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Hominis placenta Suppresses Acute Lung Inflammation by Activating Nrf2.

Authors
  • Kim, Tae Ho1
  • Choi, Jun-Yong2
  • Kim, Kyun Ha3
  • Kwun, Min Jung3
  • Han, Chang-Woo4
  • Won, Ran5
  • Lee, Jung Ju1
  • Kim, Jong-In1
  • Joo, Myungsoo3
  • 1 * Department of Clinical Korean Medicine, Graduate School, Kyung Hee University, Seoul 02447, Republic of Korea. , (North Korea)
  • 2 † Lung Cancer Clinic, Pulmonary Medicine Center, Pusan National University, Yangsan 50612, Republic of Korea. , (North Korea)
  • 3 ‡ School of Korean Medicine, Pusan National University, Yangsan 50612, Republic of Korea. , (North Korea)
  • 4 § Department of Internal Medicine, Korean Medicine Hospital of Pusan National University, Yangsan 50612, Republic of Korea. , (North Korea)
  • 5 ¶ Department of Biomedical Laboratory Science, Division of Health Sciences, Dongseo University, Busan 47011, Republic of Korea. , (North Korea)
Type
Published Article
Journal
The American journal of Chinese medicine
Publication Date
Jan 01, 2018
Volume
46
Issue
4
Pages
801–817
Identifiers
DOI: 10.1142/S0192415X18500428
PMID: 29754504
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Hominis placenta (HP), a dried human placenta, has been known to target liver, lung, or kidney meridians, improving the functions associated with these meridians in traditional Chinese or Asian medicine (TCM). Since recent studies implicate an HP extract in suppressing inflammation, we investigated whether an aqueous HP extract can ameliorate inflammation that occurred in the lungs. When administered with a single intratracheal lipopolysaccharide (LPS), C57BL/6 mice developed an acute neutrophilic lung inflammation along with an increased expression of pro-inflammatory cytokine genes. However, this was diminished by the administration HP extract via an intraperitoneal route 2 h after LPS treatment. Western blot and semi-quantitative RT-PCR analyses revealed that while suppressing the activity of a proinflammatory factor NF-[Formula: see text]B marginally, the HP extract strongly activated an anti-inflammatory factor Nrf2, with concomitant expression of Nrf2-dependent genes. Mechanistically, the HP extract suppressed the ubiquitin-mediated degradation of Nrf2, functioning similarly to a 26S proteasome inhibitor, MG132. Collectively, these results suggest that the HP extract suppresses inflammation in mouse lungs, which is in part related to the HP extract perturbing the ubiquitin-dependent degradation of Nrf2 and thus increasing the function of Nrf2.

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