4.7 Article

Puerarin attenuates smoke inhalation injury by regulation of Th1/Th2 expression and inhibition of Th17 cells in rats

Journal

INTERNATIONAL IMMUNOPHARMACOLOGY
Volume 28, Issue 1, Pages 546-553

Publisher

ELSEVIER SCIENCE BV
DOI: 10.1016/j.intimp.2015.07.023

Keywords

Smoke inhalation injury; Gunpowder; Puerarin; Th17; Th1/Th2

Funding

  1. 12th Five Year Medical Scientific Research General Program of China [CWS12J021]

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Objective: Puerarin, a kind of traditional Chinese medicine, possesses immunomodulatory property. However, the immunomodulatory effects of puerarin on smoke inhalation injury have not been determined. The aim of the current study was to investigate the therapeutic efficacy of puerarin on gunpowder smog-induced acute lung injury in rats via regulation of Th1/Th2/Th17 expression. Materials and methods: Wistar rats were equally randomized to four groups (normal control group, puerarin control group, smoke inhalation injury group, puerarin treatment plus smoke inhalation injury group). The severity of lung injury was evaluated by histopathology, myeloperoxidase (MPO) activity in lung homogenates, cell counting in bronchoalveolar lavage fluid (BALF), and lung vascular permeability parameters including lung wet to dry weight ratio and protein concentration in BALF. Flow cytometry was used to analyze the expression of Th1/Th2/Th17 lymphocytes in blood of rats. Results: Puerarin showed significant therapeutic effects against neutrophil infiltration and tissue injury, as evidenced by histopathological findings and MPO activity. Lung vascular permeability was also relieved by puerarin administration. Additionally, puerarin significantly decreased the number of neutrophils and lymphocytes in BALF compared with smoke inhalation injury group. Furthermore, puerarin increased Th1 immunity and reduced Th2 and Th17 responses and thereby altering the Th1/Th2/Th17 imbalance induced by smoke inhalation. Conclusions: Our findings suggested that puerarin suppressed inflammatory responses in gunpowder smog-induced acute lung injury by regulation of Th1/Th2/Th17 expression, and may be a potential therapeutic agent for smoke inhalation injury. (C) 2015 Elsevier B.V. All rights reserved.

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