Riboflavin attenuates lipopolysaccharide-induced lung injury in rats

Abstract

Riboflavin (vitamin B2) is an easily absorbed micronutrient with a key role in maintaining health in humans and animals. It is the central component of the cofactors flavin adenine dinucleotide (FAD) and flavin mononucleotide (FMN) and is therefore required by all flavoproteins. Riboflavin also works as an antioxidant by scavenging free radicals. The present study was designed to evaluate the effects of riboflavin against acute lungs injury induced by the administration of a single intranasal dose (20 μg/rat) of lipopolysaccharides (LPS) in experimental rats. Administration of LPS resulted in marked increase in malondialdehyde (MDA) level (p < 0.01) and MPO activity (p < 0.001), whereas marked decrease in glutathione (GSH) content (p < 0.001), glutathione reductase (GR) (p < 0.001) and glutathione peroxidase (p < 0.01) activity. These changes were significantly (p < 0.001) improved by treatment with riboflavin in a dose-dependent manner (30 and 100 mg/kg, respectively). Riboflavin (100 mg/kg, p.o.) showed similar protective effects as dexamethasone (1 mg/kg, p.o.). Administration of LPS showed marked cellular changes including interstitial edema, hemorrhage, infiltration of PMNs, etc., which were reversed by riboflavin administration. Histopathological examinations showed normal morphological structures of lungs tissue in the control group. These biochemical and histopathological examination were appended with iNOS and CAT gene expression. The iNOS mRNA expression was increased significantly (p < 0.001) and levels of CAT mRNA expression was decreased significantly (p < 0.001) in the animals exposed to LPS, while treatment with riboflavin significantly (p < 0.01) improved expression of both gene. In conclusion, the present study clearly demonstrated that riboflavin caused a protective effect against LPS-induced ALI. These results suggest that riboflavin may be used to protect against toxic effect of LPS in lungs.

The effects of riboflavin on ischemia/reperfusion induced renal injury: Role on caspase-3 expression

“…Decreased GSH levels have been reported to increase by riboflavin treatment in carbon tetrachloride-induced hepatotoxicity, stroke and lipopolysaccharide-induced lung injury models. [16][17][18]. Our data are consistent with these previous studies.…”

“…Our study indicated that riboflavin treatment reduces renal MDA levels through its antioxidative properties. It has been previously shown that riboflavin treatment decreased MDA levels in liver [16], brain [17] and lung [18] and thus protected against carbon tetrachloride-induced hepatotoxicity, stroke and lipopolysaccharideinduced lung injury respectively. Therefore, the reduction of MDA levels presented here probably contributed in great sense to the inhibition of I/R events in kidney tissues.…”

Riboflavin: The Health Benefits of a Forgotten Natural Vitamin

“…It has been demonstrated that RF reduced the hepatocellular injury and hepatotoxicity induced by LPS through elevation of malondialdehyde (MDA) level and myeloperoxidase (MPO) activity, whereas a marked decrease in GSH content, GR and glutathione peroxidase (GPx) activity. Moreover, expression of inducible nitric oxide synthase (iNOS) and catalase (CAT) gene expression was improved via RF administration [45]. In addition, RF reduces mortality rates through the reduction of the expression and release of high-mobility group protein B1 (HMGB1); however, the effect of RF was time-dependent [46].…”

Ameliorative effects of riboflavin on acetic acid‐induced colonic injury in rats

“…More recently, it was reported that administration of soymilk fermented by the RF‐producing Lactobacillus plantarum strain to mice showed anti‐inflammatory effects by lowering microbial translocation to liver and decreasing cytokine levels in intestinal fluids in a trinitrobenzene sulfonic acid‐induced intestinal inflammation model . Furthermore, RF caused a protective effect by reversing cellular changes such as interstitial edema, haemorrhage and polymorphonuclear leukocyte infiltration against lipopolysaccharide‐induced acute lung injury . In addition, RF has been shown to reduce proinflammatory activity of macrophages and exert anti‐inflammatory effects by inhibiting nuclear factor (NF)‐κB activation .…”