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Poly-lactic acid/polyhydroxybutyrate (PLA/PHB) bio-based films suppose an environmentally friendly alternative to petroleum-derived packaging. In addition, rice bran extracts (RBEs) are an interesting source of bioactive compounds. In the present study, active films were formulated with 0.3% (w/v) or 0.5% (w/v) RBE (low-RBE and high-RBE) and compared to PLA/PHB films with no RBE. The migrations of active compounds as well as the antimicrobial and the antioxidant activities were analyzed in the three film formulations. The effects of active PLA/PHB films on fresh pork meat were evaluated by measuring the instrumental color, lipid and protein oxidations, and microbiological status of meat refrigerated for 1, 5, or 9 days. The developed films presented antioxidant activity in vitro, but they did not have an antimicrobial effect against bacterial development (E. coli nor L. innocua). The PLA/PHB film with no extract prevented changes in the instrumental color of meat during storage. However, the antioxidant effect of the PLA/PHB films on fresh pork was negligible, and the inclusion of high doses of extract favored microbial development in the pork during storage. Despite the lack of activity of active PLA/PHB films on meat, their use could be a sustainable alternative to the petroleum-based films. [ABSTRACT FROM AUTHOR]

PPAR-γ anti-inflammatory functions have received significant attention since its agonists have been shown to exert a wide range of protective effects in many experimental models of neurologic diseases. Rice bran is very rich in polyunsaturated fatty acids, which are reported to act as PPAR-γ partial agonists. Herein, the anti-inflammatory effect of rice bran extract (RBE) through PPAR-γ activation was evaluated in LPS-induced neuroinflammatory mouse model in comparison to pioglitazone (PG) using 80 Swiss albino mice. RBE (100 mg/kg) and PG (30 mg/kg) were given orally for 21 days and LPS (0.25 mg/kg) was injected intraperitoneally for the last 7 days. TNF-α and COX-2 brain contents were evaluated by real-time PCR and immunohistochemical analysis. In addition, NFκB binding to its response element was evaluated alongside with the effect of treatments on IκB gene expression. Furthermore, PPAR-γ sumoylation was also studied. Finally, histopathological examination was performed for different brain areas. RBE administration was found to protect against the LPS-induced inflammatory effects by decreasing the inflammatory mediator expression in mice brains. It also decreased PPAR-γ sumoylation without significant effect on IκB expression or NFκB binding to its response element. The majority of the effects were attenuated in presence of PPAR-γ antagonist (GW9662). Level of significance was set to P < 0.05. Such findings highlight the agonistic effect of RBE component(s) on PPAR-γ and support the hypothesis of involvement of PPAR-γ activation in its neuroprotective effect. [ABSTRACT FROM AUTHOR]