Abstract

Persea americana Mill, cv. Hass, also known as avocado, has been reported to possess hypolipidemic, anti-diabetic, anti-oxidant, cardioprotective, and photoprotective potencies. However, few studies have reported its anti-colitic effects. In this study, we investigated anti-colitic effects of ethanol extract of P. americana (EEP) in dextran sulfate sodium (DSS)-induced colitic mice and the involved molecular mechanisms. EEP effectively improved clinical signs and histological characteristics of DSS-induced colitis mice. In DSS-exposed colonic tissues, EEP reduced expression levels of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and pro-inflammatory cytokines such as interleukin (IL)-6, IL-1β, and tumor necrosis factor (TNF)-α. Moreover, EEP suppressed DSS-induced activation of nuclear factor-kappa B (NF-κB) and signal transducer and activator of transcription 3 (STAT3). Consistent with in vivo results, EEP also suppressed protein and mRNA expression levels of iNOS, COX-2, and pro-inflammatory cytokines via NF-κB and STAT3 inactivation in LPS-induced RAW 264.7 macrophages. Taken together, our data indicate that ethanol extract of avocado may be used as a promising therapeutic against inflammatory bowel diseases by suppressing the NF-κB and STAT3 signaling pathway.

Highlights

  • Inflammatory bowel diseases (IBD), covering Crohn’s disease (CD) and ulcerative colitis (UC), are characterized by chronic remittent or progressive inflammatory conditions that can damage the entire gastrointestinal tract and the colonic mucosa [1]

  • Five compounds were identified by HPLC-PDA-electrospray ionization (ESI)-mass spectrometric (MS) by comparing their UV spectra and high-resolution mass number with literature data previously reported

  • Peak 1 was confirmed as homocysteine [17] while peak 2, peak 3, and peak 5 were identified as guanine, cytidine, and guanosine, respectively [18]

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Summary

Introduction

Inflammatory bowel diseases (IBD), covering Crohn’s disease (CD) and ulcerative colitis (UC), are characterized by chronic remittent or progressive inflammatory conditions that can damage the entire gastrointestinal tract and the colonic mucosa [1]. The most common age for IBD is 20 to 29 years and the second most common age is 50 to 70 years [2]. The exact etiology of IBD is not clearly understood yet, accumulating reports indicate that abnormal immune responses, complex gene–environment interactions, and genetic factors can converge to provoke disease initiation and progression [3]. 5-aminosalicylic acid (5-ASA), corticosteroids, sulfasalazine, and biological agents such as adalimumab are used to treat UC. A variety of natural products that can safely regulate pro-inflammatory signals and modulate IBD have been reported [5]

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