Previous studies have suggested that rice bran oil (RBO), an edible oil from the byproducts of rice milling, has antiinflammatory effects in inflammation inducing macrophages, known as M1 subsets. Yet the effects of RBO on the counterpart M2 subsets, the “healing” macrophages, were poorly investigated to date. In this regard, recent studies on the molecular/cellular anti-inflammatory mechanisms of dietary components have demonstrated that mitochondrial respiration contributes to macrophage functioning. Therefore, the current study examined whether RBO regulates cytokine secretion by modulating mitochondrial metabolism in wound healing M2 subsets. Palm oil (PO), enriched with medium-chain fatty acids, served as a positive control. C57BL/6 mice were fed a diet containing either corn oil (CO), PO or RBO for 4 weeks, followed by purification of bone marrow-derived macrophages (BMDM) from their tibias and femurs. Cells were further polarized to M2-BMDM, and the expression of M2 marker (CD206) on cellular surfaces were not affected by dietary intervention. In addition, the secretion of anti-inflammatory cytokine (IL-10) in the culture supernatant was not affected by dietary lipids. Oxygen consumption rate, the indicator of mitochondrial respiration in M2-BMDM was not regulated by RBO intervention and PO treatment. Taken together, this study imply that RBO did not intervene both the regulation of inflammatory responses and mitochondrial respiration in M2 macrophages.

Previous studies demonstrated that rice bran oil has an anti-inflammatory effect. The current study investigated if the immune responses and energy metabolism phenotypes were affected by rice bran oil. Rice bran oil and palm oil, which served as an experimental control, were treated to RAW 264.7 macrophages respectively, followed by LPS stimulation so as to quantify the production of pro-inflammatory cytokines such as IL-6 and TNF-α. The expression of surface markers i.e. CD 80, CD 86 and MHC-classⅡ and mitochondrial metabolism phenotypes were also tested. The data exhibited rice bran oil suppressed inflammatory responses and mitochondrial metabolism were modulated by rice bran oil. These results warrant the necessity for the compositional and/or mechanistic studies to elucidate the details.

들기름 및 미강유를 베이스로 개발한 혼합 식용유는 오메가-3 지방산인 리놀렌산 함량이 약 20% 정도로 매우 높다. 이는 기존의 일반 식용유 중 오메가-3 지방 함량이 매우 높은 콩기름과 카놀라유의 리놀렌산 함량이 각각 6% 및 10% 내외인 점을 감안하면, 이들 식용유에 비하여 새로 들기름과 미강유를 혼합한 식용유는 2~3배 높은 비율로 오메가-3 지방산을 제공할 수 있어서, 오메가-3 지방산 섭취가 부족한 현대인의 식단에서 중요한 오메가-3 지방산 급원으로서의 역할을 할 수 있을 것이다. 뿐만 아니라, 토코페롤 함량도 약 46.77 ㎎/ 100 g oil 정도인데, 가장 주목할 일은 토코페롤 동족류 중 비타민 E의 활성이 가장 강한 알파-토코페롤(31.71 ㎎/100 g oil)이 가장 많이 존재하여, 총 토코페롤의 64%를 차지하고 있어서 비타민 E로서의 기능이 높다. 혈중 콜레스테롤 함량을 낮추는 기능성이 알려진 파이토스테롤 함량이 들기름과 미강유를 혼합한 식용유에 약 7,200 ppm 함유되어 있어, 일반적인 식용유의 3,000 ppm의 약 2.3배에 달한다. 본 연구에서 개발한 들기름과 미강유를 혼합한 식용유는 일반적인 식용유인 콩기름과 거의 유사한 산화안정성을 갖는 것으로 확인되어, 일반 들기름에 비하여 현저히 높은 산화안정성이 확보되었다.

쌀 도정시 발생하는 미강의 부가가치를 높이기 위하여,미강내 생리기능성 물질를 고농도로 농축하기 위한 전처리방법 및 농축조건을 확립하고자 하였다. 미강으로부터 추출한 조미강유중 지방산을 분리하기 위하여 산 또는 효소촉매를 이용하여 지방산 에틸 에스터를 제조하였다. 산 촉매 에스터 반응시 tocopherol류의 함량은 크게 영향을 받지 않았으나, tocotrienol류의 함량은 크게 감소하였고, 특히 γ-tocotrienol은 52% 감소하였다. 효소 촉매 에스터반응시 tocopherol류와 tocotrienol류 모두 크게 변화가 없었으므로 효소촉매를 이용한 에틸 에스터 반응이 생리활성물질농축에는 더 적합하였다. 효소 촉매 반응을 이용하여 생산한 미강유 에틸 에스터를 초임계 이산화탄소를 이용하여분리하고, 생리활성물질을 농축하였다. 온도 조건은 45oC,50oC, 55oC, 압력조건은 9.62MPa, 10.34MPa, 11.03MPa이었다. Tocols는 소량이지만, 1-5번 추출 분획에서 모두검출되었으며, 5번 분획에 가까워질수록 더 많은 양의tocols이 추출되었다. γ-Oryzanol도 매우 소량이기는 하나 1-5번 분획에서 추출되었다. Policosanol과 phytosterol은 1-5번 분획에서 전혀 추출되지 않았다. 특히 초임계 이산화탄소의 밀도와 지방산 에스터와 함께 추출되는 tocols 및 γ-oryzanol의 양은 높은 상관관계를 가지고 있었다(R2tocols=0.9306, R2oryzanol=0.7934). Tocols와 phytosterol은 55oC,9.62MPa에서 농축시 농축률이 가장 높았으며, γ-oryzanol과policosanol은 각 조건별로 농축률에 변화가 없었다. 또한초임계 이산화탄소의 밀도가 클수록 농축속도는 매우 빨랐으나 농축물질의 선택성은 낮았다. 따라서 생리활성물질을농축하는데에는 상대적으로 낮은 밀도의 초임계 이산화탄소를 적용하는 것이 더 효과적이었으며, 이러한 결과는 건강기능식품등에 이용하는 생리활성물질의 농축 및 정제 공정에 효율적으로 적용될 수 있을 것이다.

This study was carried out to determine the pesticide residues in rice bran, crude rice bran oil and the oil of various stages of refining process. Each samples were analyzed for 41 pesticide residues by multiclass multiresidue methods with GC-ECD, NPD and identified by GC-MSD. Rice bran were detected cypermethrin, diazinon, dichlofluanid, and its level were ranged from 0.01-0.122 ppm. Crude rice bran oil were detected cypermethrin, diazinon, dichlofluanid, dimethoate, etrimfos, flucythrinate, and its level were ranged from 0.015-0.654 ppm. Crude rice bran oil has the higher level of pesticide residues and more varieties of pesticides than rice bran. But pesticide residues in the crude rice bran oil was found to be almost removed when pigment was decolorized by absorption using active carbon and clealy removed by thermolysis for deodorization.

To investigate the protective action of various antioxidants on the photooxidation of rice bran oil, it was irradiated with red and visible light in presence and absence antioxidants with or without sensitizer (methylene blue). 1. Rice bran oil with and without sensitizer in chloroform-ethanol (4:1, v/v) media was largely oxidized under visible light irradiation. on the other hand, rice bran oil without sensitizer was hardly oxidized under red light irradiation. 2. Rice bran oil with sensitizer was oxidized much faster than that without. And the absorbance of it irradiated with visible was increased more than that with red light. 3. The effectiveness of antioxidants on the rice bran oil photooxidation was same order as follows: Irradiation with visible light, no addition of sensitizer β-carotene 〉 dl-α-tocopherol 〉 BHT 〉 BHA Irradiation with visible light, addition of sensitizer β-carotene 〉 BHT 〉 dl-αtocopherol 〉 BHA Irradiation with red light, addition of sensitizer β-carotene 〉 BHA 〉 BHT 〉 dl-α-tocopherol From these results, we concluded that rice bran oil was largely oxidized under visible light irradiation, therefore it must be protected from photooxidative deterioration by the addition of antioxidants.

Background : Ischemic stroke is a common cause of adult disability and death worldwide. Excessive oxidative stress is an important pathogenic mechanism in ischemic stroke. Major reduction of endogenous antioxidative systems increases production of free radicals inducing peroxidation of lipid, protein, and nucleic acid. 1,3-Dipalmitoyl-2-oleoylglycerol (DPOG) is a triglyceride found in oils from various natural sources such as palm kernels, sunflower seeds and rice bran. We found DPOG as an active constituent of rice bran oil. In the present study, we investigated neuroprotective effect of DPOG derived from rice bran oil on excitotoxicity in cultured neurons and on ischemic brain injury in rats. Methods and Results : Transient focal ischemic brain damage was induced by 2 h middle cerebral artery occlusion followed by 24h reperfusion (MCAO/reperfusion) in rats. After MCAO/reperfusion, the infarct and edema volume of brain tissue was measured by 2,3,5-triphenyltetrazolium chloride (TTC) staining methods. Glutathione concentration and lipid peroxidation rate were measured in brain tissue. The expression levels of phosphorylated mitogen activated proteins kinases (MAPKs), inflammatory factors, and anti-apoptotic and pro-apoptotic proteins in brain tissue were detected by Western blot. Cerebral cortical neuronal cells were cultured in 15-days-old fetus. Cortical neurons were incubated with 1 mM N-methyl-D-aspartate (NMDA) for 14 h to produce excitotoxicity. Cell viability was measured by MTT assay. DPOG (1-5 mg/kg) significantly reduced MCAO/reperfusion-induced infarction and edema formation, neurological deficits, and brain cell death. Depletion of glutathione level and lipid peroxidation induced by MCAO/reperfusion were inhibited by administration of DPOG. The increase of phosphorylated MAPKs, inflammatory factors, and proapoptotic proteins and the decrease of antiapoptotic protein in ischemic brain were significantly inhibited by treatment with DPOG. DPOG (0.1-10 uM) inhibited 1 mM NMDA-induced neuronal cell death in cultured cortical neurons. Conclusion : From the above results, the present study provides an evidence that DPOG derived from rice bran oil might be effectively applied for the treatment of ischemic stroke.

Background : Alzheimer’s disease (AD) is a neurodegenerative disease characterized by progressive memory loss, cognitive impairment and personality defects accompanied by diffuse structural abnormalities in the brain. The major pathological hallmarks of AD include beta amyloid (Aß) protein deposition, presence of neurofibrillary tangles and neurodegeneration of cholinergic neurons. Aß, a 39-43 amino acid proteolytic fragment of amyloid precursor protein, is the major constituent of the senile plaques. Rice bran, the major byproduct of the rice milling industry, is the source of a high quality vegetable oil. Rice bran oil (RBO) has attracted much medicinal attention for its strong hypocholesterolemic properties because of its balanced fatty acid composition and high levels of antioxidant phytochemicals such as oryzanols, tocopherols and tocotrienols. The present study aims to investigate the protective effect of RBO against Aß (25-35)-induced neurotoxicity in in vitro and in vivo. Methods and Results : Memory impairment was produced by intracerebroventricular (i.c.v) microinjection of 15 nmol Aß (25-35) and measured by passive avoidance test in ICR mice. Glutathione concentration, lipid peroxidation rate and acetylcholine esterase activity were measured in mice brain. The expression levels of phosphorylated mitogen activated proteins kinases (MAPKs), inflammatory factors, and anti-apoptotic and pro-apoptotic proteins in mice brains were detected by Western blot. Cerebral cortical neuronal cells were cultured from 15-days-old fetus. Cortical neurons were incubated with 10 μM Aß (25-35) for 36 h. Cell viability was measured by MTT assay. Chronic treatments of RBO (0.1-1 ml/kg, 8 days, p.o.) protected against memory impairment induced by Aß (25-35). Depletion of glutathione level, lipid peroxidation and increased acetylcholine esterase activity by the treatment with Aß (25-35) were inhibited by administration of RBO. The increase of phosphorylated MAPKs, inflammatory factors, and proapoptotic proteins and the decrease of antiapoptotic protein in Aß (25-35)-administered mice brain were significantly inhibited by treatment with RBO. RBO (0.1-5ul/ml) inhibited 10μM Aß (25-35)-induced neuronal cell death in cultured cortical neurons. Conclusion : The present study suggests the role of RBO as a promising therapeutic for neurodegenerative diseases like AD and stroke.

Background : Rice bran is the outer brown layer of the rice grain and produced when rice is milled. The basic components of rice bran are fiber, lipids, amino acids, vitamins, and minerals. The oil extracted from this bran is called rice bran oil. Although whole rice bran in itself does not have anti-cholesterol properties, its oil offers significant benefits. Ischemic stroke is a major cause of morbidity and mortality worldwide. The cessation or critical reduction of blood flow in brain during acute stroke results in deprivation of the oxygen and glucose supplies, which can produce a local brain ischemia and injury. It is well established that excitotoxicity, a type of neurotoxicity evoked by elevated extracellular glutamate level, is a primary contributor to ischemic neuronal death. The present study aims to investigate the neuroprotective effect of Rice bran oil (RBO) on ischemic brain injury in rats and on excitotoxicity in cultured neurons. Methods and Results : Transient focal ischemic brain damage was induced by 2 h middle cerebral artery occlusion followed by 24 h reperfusion (MCAO/reperfusion) in rats. After MCAO/reperfusion, the infarct and edema volumes of brain tissues were measured using 2,3,5-triphenyltetrazolium chloride (TTC) staining methods. The expression levels of phosphorylated mitogen activated proteins kinases (MAPKs), inflammatory factors, and anti-apoptotic and pro-apoptotic proteins in brain tissue were detected by Western blot. Primary cortical neuronal cultures were prepared using SD rat fetuses on embryonic days 15. Cortical neurons were treated with N-methyl-D-aspartate (NMDA) (1 mM) for 14 h to produce neuronal cell death. Cell viability was measured by MTT assay. RBO inhibited the formation of infartion and edema in MCAO/reperfusion–induced ischemic brains. The increase of phosphorylated MAPKs, inflammatory factors, and proapoptotic proteins and the decrease of antiapoptotic protein in ischemic brains were significantly inhibited by treatment with RBO. RBO (0.01-1ul/ml) inhibited 1 mM NMDA-induced neuronal cell death in cultured cortical neurons. Conclusion : These results suggest that RBO might be a promising therapeutic for neurodegenerative disease such as stroke.

Due to the fact that tocopherols and tocotrienols have antioxidant and anticancer properties, the commercial utilization of unsaponifiable fractions in rice bran is increasing. These nutraceutical compounds, however, are fairly unstable and readily break down when exposed to oxygen or lighting conditions. To compare the relative sensitivity of vit E isomers to heat and oxygen, concentrated unsaponifiable fractions extracted from crude rice bran oil were exposed to various temperature, oxygen (nitrogen-balanced), and bathing solvent conditions and resultant concentration changes in α- and γ-tocopherols (T) and tocotrienols (T3) were evaluated. Each isomer exhibited different heat stability. Among them, α-T3 degraded more rapidly compared to other vit E isomers while α-T was the most stable isomer. Oxygen level also showed significant impact on each isomer's stability where severe reductions of γ-T (by 20%) and γ-T3 (by 29%) were observed under 2% oxygen conditions, while under 0% oxygen conditions no degradation could be observed even after exposure to 95℃ for 4 hours. When various blending solvents were mixed with concentrated unsaponifiable fractions, organic solvents such as isooctane and hexane were more effective in maintaining the stability of γ- T3 compared to edible oils, among which com oil was more efficient than soybean and rice bran oils.