Does krill oil enhancing the new bone formation in orthopedically expanded median palatal suture in rat model? A micro-CT and immunohistochemical analysis.

BACKGROUND: The purpose of this study was to assess the effects of systemically given krill oil (KO) on the development of new bone formation in the sutura palatina media following rapid maxillary expansion (RME). METHODS: 28 4-5 week-old male Wistar albino rats were randomly divided into 4 groups: Control (C), Only Expansion (OE) (no supplement but undergoing expansion and retention), KE (supplemented during both the expansion and retention phases), Krill Oil Nursery Group (KN) (supplemented during the 40-day nursery phase as well as during the expansion and retention phases). A 5-day RME was followed by a 12-day retention period. All rats were euthanized simultaneously. Micro-computerized tomography (Micro-CT), hemotoxylen-eosin (H&E) staining, and immunohistochemical analysis were conducted. Kruskal-Wallis and Dunn tests with Bonferonni corrrection were applied (p < 0.05). RESULTS: Expansion and KO supplementation did not cause a statistically significant change in bone mineral density (BMD), bone volume fraction (BV/TV), spesific bone surface (BS/BV) and trabecular thickness (Tb.Th). While the expansion prosedure increased the trabecular seperation (Tb.Sp), KO supplemantation mitigated this effect. The KE group exhibited a statistically significantly increase in trabecular number (Tb.N) compared to the OE group. Although receptor activator of nuclear factor-kappa-Β ligand (RANKL)/osteoprotegerin (OPG) ratios did not show significant differences between groups, the KE and OE groups demonstrated the lowest and highest value, respectively. KE showed a reduced amount of tartrate-resistant acid phosphatase (TRAP) compared to the OE. CONCLUSION: KO positively affected the architecture of the new bone formed in the mid-palatal suture. In this rat model of RME, results support the idea that administering of KO during the expansion period or beginning before the RME procedure may reduce relapse and enhance bone formation within the mid-palatal suture.

Krill Oil Ameliorates Liver Injury in Diabetic Mice by Activating Antioxidant Capacity and Inhibiting Ferroptosis.

Diabetic liver injury (DLI) has raised attention in recent years. Liver injury results from type 2 diabetes mellitus (T2DM), and in turn accelerates T2DM development by exacerbating insulin resistance. However, effective approaches for mitigating DLI are surprisingly rare. Krill oil (KO) is an alternative source of omega-3 polyunsaturated fatty acids, possessing antioxidant and anti-inflammatory capacities. Here we investigated the effect of KO supplementation on DLI in a mouse model of T2DM induced by streptozotocin and high-fat diet. The diabetic mice developed glucose intolerance, elevated serum alanine aminotransferase and aspartate aminotransferase, and hepatic pathological injuries such as vacuolation, lipid accumulation and fibrosis deposition, the effects of which were mitigated by KO. Further investigation showed that KO ameliorated the DM-induced expression of fibrotic and inflammatory genes. Notably, KO dramatically reduced hepatic oxidative gene expression, lipid peroxidation and ROS production, all of which are hallmarks of ferroptosis. The inhibitory effect of KO on ferroptosis was confirmed by the KO-decreased hepatic expression of GPX4, COX2 and ACSL4, as well as the KO-reduced hepatic iron deposition. Further, KO restored hepatic NRF2 antioxidant signaling which combats ferroptosis. The present study may provide KO supplementation as a viable approach for the intervention of DLI.

Emu oil alleviates atopic dermatitis-like responses by inhibiting Cdc42 signaling of keratinocyte.

Emu oil is the oil extracted from the body fat of the Australian bird emu. Although previous studies have reported that emu oil has anti-inflammatory effects, the effect and mechanism of emu oil on the treatment of atopic dermatitis have not been reported. Here, 2, 4-dinitrofluorobenzene was used to induce atopic dermatitis-like appearance on the back skin of C57BL/6 mice. And then, the effect of emu oil in the atopic dermatitis treatment was evaluated. We found that emu oil reduced the transdermal water loss in the atopic dermatitis model. Additionally, the epidermal thickness treated with emu oil was significantly thinner. The number of mast cells and inflammatory cells were significantly decreased. The thymic stromal lymphopoietin (TSLP), which is secreted by keratinocyte, was decreased significantly after treatment. Moreover, the serum levels of cytokines TSLP, interleukin-4, interleukin-13, and immunoglobulin (Ig) E were decreased after emu oil treatment. Surprisingly, we found that the high level of Cdc42 expression in the atopic dermatitis, which was decreased after emu oil treatment. To detect the role of Cdc42 in atopic dermatitis, we constructed atopic dermatitis model in mice with sustained activation of Cdc42 signaling. Furthermore, we have confirmed that emu oil demonstrates anti-inflammatory effects in atopic dermatitis by inhibiting the expression of Cdc42 signaling in keratinocytes. In conclusion, we discovered a new role of Cdc42 in the development of atopic dermatitis, which mediated the therapeutic effect of emu oil on atopic dermatitis.

Beneficial Effects of Capybara Oil Supplementation on Steatosis and Liver Apoptosis in Obese Mice.

Obesity is a complex chronic disease characterized by excess body fat (adipose) that is harmful to health and has been a major global health problem. It may be associated with several diseases, such as nonalcoholic fatty liver disease (NAFLD). Polyunsaturated fatty acids (PUFA) are lipid mediators that have anti-inflammatory characteristics and can be found in animals and plants, with capybara oil (CO) being a promising source. So, we intend to evaluate the hepatic pathophysiological alterations in C57Bl/6 mice with NAFLD, caused by obesity, and the possible beneficial effects of OC in the treatment of this disease. Eighteen 3-month-old male C57Bl/6 mice received a control or high-fat diet for 18 weeks. From the 15th to the 18th week, the animals received treatment-through orogastric gavage-with placebo or free capybara oil (5 g/kg). Parameters inherent to body mass, glucose tolerance, evaluation of liver enzymes, percentage of hepatic steatosis, oxidative stress, the process of cell death with the apoptotic biomarkers (Bax, Bcl2, and Cytochrome C), and the ultrastructure of hepatocytes were analyzed. Even though the treatment with CO was not able to disassemble the effects on the physiological parameters, it proved to be beneficial in reversing the morphological and ultrastructural damage present in the hepatocytes. Thus, demonstrating that CO has beneficial effects in reducing steatosis and the apoptotic pathway, it is a promising treatment for NAFLD.

Krill Oil and Its Bioactive Components as a Potential Therapy for Inflammatory Bowel Disease: Insights from In Vivo and In Vitro Studies.

Krill oil is extracted from krill, a small crustacean in the Antarctic Ocean. It has received growing attention because of krill oil's unique properties and diverse health benefits. Recent experimental and clinical studies suggest that it has potential therapeutic benefits in preventing the development of a range of chronic conditions, including inflammatory bowel disease (IBD). Krill oil is enriched with long-chain n-3 polyunsaturated fatty acids, especially eicosapentaenoic and docosahexaenoic acids, and the potent antioxidant astaxanthin, contributing to its therapeutic properties. The possible underlying mechanisms of krill oil's health benefits include anti-inflammatory and antioxidant actions, maintaining intestinal barrier functions, and modulating gut microbiota. This review aims to provide an overview of the beneficial effects of krill oil and its bioactive components on intestinal inflammation and to discuss the findings on the molecular mechanisms associated with the role of krill oil in IBD prevention and treatment.

Preparation and characterization of Antarctic krill oil/quercetin co-loaded liposomes and their protective effect on oleic acid-induced steatosis and oxidative stress in vitro.

This study aims to introduce a new liposome to co-load Antarctic krill oil (AKO) and quercetin (QC) as a new delivery formulation to enrich the application of AKO and QC. The stability of liposomes could be increased by adding an appropriate quantity of soy lecithin (SL). Changes in the composition of the phospholipid membrane were strongly correlated with the stability and release capacity of loaded nutrients. SL2@QC/AKO-lips displayed a nearly spherical shape with higher oxidative stability and controlled the in vitro release performance of QC in simulated digestion. Moreover, in vitro studies indicated that new liposomes had no adverse effects on cell viability and could combine the physiological functions of AKO and QC to protect the HepG2 cells from oleic acid-induced steatosis and oxidative stress. The findings demonstrated that the AKO and QC co-loaded liposomes prepared with the addition of an appropriate quantity of SL had excellent loading efficiency of AKO/QC and good oxidative stability, security and functional activity.

Ovicidal and Pediculicidal Activity of Indigofera suffruticosa Mill. Leaf Oil on Pediculus humanus capitis Egg to Adult Stages.

PURPOSE: Pediculosis capitis, commonly known as head lice infestation, represents a significant health 26 problem for school children worldwide. Repeated and long-term usages of highly toxic pediculicides have resulted in the development of increased levels of resistance and do not kill louse eggs. Alternative pediculicides, such as herbal products, have recently been proposed for the treatment of head lice infestation, thereby decreasing toxicity. METHODS: This study analyzed the chemical composition of I. suffruticosa leaf extracts using GC-MS and evaluated the effects of Indigofera suffruticosa Mill. (I. suffruticosa) leaf extract on the mortality of head lice and their eggs. RESULTS: The major five components of the tested oils identified were as follows: n-hexadecanoic acid, hexadecanoic acid, ethyl ester, oleic acid, (E)-9-octadecenoic acid ethyl ester, and linoleic acid ethyl ester. The effective pediculicide of the I. suffruticosa leaf extracts affected head lice in all stages (egg, nymph, and adults). The concentrations of I. suffruticosa leaf extracts at 500 mg/mL produced the highest effective ovicidal on egg with 96.6% unhatching and pediculicide on nymphs and adults with 96.7 ± 5.7% and 86.7 ± 5.7% mortality, respectively, at 60 min (LT50 value < 10 min). The analysis of the external structure of the adult-stage head lice by SEM examination revealed that dead lice exposed to I. suffruticosa leaf extract displayed damage to the outer smooth architecture and obstructed the respiratory spiracles. CONCLUSION: We may conclude that the application of I. suffruticosa leaf extract produces an effective herbal pediculicide capable of affecting all stages of head lice.

Toxicity assessment of common acaricides and mineral oils on Anagyrus vladimiri, an effective biocontrol agent of citrus mealybug.

Chemical pesticides, while playing an important role in the suppression of insect pests, should be used in a manner that minimizes negative effects on natural enemies. The parasitoid, Anagyrus vladimiri Triapitsyn (Hymenoptera: Encyrtidae), plays an important role in the management of mealybug pests of citrus groves in the Mediterranean region. This study was conducted to evaluate the effect of commonly used acaricides (Spirodiclofen, Spirotetramat, Sulfur, Fenpyroximate, Abamectin) and mineral oils (Levanola, EOS, JMS, and Ultrapaz) on acute mortality of A. vladimiri. Toxicity was assessed in 4 cases: (i) direct spray application on adults, (ii) pesticide application on the mummified host, (iii) feeding with contaminated food, and (iv) contact with pesticide residue. The pesticide Abamectin, applied alone and with Levanola oil was highly toxic to adults in all bioassays, with the exception of direct spray application on the mummified host. Fenpyroximate was found to be highly toxic only when sprayed directly on adults, and sulfur was slightly harmful. Mineral oils were harmful when ingested with food; otherwise, they did not cause appreciable adult mortality. The findings of the present study suggest that all tested materials, with the exception of Abamectin and Fenpyroximate, are compatible with the survival of A. vladimiri. Direct ingestion of oils can, however, cause a degree of mortality. Given that indiscriminate use of these pesticides may affect the population ecology of A. vladimiri, they should be used with caution.

Krill Oil Inhibits Cholesterol Synthesis and Stimulated Cholesterol Excretion in Hypercholesterolemic Rats.

The present study aimed to investigate the antihypercholesterolemic effects of krill oil supplementation in high-cholesterol diet-induced hypercholesterolemic rats, and the mechanisms underlying these effects. Rats were divided into five groups: normal control, control (high-cholesterol diet), krill oil 100 mg/kg b.w. (high-cholesterol diet with Krill oil 100 mg/kg b.w.), and krill oil 200 mg/kg b.w. (high-cholesterol diet with Krill oil 200 mg/kg b.w.). After 12 weeks, the rats were sacrificed to observe the effects of krill oil on cholesterol synthesis and excretion. We found that krill oil supplementation suppressed total triglycerides, total cholesterol, and LDL-cholesterol levels, as well as HMG-CoA reductase activity. It stimulated AMPK phosphorylation, LDL receptor and ACAT2 expression in the liver, and the fecal output of cholesterol. Furthermore, it decreased the levels of P-selectin, sVCAM-1, and NO, as well as aortic wall thickness, demonstrating its role in the prevention of atherosclerosis. Thus, we suggest that krill oil supplementation can reduce LDL-cholesterol levels in the blood during hypercholesterolemia by stimulating the uptake of LDL-cholesterol into tissue and cholesterol excretion, as well as inhibition of cholesterol synthesis.

Ovicidal Aroma Shields for Prevention of Blow Fly Strikes Caused by Lucilia sericata (Meigen), Diptera: Calliphoridae.

The blow fly, Lucilia sericata (Meigen) (Diptera: Culicidae) is a primary facultative ectoparasite controlled by insecticides that have environmental and safety concerns; therefore, its natural and safe control is crucial. L. sericata eggs were subjected to 400 µL of 5% of 24 materials of plant-borne origin. The number of hatched and unhatched eggs were counted 24 h postexposure. Stopmyasis® expressed the highest ovicidal effect, followed by cedarwood, orange, and tea tree oils. The mean ovicidal results were 46.09-95.24% grouped as Class A, which provided the lowest hatchability rates. Even though benzoin, vanillin, citronella, and camphor oils grouped as Class B provided moderate ovicidal effects (33.69-43.92%), their efficacy differed significantly from those of the treatments in Classes A and C containing the control group and vetiver, eucalyptus, Olbas®, neem, sunflower, oil blends, patchouli, frankincense, p-menthane-3,8 diol (PMD), lavender, peppermint, cinnamon, calry sag, myrtle, and silicone oil. According to our knowledge, most (19 out of 24) applied materials were used as ovicides against L. serricata for the first time, except orange, eucalyptus, patchouli, cinnamon oils, and six of them were applied as ovicides against pests for the first time. Stopmyasis containing Géraniol and PMD is the drug of choice as an ecofriendly product to prevent blow fly strikes through correct diagnosis and prompt treatment preventing a disastrous and destructive course of the disease and improving quality of life.

Nitric Oxide-Releasing Silicone Oil with Tunable Payload for Antibacterial Applications.

Bacterial infections are a hurdle to the application of medical devices, and in the United States alone, more than one million infection cases are reported annually from indwelling medical devices. Infections not only affect the function of medical devices but also risk the lives and health of patients. Nitric oxide (NO) has been used as an antibacterial therapy that kills bacteria without causing resistance and provides many therapeutic effects such as anti-inflammation, antithrombosis, and angiogenesis. Silicone oils have been widely utilized in manufacturing consumer goods, healthcare products, and medical products. Specifically, liquid silicone oils are used as a medical lubricant that creates lubricated interfaces between medical devices and the exterior physiological environment to improve the performance of medical devices. Herein, we report the first primary S-nitrosothiol-based NO-releasing silicone oil (RSNO-Si) that exhibits proactive antibacterial effects. S-nitrosothiol silicone oils (RSNO-Si) were synthesized and the NO payloads ranged from 34.0 to 603.9 µM. The increased NO payload induced higher-viscosity RSNO-Si oils, as RSNO0.1-Si, RSNO0.5-Si, and RSNO1-Si had viscosities of 12.8 ± 0.1 cP, 32.0 ± 0.2 cP, and 35.1 ± 0.3 cP, respectively. RSNO-Si-SR interfaces were fabricated by infusing silicone rubber (SR) in RSNO-Si oil, and the resulting RSNO-Si-SR disks demonstrated NO release without NO donor leaching. RSNO0.1-Si-SR, RSNO0.5-Si-SR, and RSNO1-Si-SR exhibited maximum NO flux at 0.8, 6.5, and 21.5 × 10 -10 mol cm-2 min-1 in 24 h, respectively. RSNO-Si-SR disks also demonstrated 97.45, 95.40, and 96.08% of inhibition against S. aureus in a 4 h bacterial adhesion assay. Considering the easy synthesis, simple fabrication of non-leaching NO-releasing interfaces, tunable payloads, NO flux levels, and antimicrobial effects, RSNO-Si oils exhibited their potential use as platform chemicals for creating antimicrobial medical device surfaces and other antibacterial materials.

An active ingredient isolated from Ganoderma lucidum promotes burn wound healing via TRPV1/SMAD signaling.

The mushroom Ganoderma lucidum is a traditional Chinese medicine and G. lucidum spore oil (GLSO) is the lipid fraction isolated from Ganoderma spores. We examined the effect of GLSO on burn wound healing in mice. Following wounding, GLSO was applied on the wounds twice daily. Repair analysis was performed by Sirius-Red-staining at different time points. Cell proliferation and migration assays were performed to verify the effect of GLSO on growth. Network pharmacology analysis to identify possible targets was also carried out, followed by Western blotting, nuclear translocation, cell proliferation, and immunofluorescence assays for in-depth investigation of the mechanism. Our study showed that GLSO significantly promoted cell proliferation, and network pharmacology analysis suggested that GLSO might act through transient receptor potential vanilloid receptor 1 (TRPV1)/SMAD signaling. Furthermore, GLSO elevated SMAD2/3 expression in skin burn and promoted its nuclear translocation, and TRPV1 expression was also increased upon exposure to GLSO. Cell proliferation and immunofluorescence assays with TRPV1 inhibitor showed that GLSO accelerated skin burn wound healing through TRPV1 and SMADs signaling, which provides a foundation for clinical application of GLSO in the healing of deep skin burns.

Krill Oil Inhibits NLRP3 Inflammasome Activation in the Prevention of the Pathological Injuries of Diabetic Cardiomyopathy.

Diabetic cardiomyopathy (DCM) is a common complication of diabetes mellitus (DM), resulting in high mortality. Myocardial fibrosis, cardiomyocyte apoptosis and inflammatory cell infiltration are hallmarks of DCM, leading to cardiac dysfunction. To date, few effective approaches have been developed for the intervention of DCM. In the present study, we investigate the effect of krill oil (KO) on the prevention of DCM using a mouse model of DM induced by streptozotocin and a high-fat diet. The diabetic mice developed pathological features, including cardiac fibrosis, apoptosis and inflammatory cell infiltration, the effects of which were remarkably prevented by KO. Mechanistically, KO reversed the DM-induced cardiac expression of profibrotic and proinflammatory genes and attenuated DM-enhanced cardiac oxidative stress. Notably, KO exhibited a potent inhibitory effect on NLR family pyrin domain containing 3 (NLRP3) inflammasome that plays an important role in DCM. Further investigation showed that KO significantly upregulated the expression of Sirtuin 3 (SIRT3) and peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α), which are negative regulators of NLRP3. The present study reports for the first time the preventive effect of KO on the pathological injuries of DCM, providing SIRT3, PGC-1α and NLRP3 as molecular targets of KO. This work suggests that KO supplementation may be a viable approach in clinical prevention of DCM.

Nanostructured systems increase the in vitro cytotoxic effect of bullfrog oil in human melanoma cells (A2058).

The aim of this work was to investigate the in vitro cytotoxic effect of previously developed nanocapsules, nanoemulsion, and microemulsion based on bullfrog oil (BFO) against human melanoma cells (A2058). The nanosystems were produced as described in previous studies and characterized according to droplet/particle distribution and zeta potential. The biocompatibility was evaluated by the determination of the hemolytic potential against human erythrocytes. The cytotoxicity assessment was based on MTT and cell death assays, determination of Reactive Oxygen Species (ROS) levels, and cell uptake. The nanosystems were successfully reproduced and showed hemolytic potential smaller than 10% at all oil concentrations (50 and 100 µg.mL-1) (p < 0.05). The MTT assay revealed that the nanosystems decreased the mitochondrial activity up to 92 ± 2% (p < 0.05). The study showed that the free BFO induced cell apoptosis, while all the nanostructured systems caused cell death by necrosis associated with a ROS overproduction. This can be related to the increased ability of the nanostructured systems to deliver the BFO across all cellular compartments (membrane, cytoplasm, and nucleus). Finally, these results elucidate the in vitro BFO nanosystems cytotoxic effect against human melanoma cells (A2058), revealing the emulsified ones as the most cytotoxic systems. Overall, the findings suggest that the safety and antineoplastic activity of these systems can be further investigated by in vivo studies.

In-vitro and in-vivo evaluation of taste-masked ibuprofen formulated in oral dry emulsions.

OBJECTIVE: The aim of this study was to develop a pediatric oral preparation for ibuprofen. SIGNIFICANCE: Ibuprofen is widely used for defervescence in children, but medication compliance is poor due to its bitter taste. Dry emulsions possess good stability and can be transported and stored in solid form; they can be dispersed into liquid emulsions with water and easily administered to children. METHODS: In this study, a dry emulsion excipient was prepared by spray drying: a mixture of orange peel and corn oils (3:7, w/w) was used as the oil phase and solvent for ibuprofen; gum arabic and gum tragacanth were chosen as emulsifiers; and maltodextrin was used as a solid carrier. RESULTS: The particle sizes of the liquid and reconstituted emulsions were 5.75 µm and 6.11 µm, respectively; the average particle size distribution of the dry emulsion powder was 8.13 µm; scanning electron microscopy showed that the dry emulsion powder was composed of evenly distributed smooth spheres. At a drug loading of 36.52 ± 1.15 mg/g, 90% of ibuprofen was released from the dry emulsion excipient within 30 min. Sensory evaluations using human volunteers, rats, and an electronic tongue demonstrated that the emulsion had a taste-masking effect on ibuprofen. It was further corroborated by in vivo studies using a rat model that highlighted a 1.76-fold increase in ibuprofen absorption when the drug was administered as an emulsion compared with granules. CONCLUSIONS: These results indicate that the dry emulsion for taste-masking is promising and valuable in the development of ibuprofen for pediatrics.

Krill Oil Treatment Increases Distinct PUFAs and Oxylipins in Adipose Tissue and Liver and Attenuates Obesity-Associated Inflammation via Direct and Indirect Mechanisms.

The development of obesity is characterized by the metabolic overload of tissues and subsequent organ inflammation. The health effects of krill oil (KrO) on obesity-associated inflammation remain largely elusive, because long-term treatments with KrO have not been performed to date. Therefore, we examined the putative health effects of 28 weeks of 3% (w/w) KrO supplementation to an obesogenic diet (HFD) with fat derived mostly from lard. The HFD with KrO was compared to an HFD control group to evaluate the effects on fatty acid composition and associated inflammation in epididymal white adipose tissue (eWAT) and the liver during obesity development. KrO treatment increased the concentrations of EPA and DHA and associated oxylipins, including 18-HEPE, RvE2 and 14-HDHA in eWAT and the liver. Simultaneously, KrO decreased arachidonic acid concentrations and arachidonic-acid-derived oxylipins (e.g., HETEs, PGD2, PGE2, PGF2α, TXB2). In eWAT, KrO activated regulators of adipogenesis (e.g., PPARγ, CEBPα, KLF15, STAT5A), induced a shift towards smaller adipocytes and increased the total adipocyte numbers indicative for hyperplasia. KrO reduced crown-like structures in eWAT, and suppressed HFD-stimulated inflammatory pathways including TNFα and CCL2/MCP-1 signaling. The observed eWAT changes were accompanied by reduced plasma leptin and increased plasma adiponectin levels over time, and improved insulin resistance (HOMA-IR). In the liver, KrO suppressed inflammatory signaling pathways, including those controlled by IL-1ß and M-CSF, without affecting liver histology. Furthermore, KrO deactivated hepatic REL-A/p65-NF-κB signaling, consistent with increased PPARα protein expression and a trend towards an increase in IkBα. In conclusion, long-term KrO treatment increased several anti-inflammatory PUFAs and oxylipins in WAT and the liver. These changes were accompanied by beneficial effects on general metabolism and inflammatory tone at the tissue level. The stimulation of adipogenesis by KrO allows for safe fat storage and may, together with more direct PPAR-mediated anti-inflammatory mechanisms, attenuate inflammation.

A low proportion n-6/n-3 PUFA diet supplemented with Antarctic krill (Euphausia superba) oil protects against osteoarthritis by attenuating inflammation in ovariectomized mice.

Osteoarthritis (OA), the most common form of arthritis, is characterized by cartilage destruction, and its incidence is much higher in the osteoporotic population. There is increasing evidence that the occurrence and development of OA are modulated by the dietary intake of polyunsaturated fatty acids (PUFA). This study investigated the effects of dietary PUFA, including n-3/n-6 PUFA proportion and the molecular form of n-3 PUFA, on OA using osteoporotic osteoarthritis dual model mice, where phospholipid type n-3 PUFA were specifically examined. The results revealed that a low proportion of n-6/n-3 PUFA in diets from 1 : 1 to 6 : 1 significantly improved the cartilage structure and inhibited articular cartilage polysaccharide loss. Furthermore, the low proportion n-6/n-3 PUFA diets inhibited the NF-κB signaling pathway by activating G-protein coupled receptor 120 (GPR120) to reduce inflammation and inhibit catabolism. Antarctic krill (Euphausia superba) oil (AKO), rich in phospholipid-type n-3 PUFA, had a better effect on OA than linseed oil (plant-derived n-3 PUFA), which may be due to peroxisome proliferator-activated receptor-gamma (PPAR γ). These findings suggested that the low proportion n-6/n-3 PUFA diets, particularly with AKO, alleviated inflammation and inhibited articular cartilage degeneration. Therefore, dietary intervention can be a potential treatment for OA.

Shrimp Oil Extracted from Shrimp Processing By-Product Is a Rich Source of Omega-3 Fatty Acids and Astaxanthin-Esters, and Reveals Potential Anti-Adipogenic Effects in 3T3-L1 Adipocytes.

The province of Newfoundland and Labrador, Canada, generates tons of shrimp processing by-product every year. Shrimp contains omega (n)-3 polyunsaturated fatty acids (PUFA) and astaxanthin (Astx), a potent antioxidant that exists in either free or esterified form (Astx-E). In this study, shrimp oil (SO) was extracted from the shrimp processing by-product using the Soxhlet method (hexane:acetone 2:3). The extracted SO was rich in phospholipids, n-3 PUFA, and Astx-E. The 3T3-L1 preadipocytes were differentiated to mature adipocytes in the presence or absence of various treatments for 8 days. The effects of SO were then investigated on fat accumulation, and the mRNA expression of genes involved in adipogenesis and lipogenesis in 3T3-L1 cells. The effects of fish oil (FO), in combination with Astx-E, on fat accumulation, and the mRNA expression of genes involved in adipogenesis and lipogenesis were also investigated. The SO decreased fat accumulation, compared to untreated cells, which coincided with lower mRNA expression of adipogenic and lipogenic genes. However, FO and FO + Astx-E increased fat accumulation, along with increased mRNA expression of adipogenic and lipogenic genes, and glucose transporter type 4 (Glut-4), compared to untreated cells. These findings have demonstrated that the SO is a rich source of n-3 PUFA and Astx-E, and has the potential to elicit anti-adipogenic effects. Moreover, the SO and FO appear to regulate adipogenesis and lipogenesis via independent pathways in 3T3-L1 cells.

Egg yolk oils exert anti-inflammatory effect via regulating Nrf2/NF-κB pathway.

ETHNOPHARMACOLOGICAL RELEVANCE: Egg yolk oils (EYO) is a traditional Chinese medicine obtained from Gallus gallus domesticus Brisson, which has been used to treat inflammatory related diseases such as cheilitis, ulceration and acute anal fissure. However, the detailed anti-inflammatory mechanism of EYO is still unknown. AIM OF THE STUDY: The anti-inflammatory activity and mechanism of EYO were investigated in tumor necrosis factor (TNF)-α induced Caco-2 cells. MATERIALS AND METHODS: EYO was obtained by direct-heat extraction (HE), ethanol extraction (EE) and petroleum ether extraction (PE), respectively. Fatty acid compositions of three EYO were measured by gas chromatography (GC). Cell viability, enzyme-linked immunosorbent assay (ELISA), transcriptome, RT-PCR and Western blotting were also performed. RESULTS: Fatty acid compositions of three EYO were different with varied extraction methods. EYO significantly reduced interleukin (IL)-8 secretion. EYO exerted anti-inflammatory effect via coordinating regulation of Nrf2/NF-κB pathways based on the results of transcriptome, Q-PCR and Western blotting. In detail, PE and HE inhibited the NF-κB pathway, whereas EE exerted anti-inflammatory activity via the Nrf2/NF-κB pathways. CONCLUSIONS: The aforementioned results showed the anti-inflammatory mechanism of EYO. These findings might be beneficial to clinical applications of EYO.

Microalgal Bioprocess Toward the Production of Microalgal Oil Loaded Bovine Serum Albumin Nanoparticles.

Microalgal biotechnology has increased rapidly owing to have high value bioactive compounds and numerous consumer products that can be utilized from microalgae. With the development of novel cultivation and processing methods, microalgal biotechnology can meet the high demands of food, energy and pharmaceutical industries. In this context, especially for food and pharmaceutical applications, encapsulation of microalgal bioactive compounds is carried out to protect the compound from oxidation and degradation. In this study, a microalgal production process was carried out and microalgal oil loaded bovine serum albumin (BSA) nanoparticle production using glucose as cross-linking agent was investigated. The influences of different process parameters such as initial BSA concentration, glucose concentration and desolvation temperature on the size of BSA nanoparticles were investigated to achieve very small size nanoparticles. Furthermore, data obtained from the experiments were assessed statistically to model the process. It was found that the obtained nanoparticles showed spherical shape with the mean particle size of around 200-300 nm with zeta potential of about - 23 mV. Also, stability test showed that, there was not any change in particle size for one month storage and nanoparticle structure enhance the protection of microalgae oil from oxidation. At last, antibacterial effect of nanoparticles was presented against E. coli ATCC 8739 and L. monocytogenes ATCC 13932. In here, we demonstrated a microalgal bioprocess which consists of microalgae production to obtain microalgal oil riched in bioactive and, encapsulation of microalgal oil to protect it from environmental conditions.