIGN: The effects of CA phytosome on atopic dermatitis were examined by using phthalic anhydride (PA)-induced AD mouse model and RAW 264.7 murine macrophages. METHODS: An AD-like lesion was induced by a topical application of 5% phthalic anhydride (PA) to the dorsal skin or ear of HR-1 mice. After AD induction, 100 µl (20 µl/cm2) of 0.2% and 0.4% CA phytosome was spread on the dorsal skin and ear of the mice three times a week for four weeks. We evaluated histopathological changes and changes in protein expression by Western blotting for iNOS and COX-2; NF-κB activity was determined by EMSA. We also measured TNF-α, IL-1β, and IgE concentration in the blood of AD mice by ELISA. RESULTS: Histological analysis showed that CA phytosome inhibited infiltration of inflammatory cells. CA phytosome treatment inhibited the expression of iNOS and COX-2, activity of NF-κB, and release of TNF-α, IL-1β, and IgE. In addition, CA phytosome (5, 10, and 20 µg/ml) potently inhibited LPS (1 µg/ml)-induced NO production as well as iNOS and COX-2 expression in RAW 264.7 macrophage. Furthermore, CA phytosome inhibited LPS-induced DNA binding activities of NF-κB, and this was associated with the discontinuation of IκBα degradation and subsequent decreases in the translocation of p65 and p50 into the nucleus. CONCLUSION: From our data, CA phytosome application, which operates via NF-κB signaling inhibition, seems to be a promising AD treatment. Herein, we investigated the effects of Centella asiatica phytosome (CA phytosome) on inflammatory responses by macrophages in an atopic dermatitis (AD) mouse model. An AD-like lesion was induced by the topical application of 5% phthalic anhydride (PA) to the dorsal skin or ear of HR-1 mice. After AD induction, 100 µl (20 µl/cm2) of 0.2% and 0.4% CA phytosome was spread on the dorsal skin and ear of the mice three times a week for four weeks. We evaluated dermatitis severity, histopathological changes, and changes in protein expression by Western blotting for iNOS and COX-2; NF-κB activity was determined by gel electromobility shift assay (EMSA). We also measured TNF-α, IL-1β, and IgE concentration in the blood of AD mice by enzyme-linked immunosorbent assay (ELISA). CA phytosome attenuated the development of PA-induced AD. Histological analysis showed that CA phytosome inhibited hyperkeratosis, proliferation of mast cells, and infiltration of inflammatory cells. Furthermore, CA phytosome treatment inhibited the expression of iNOS and COX-2, activity of NF-κB, and release of TNF-α, IL-1β, and IgE. In addition, CA phytosome (5, 10, and 20 µg/ml) potently inhibited lipopolysaccharide (LPS) (1 µg/ml)-induced NO production as well as iNOS and COX-2 expression in RAW 264.7 macrophage cells. Furthermore, CA phytosome inhibited LPS-induced DNA binding activities of NF-κB, and this was associated with the discontinuation of IκBα degradation and subsequent decreases in the translocation of p65 and p50 into the nucleus. From our data, CA phytosome application, which operates via NF-κB signaling inhibition, seems to be a promising AD treatment.
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