Abstract
Royal Jelly (RJ) is widely consumed in diets throughout the world due to its beneficial effects: antioxidant, antitumor and anti-inflammatory. We have investigated the role of RJ in the development of TNBS colitis in mice. Colitis was induced by a rectal instillation of TNBS at 0.1 mL per mouse. Intestine samples of the animals orally treated with RJ (100, 150, and 200 mg/kg) were collected for antioxidant assays (GSH and GSH-Px), proinflammatory protein quantification (COX-2 and NF-κB), and histological analyses. RJ 100 mg/kg maintained GSH levels and increased the activity of GSH-Px, downregulated key inflammatory mediators (COX-2 and NF-κB), and decreased the lesions caused by TNBS as shown by the histological analyses. In conclusion, RJ showed anti-inflammatory and antioxidant properties in experimental colitis, resulting in the amelioration of the macroscopic and histological analyses. These results corroborate with the RJ supplementation in diets.
Highlights
Royal jelly (RJ) is an important functional food item that possesses several health-promoting properties and has been widely used in commercial medical products, healthy foods, and cosmetics in many countries [1]
According to the results shown and the data published, RJ remains as a prominent nutrient
We demonstrated that oral pretreatment with RJ may be effective in protecting the mucosa of mice in Trinitrobenzene sulfonic acid (TNBS)-induced colitis, partly explained by its antioxidant property, which prevents proinflammatory mediators from acutely increasing
Summary
Royal jelly (RJ) is an important functional food item that possesses several health-promoting properties and has been widely used in commercial medical products, healthy foods, and cosmetics in many countries [1]. Some of its accredited properties are immunomodulation [3] anti-inflammatory [4], healing [5], and antiaging [6]. It is a nourishing substance secreted by the mandibular and hypopharyngeal glands of worker honey bees Apis mellifera [7]. It is already known that highly reactive free radicals are formed by either exogenous chemicals or endogenous metabolic processes of the body These free radicals are capable of oxidizing biomolecules, resulting in tissue damage and consequent cell death [11] in various pathological processes including inflammatory bowel disease [12, 13]
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