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Dietary Rice Bran Oil and γ‐Oryzanol Attenuates Toll Like Receptor‐mediated IκBα Phosphorylation, NF‐κB p65 Activation and Matrix Metallo Protease‐9 Expression in Peritoneal Macrophages from Rats Fed Partially Hydrogenated Vegetable Fat and thereby Exhibit Anti‐Inflammatory Activity

In spite of warning issued by regulatory agencies all over the world, South Asian countries are continuing to use Partially Hydrogenated Vegetable Fat (PHVF) in many food products. PHVF contains trans fatty acid known as elaidic acid which is pro‐inflammatory. NF‐κB p65 and Matrix Metallo Proteases‐9 (MMP‐9) play an important role in promoting inflammation. Dietary Rice bran oil (RBO) and γ‐ORY reduce the secretion of inflammatory mediators from macrophages as compared to those obtained from rats fed diet containing PHVF and thereby exhibit anti‐inflammatory activity. The present study was focused on specific role of RBO and γ‐ORY on the phosphorylation of IκBα, subsequent activation of NF‐κB p65 and secretion of Matrix Metallo Proteases (MMP‐9) a mechanism by which RBO and γ‐ORY may be exhibiting their anti‐inflammatory activity. Male wistar rats were fed AIN‐93 diet for 60 days. The diet was supplemented with one of the following fat/oil at 10wt%level: PHVF, RBO‐N (unfrationated oil), RBO‐MCR (Minor Constituents Removed oil), RBO‐MCR+Unsaponifiable Matter from Rice Bran Oil added back to RBO‐MCR (UM RBO‐MCR), RBO‐MCR+ γ‐ORY(700mg/kg diet), PHVF+RBO‐N (5.0+5.0wt%), PHVF+ γ‐ORY (700mg/kg diet). The macrophages from rats fed diet containing PHVF showed increased phosphorylation of IκB, translocation of NF‐κB p65, enhanced secretion of MMP‐9 indicating pro‐inflammatory nature of dietary PHVF. Diet containing RBO‐N, RBO‐MCR, UM RBO‐MCR and RBO‐MCR+ γ‐ORY significantly reduced phosphorylation of IκB, translocation of NF‐κB p65 and expression of MMP‐9 in macrophages all of which were enhanced when PHVF diets were fed to rats. Thus RBO and its components like γ‐ORY exhibit anti‐inflammatory activity by modulating expression of NF‐κB p65 which ultimately results in decreased secretion of pro‐inflammatory mediators by macrophages.