Abstract

Air pollutants, commonly derived from combustion reaction, are correlated with systematic inflammation, causing bronchial and asthmatic disorders. Therefore, it is very important to develop the ingredients which protect people from pulmonary damage caused by air pollutants. This study aimed at examining the anti‐inflammatory activity of Zizyphus jujube extract. Jujube fruit harvested from Gyeongsan region, Republic of Korea was ground, heated, and extracted in aqueous ethanol with or without enzymatic hydrolysis using Viscozyme® L (Novozyme, Bagsvaerd, Denmark). The jujube ethanolic extract prepared after treatment with heat and the enzyme (HJE) was found to effectively scavenge radicals as well as contain the considerable levels of total phenolics and flavonoids compared to non‐hydrolyzed extract (NHJE). In vitro studies using various types of cell lines demonstrated that HJE (1) decreased nitric oxide (NO) production from lipopolysaccharide (LPS)‐treated Raw 264.7 murine macrophages in a concentration‐dependent manner, (2) lowered secretions of pro‐inflammatory cytokines including tumor necrosis factor α (TNFα), interleukin‐6 (IL‐6) and interleukin‐1β (IL‐1β) from O‐tetradecanoylphorbol‐13‐acetate (TPA)‐treated THP‐1 human monocytes, and (3) reduced expressions of inflammation‐associated proteins, such as cytoplasmic COX‐2, iNOS, and nuclear NF‐κB in A549 human lung epithelial cells. To further examine the anti‐inflammatory effect of dietary HJE in animal, C57BL/6J mice were orally fed HJE for 2 weeks, followed by induction of lung inflammation by i.p. administration of benzo(a)pyrene (50 mg/kg B.W). A total of forty eight C57BL/6J mice (6‐week old male, 20–25 g) were divided into 6 groups (n = 8) as follows: (1) control, (2) B(a)P alone, (3) B(a)P+NHJE‐L (0.75 g/Kg B.W), (4) B(a)P+NHJE‐H (1.5 g/Kg B.W), (5) B(a)P+HJE‐L (0.75 g/Kg B.W), and (6) B(a)P+HJE‐H (1.5 g/kg B.W). Oral supplementation of HJE notably diminished the B(a)P‐induced elevation of pro‐inflammatory cytokine levels in the plasma and attenuated B(a)P‐induced pulmonary inflammation as evaluated by histological observation. These findings suggest that HJE can protect the lung epithelial cells from B(a)P‐induced injury presumably through attenuating macrophage‐associated inflammatory response and could be developed into the agent that suppresses air pollutant‐induced lung inflammation.Support or Funding InformationThis study was funded by the Forest Resources Development Institute of Gyeongsangbuk‐do, and the National Research Foundation of Korea grant (Grant No. 2017R1A2B4005087) by the Ministry of Science and ICT, Republic of Korea.

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