2. Academic Validation
  3. Inhibitory effects of collismycin C and pyrisulfoxin A on particulate matter-induced pulmonary injury

Inhibitory effects of collismycin C and pyrisulfoxin A on particulate matter-induced pulmonary injury

  • Phytomedicine. 2019 Sep:62:152939. doi: 10.1016/j.phymed.2019.152939.
Hyukjae Choi 1,  Wonhwa Lee 2,  Eonmi Kim 1,  Sae-Kwang Ku 3,  Jong-Sup Bae 4
Affiliations

Affiliations

  • 1 College of Pharmacy, Yeungnam University, Gyeongsan 38541, Republic of Korea.
  • 2 Aging Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon 34141, Republic of Korea.
  • 3 Department of Histology and Anatomy, College of Korean Medicine, Daegu Haany University, Gyeongsan-si 38610, Republic of Korea. Electronic address: gucci200@hanmail.net.
  • 4 College of Pharmacy, CMRI, Research Institute of Pharmaceutical Sciences, BK21 Plus KNU Multi-Omics based Creative Drug Research Team, Kyungpook National University, Daegu 41566, Republic of Korea. Electronic address: baejs@knu.ac.kr.
PMID: 31100678 DOI: 10.1016/j.phymed.2019.152939
Abstract

Background: Inhalation of fine particulate matter (PM2.5) is associated with elevated pulmonary injury caused by the loss of vascular barrier integrity. Marine microbial Natural Products isolated from microbial culture broths were screened for pulmonary protective effects against PM2.5. Two 2,2'-bipyridine compounds isolated from a red alga-associated Streptomyces sp. MC025-collismycin C (2) and pyrisulfoxin A (5)-were found to inhibit PM2.5-mediated vascular barrier disruption.

Purpose: To confirm the inhibitory effects of collismycin C and pyrisulfoxin A on PM2.5-induced pulmonary injury STUDY DESIGN: In this study, we investigated the beneficial effects of collismycin C and pyrisulfoxin A on PM-induced lung endothelial cell (EC) barrier disruption and pulmonary inflammation.

Methods: Permeability, leukocyte migration, proinflammatory protein activation, Reactive Oxygen Species (ROS) generation, and histology were evaluated in PM2.5-treated ECs and mice.

Results: Collismycin C and pyrisulfoxin A significantly scavenged PM2.5-induced ROS and inhibited the ROS-induced activation of p38 mitogen-activated protein kinase as well as activated Akt, which helped in maintaining endothelial integrity, in purified pulmonary endothelial cells. Furthermore, collismycin C and pyrisulfoxin A reduced vascular protein leakage, leukocyte infiltration, and proinflammatory cytokine release in the bronchoalveolar lavage fluid of PM-treated mice.

Conclusion: These data suggested that collismycin C and pyrisulfoxin A might exert protective effects on PM-induced inflammatory lung injury and vascular hyperpermeability.

Keywords

Akt; Collismycin C; Particulate matter; Pyrisulfoxin A; Vascular permeability.

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