Abstract
Inflammatory bowel disease is a multifactorial inflammatory condition. This study aimed to test the protective effects of Spirulina platensis against ulcerative colitis (UC). UC was induced in thirty-six male Wistar rats by adding dextran sulfate sodium (DSS) to their drinking water, while a control group received only drinking water. UC rats were equally-divided into six groups that received a single oral daily dose of vehicle (DSS), sulfasalazine (SSZ, 50 mg/kg/day), chloroform or the hydroalcoholic extracts of Spirulina platensis (100 or 200 mg/kg/day) for 15 days, and then blood and colon samples were harvested for determination of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), erythrocyte sedimentation rate (ESR), myeloperoxidase (MPO), and histopathology. At the end of the study, compared to time-matched controls, UC rats showed increased TNF-α (1.64-fold), IL-6 (5.73-fold), ESR (3.18-fold), and MPO (1.61-fold), along with loss of body weight (24.73%) and disease activity index (1.767 ± 0.216 vs. 0 ± 0), p < 0.001. These effects were prevented by SSZ treatment (p < 0.001 vs. DSS). The hydroalcoholic extract of Spirulina platensis dose-dependently modulated all DSS-induced inflammatory changes. However, the chloroform extract significantly lowered only IL-6 and ESR, but not TNF-α or MPO levels. The protective effects of the hydroalcoholic extract of Spirulina platensis against experimental UC involved mitigation of DSS-induced inflammation.
Highlights
Inflammatory bowel disease (IBD) is an inflammatory condition of multifactorial etiology that is characterized by increased inflammation, which can further deteriorate and induce serious complications such as colon cancer [1]
This experiment confirmed that the HA extract of Spirulina platensis contained carotenoids
Gas Chromatography–Mass Spectrometry (GC-MS) analysis of the sample resulted in the isolation of 24 metabolites with small molecular weight, which were identified by matching the mass spectrum of each compound using the NIST-17 mass spectral library, as shown in Figure 2 and Tables 1 and 2
Summary
Inflammatory bowel disease (IBD) is an inflammatory condition of multifactorial etiology that is characterized by increased inflammation, which can further deteriorate and induce serious complications such as colon cancer [1]. UC affects only the rectum and the colon, with the lesions being more homogeneous and continuous [3,4]. Familial and genome-wide association studies have revealed the complex nature of IBD pathogenesis [3,5,6]. The interplay between altered genetic, immune, and environmental factors determines both the incidence and severity of IBD. In spite of the complexity of the signaling pathways involved in the inflammatory pathogenesis of IBD, the emergence of tumor necrosis factor-α (TNF-α) as a common player in clinical and experimental models is not surprising [7]. Many of the interleukins (ILs) including IL-6, IL-17, IL-23, and IL-26, among others, have been implicated in IBD pathogenesis and its complications [8,9,10], while IL-10 signaling through its receptors plays a protective role against IBD development [11,12,13]
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