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J Clin Biochem Nutr. 2015 May;56(3):186-94. doi: 10.3164/jcbn.14-75. Epub 2015 Jan 28.

Pruni cortex ameliorates skin inflammation possibly through HMGB1-NFκB pathway in house dust mite induced atopic dermatitis NC/Nga transgenic mice.

Journal of clinical biochemistry and nutrition

Kenichi Watanabe, Vengadeshprabhu Karuppagounder, Somasundaram Arumugam, Rajarajan A Thandavarayan, Vigneshwaran Pitchaimani, Remya Sreedhar, Rejina Afrin, Meilei Harima, Hiroshi Suzuki, Kenji Suzuki, Takashi Nakamura, Mayumi Nomoto, Shizuka Miyashita, Kyoko Fukumoto, Kazuyuki Ueno

Affiliations

  1. Department of Clinical Pharmacology, Faculty of Pharmaceutical Sciences, Niigata University of Pharmacy and Applied Life Sciences, 265-1 Higashijima, Akiha-ku, Niigata 956-8603, Japan.
  2. Department of Gastroenterology, Niigata University Graduate School of Medical and Dental Sciences, 1-757 Asahimachidori, Chuo-ku, Niigata 951-8510, Japan.
  3. Department of Pharmaceutical Sciences, Niigata University of Pharmacy and Applied Life Sciences, 265-1 Higashijima, Akiha-ku, Niigata 956-8603, Japan.

PMID: 26060348 PMCID: PMC4454076 DOI: 10.3164/jcbn.14-75

Abstract

Pruni cortex, the bark of Prunus jamasakura Siebold ex Koidzumi, has been used in the Japanese systems of medicine for many years for its anti-inflammatory, antioxidant and antitussive properties. In this study, we investigated the effect of pruni cortex on atopic dermatitis NC/Nga mouse model. Atopic dermatitis-like lesion was induced by the application of house dust mite extract to the dorsal skin. After induction of atopic dermatitis, pruni cortex aqueous extract (1 g/kg, p.o.) was administered daily for 2 weeks. We evaluated dermatitis severity, histopathological changes and cellular protein expression by Western blotting for nuclear and cytoplasmic high mobility group box 1, receptor for advanced glycation end products, nuclear factor κB, apoptosis and inflammatory markers in the skin of atopic dermatitis mice. The clinical observation confirmed that the dermatitis score was significantly lower when treated with pruni cortex than in the atopic dermatitis group. Similarly pruni cortex inhibited hypertrophy and infiltration of inflammatory cells as identified by histopathology. In addition, pruni cortex significantly inhibited the protein expression of cytoplasmic high mobility group box 1, receptor for advanced glycation end products, nuclear p-nuclear factor kappa B, apoptosis and inflammatory markers. These results indicate that pruni cortex may have therapeutic potential in the treatment of atopic dermatitis by attenuating high mobility group box 1 and inflammation possibly through the nuclear factor κB pathway.

Keywords: High mobility group box protein 1; atopic dermatitis; inflammation; nuclear factor κB; pruni cortex

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