Abstract

Electroacupuncture (EA) is reported to possess anti-inflammatory properties and has beneficial effects on acute respiratory distress syndrome (ARDS). However, the underlying mechanisms of the effects of EA on ARDS remain unclear. This study aims to investigate the protective effect of EA on LPS-induced ARDS. In this study, Sprague-Dawley male rats were treated with EA at Hegu (LI4) for 45 minutes before LPS instillation (0.4 mg/kg, 100 ul). H&E staining, wet-to-dry weight (W/D) ratio, PaO2, and protein content in BALF were employed to determine the function of lung tissues. Inflammatory cytokines in serum and BALF were detected by enzyme-linked immunoassay assay (ELISA). The levels of oxidative stress markers were detected to determine the oxidative stress status. Cell apoptosis was observed by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining and western blot. Here, we found that EA pretreatment effectively alleviated lung pathological damage. Moreover, EA suppressed the oxidative stress damage by upregulating glutathione and superoxide dismutase and downregulating malondialdehyde. EA pretreatment also regulated apoptosis-related proteins, such as Bax and Bcl-2. We found that peroxisome proliferators-activated receptors γ (PPARγ) play a critical role during ARDS, EA up-regulated the expression of PPARγ, which inhibited the activation of nuclear factor-kappa B (NF-κB) and decreased the inflammatory cytokines (interleukin-1β, interleukin-6, and tumor necrosis factor-α). When rats were treated with GW9662, a selective PPARγ antagonist, these effects of EA were reversed. Our study demonstrated that EA pretreatment had a beneficial effect on LPS-induced ARDS in rats by anti-inflammatory, antioxidative, and antiapoptotic properties which was regulated via PPARγ/NF-κB signaling pathway.

Highlights

  • Acute respiratory distress syndrome (ARDS) is a lifethreatening form of respiratory failure

  • Compared with negative control (NC) group, LPS instillation decreased the expression of peroxisome proliferators-activated receptors c (PPARc), while EA pretreatment upregulated the expression of PPARc

  • When pretreated with EA, the downregulation of PPARc was prevented in the rat lung tissues. e results in IHC were similar to that detected by western blot, in the R + EA group, the expression of PPARc was upregulated and, in G + EA group, the expression of PPARc was decreased (Figure 1(c))

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Summary

Introduction

Acute respiratory distress syndrome (ARDS) is a lifethreatening form of respiratory failure. ARDS accounts for 10% of intensive care unit admissions, representing more than 3 million patients annually [1]. ARDS is characterized by noncardiogenic pulmonary edema, lifethreatening hypoxemia, oxidative stress, and imbalance of proinflammatory and anti-inflammatory cytokines [2]. There is still no effective therapy for this life-threatening disorder because of the limited understanding about its pathogenesis. Acupuncture is a popular folk practice in traditional Chinese medicine (TCM) with a history over 5000 years. In Europe and the USA, this traditional Chinese medicine has become one of the treatment strategies and has steadily claimed its usefulness in complementary medicine [4]. Electroacupuncture (EA), a kind of therapy, combines traditional Chinese medicine with modern technique

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