Effect of vegetable oils on the experimental infection of mice with Trypanosoma congolense.

Vegetable oils are frequently used as solvents for lipophilic materials; accordingly, the effects of their components should be considered in animal experiments. In this study, the effects of various vegetable oils on the course of Trypanosoma congolense infection were examined in mice. C57BL/6J mice were orally administered four kinds of oils (i.e., coconut oil, olive oil, high oleic safflower oil, and high linoleic safflower oil) with different fatty acid compositions and infected with T. congolense IL-3000. Oil-treated mice infected with T. congolense showed significantly higher survival rates and lower parasitemia than those of control mice. Notably, coconut oil, which mainly consists of saturated fatty acids, delayed the development of parasitemia at the early stage of infection. These results indicated that vegetable oil intake could affect T. congolense infection in mice. These findings have important practical implications; for example, they suggest the potential effectiveness of vegetable oils as a part of the regular animal diet for controlling tropical diseases and indicate that vegetable oils are not suitable solvents for studies of the efficacy of lipophilic agents against T. congolense.

Comparison of Dietary Oils with Different Polyunsaturated Fatty Acid n-3 and n-6 Content in the Rat Model of Cutaneous Wound Healing.

Dietary supplementation with polyunsaturated fatty acids (PUFA) n-3 can affect cutaneous wound healing; however, recent findings demonstrate the variable extent of their influence on the quality of healing. Here, we compare the effect of several dietary oils, containing different levels of PUFA n-3 and PUFA n-6, on wound healing in the rat model. Rats were fed the feed mixture with 8% palm oil (P), safflower oil (S), fish oil (F) or Schizochytrium microalga extract (Sch) and compared to the animals fed by control feed mixture (C). Dorsal full-thickness cutaneous excisions were performed after 52 days of feeding and skin was left to heal for an additional 12 days. Histopathological analysis of skin wounds was performed, including immune cells immunolabeling and the determination of hydroxyproline amount as well as gene expression analyses of molecules contributing to different steps of the healing. Matrix-assisted-laser-desorption-ionization mass-spectrometry-imaging (MALDI-MSI) was used to determine the amount of collagen α-1(III) chain fragment in healing samples. Treatment by Schizochytrium extract resulted in decrease in the total wound area, in contrast to the safflower oil group where the size of the wound was larger when comparing to control animals. Diet with Schizochytrium extract and safflower oils displayed a tendency to increase the number of new vessels. The number of MPO-positive cells was diminished following any of oil treatment in comparison to the control, but their highest amount was found in animals with a fish oil diet. On the other hand, the number of CD68-positive macrophages was increased, with the most significant enhancement in the fish oil and safflower oil group. Hydroxyproline concentration was the highest in the safflower oil group but it was also enhanced in all other analyzed treatments in comparison to the control. MALDI-MSI signal intensity of a collagen III fragment decreased in the sequence C > S > Sch > P > F treatment. In conclusion, we observed differences in tissue response during healing between dietary oils, with the activation of inflammation observed following the treatment with oil containing high eicosapentaenoic acid (EPA) level (fish oil) and enhanced healing features were induced by the diet with high content of docosahexaenoic acid (DHA, Schizochytrium extract).

Dietary-fat-induced taurocholic acid promotes pathobiont expansion and colitis in Il10-/- mice.

The composite human microbiome of Western populations has probably changed over the past century, brought on by new environmental triggers that often have a negative impact on human health. Here we show that consumption of a diet high in saturated (milk-derived) fat, but not polyunsaturated (safflower oil) fat, changes the conditions for microbial assemblage and promotes the expansion of a low-abundance, sulphite-reducing pathobiont, Bilophila wadsworthia. This was associated with a pro-inflammatory T helper type 1 (T(H)1) immune response and increased incidence of colitis in genetically susceptible Il10(−/−), but not wild-type mice. These effects are mediated by milk-derived-fat-promoted taurine conjugation of hepatic bile acids, which increases the availability of organic sulphur used by sulphite-reducing microorganisms like B. wadsworthia. When mice were fed a low-fat diet supplemented with taurocholic acid, but not with glycocholic acid, for example, a bloom of B. wadsworthia and development of colitis were observed in Il10(−/−) mice. Together these data show that dietary fats, by promoting changes in host bile acid composition, can markedly alter conditions for gut microbial assemblage, resulting in dysbiosis that can perturb immune homeostasis. The data provide a plausible mechanistic basis by which Western-type diets high in certain saturated fats might increase the prevalence of complex immune-mediated diseases like inflammatory bowel disease in genetically susceptible hosts.

Safflower (Carthamus tinctorius L.) oil during pregnancy and lactation influences brain excitability and cortex oxidative status in the rat offspring.

OBJECTIVES: To evaluate how safflower oil (SFO) influences brain electrophysiology and cortical oxidative status in the offspring, mothers received a diet with SFO during brain development period. METHODS: Beginning on the 14th day of gestation and throughout lactation, rats received safflower (safflower group - SG) or soybean oil (control group - CG) in their diet. At 65 days old, cortical spreading depression (CSD) and cortex oxidative status were analyzed in the offspring. RESULTS: SG presented reduction of the CSD velocity as compared to the CG (SG: 3.24 ± 0.09; CG: 3.37 ± 0.07 mm/min). SFO reduced levels of lipid peroxidation by 39.4%. SG showed the following increases: glutathione-S-transferase, 40.8% and reduced glutathione, 34.3%. However, SFO decreased superoxide dismutase by 40.4% and catalase by 64.1%. To control for interhemispheric effects, since CSD was recorded only in the right cortex, we evaluated the oxidative status in both sides of the cortex; no differences were observed. DISCUSSION: Data show that when SFO is consumed by the female rats during pregnancy and lactation, the offspring present long-term effects on brain electrophysiology and cortical oxidative state. The present study highlights the relevance of understanding the SFO intake of pregnant and lactating mammals.

Transcriptome Analysis of Long Non-Coding RNA in the Bovine Mammary Gland Following Dietary Supplementation with Linseed Oil and Safflower Oil.

This study aimed to characterize the long non-coding RNA (lncRNA) expression in the bovine mammary gland and to infer their functions in dietary response to 5% linseed oil (LSO) or 5% safflower oil (SFO). Twelve cows (six per treatment) in mid lactation were fed a control diet for 28 days followed by a treatment period (control diet supplemented with 5% LSO or 5% SFO) of 28 days. Mammary gland biopsies were collected from each animal on day-14 (D-14, control period), D+7 (early treatment period) and D+28 (late treatment period) and were subjected to RNA-Sequencing and subsequent bioinformatics analyses. Functional enrichment of lncRNA was performed via potential cis regulated target genes located within 50 kb flanking regions of lncRNAs and having expression correlation of >0.7 with mRNAs. A total of 4955 lncRNAs (325 known and 4630 novel) were identified which potentially cis targeted 59 and 494 genes in LSO and SFO treatments, respectively. Enrichments of cis target genes of lncRNAs indicated potential roles of lncRNAs in immune function, nucleic acid metabolism and cell membrane organization processes as well as involvement in Notch, cAMP and TGF-ß signaling pathways. Thirty-two and 21 lncRNAs were differentially expressed (DE) in LSO and SFO treatments, respectively. Six genes (KCNF1, STARD13, BCL6, NXPE2, HHIPL2 and MMD) were identified as potential cis target genes of six DE lncRNAs. In conclusion, this study has identified lncRNAs with potential roles in mammary gland functions and potential candidate genes and pathways via which lncRNAs might function in response to LSO and SFA.

Effect of dietary fatty acid supplements, varying in fatty acid composition, on milk fat secretion in dairy cattle fed diets supplemented to less than 3% total fatty acids.

Dietary fatty acids can affect both milk fat yield and fatty acid (FA) composition. This relationship is well established when the dietary level of FA exceeds 3% of diet dry matter (DM). We could find no reports directly examining the effects of dietary FA profile on milk fat at levels below 3%. Twenty-four primiparous and 36 multiparous lactating cows were paired by production (1 high with 1 low, within parity) to form 30 experimental units. Pairs were fed 6 diets in five 6×6 balanced Latin squares with 21-d periods, and data were collected during the last 5d of each period. Two control diets were fed: a corn control diet (CC; 29% corn silage, 16% alfalfa silage, 19% corn grain, and 8% distillers grain on a DM basis) containing 1.8% FA; and a low-oil control diet (LOC; 9% corn silage, 35% alfalfa silage, 20% food-grade corn starch, and 8% corn gluten feed on a DM basis) containing 1.2% FA. A portion of the food-grade corn starch in LOC was replaced with 4 different FA supplements to create the 4 treatment diets. Treatments were 1.7% (DM basis) of a 50:50 blend of corn oil and high-linoleic safflower oil (LO), 1.7% high-oleic sunflower oil (OO), 1.7% palm oil (PO), or 1.8% calcium salts of palm fatty acids (PFA). The resultant diets were thus enriched in linoleic (LO), oleic (OO), or palmitic acid (PO and PFA). Dietary treatments did not affect dry matter intake. Addition of any of the fat sources to LOC resulted in increased milk yield, but milk fat yields and milk FA composition were variable for the different treatments. The LO treatment resulted in lower milk fat yield, fat concentration, and C16:0 yield but increased both trans-10 C18:1 and trans-10,cis-12 C18:2 yields compared with the other added FA treatments. Diets PO and PFA resulted in increased milk C16:0 yield and decreased total milk C18 yield compared with OO. Regression analysis revealed a negative coefficient for dietary linoleic acid content over basal (LOC) for both milk short-chain FA yield and C16:0 yield. Dietary linoleic acid content also had a positive coefficient for milk trans-10 C18:1 and trans-10,cis-12 conjugated linoleic acid yield. These results demonstrate that even when total dietary FA are below 3%, free oils rich in linoleic acid can reduce milk fat yield by reducing secretion of milk FA with fewer than 18 carbons. Fatty acid composition of fat supplements is important even at this low level of total dietary fat.

Lymphatic diamine oxidase secretion stimulated by fat absorption is linked with histamine release.

Diamine oxidase (DAO) is abundantly expressed in mammalian small intestine catalyzing the oxidative breakdown of polyamines and histamine. The aim of this study was to determine the relationship between stimulation of intestinal diamine oxidase secretion with intestinal fat absorption and histamine release. Conscious intestinal lymph fistula rats were used. The mesenteric lymph ducts were cannulated and intraduodenal tubes were installed for the infusion of Liposyn II 20% (an intralipid emulsion). Lymphatic DAO activity and protein secretion were analyzed by radiometric assay and Western blot, respectively. Lymphatic histamine concentration was measured by ELISA. Infusion of Liposyn II (4.43 kcal/3 ml) resulted in a ~3.5-fold increase in lymphatic DAO protein secretion and DAO activity, peaking at 1 h and lasting for 3 h. Liposyn II infusion also increased the lymphatic histamine release, a substrate for DAO. To determine the relationship of DAO release with histamine release, histamine was administered intraperitoneally (10 mg/kg) in fasting rats and resulted in a significant doubling in lymphatic DAO activity, supporting a link between histamine and DAO. In addition, ip administration of the histamine H4 receptor antagonist JNJ7777120 significantly reduced the Liposyn II-induced DAO output by 65.9%, whereas H(1) (pyrilamine maleate), H(2) (ranitidine), and H(3) (thioperamide maleate) receptor antagonists had little effect. We conclude that DAO secretion may contribute to the catabolism of histamine released during fat absorption and this is probably mediated through the histamine H(4) receptor.

The effects of fish oil consumption on cardiovascular remodeling in ApoE deficient mice.

Owing to their spontaneous development of atherosclerosis, apolipoprotein E knockout mice (ApoE(KO)) are one of the best studied animal models for this disease. Little is known about the utility of various omega-3 fatty acid regimens, in particular fish oils, in preventing cardiac disease in ApoE(KO) mice. The purpose of this study was to determine the cardiovascular effects of omega-3 fatty acid supplementation with either safflower oil (control), fish oil, flaxseed oil, or designed oil in ApoE(KO) mice fed a high-fat diet for a total of 16 weeks. In-vivo cardiac function was assessed weekly using murine echocardiography. Blood pressure, plasma lipid levels, and brain natriuretic peptide (BNP) were serially measured. The results show that ApoE(KO) mice fed fish oil demonstrated an increase in left ventricular wall thickness as a result of increased afterload. Despite chronic treatment with fish oil over 16 weeks, blood pressure increased in ApoE(KO) mice by 20% compared with the baseline. Both echocardiographic evidence of left ventricular hypertrophy and biochemical increase in BNP levels confirmed diastolic dysfunction in ApoE(KO) mice fed fish oil. This suggests that high-fat diet supplemented with fish oil may lead to adverse cardiovascular effects in ApoE deficient mice.

Do edible oils reduce bacterial colonization of enamel in situ?

OBJECTIVE: Edible oils are an empiric approach for the prevention of oral diseases. The present in situ study investigated the effect of edible oils on initial bacterial colonization of enamel surfaces. METHODS AND MATERIALS: Initial biofilm formation was performed on enamel specimens mounted on maxillary splints and carried by eight subjects. After 1 min of pellicle formation, rinses with safflower oil, olive oil and linseed oil were performed for 10 min. Application of chlorhexidine for 1 min served as positive control. Afterwards, the slabs were carried for 8 h overnight. Samples carried for 8 h without any rinse served as negative controls. The amount of adherent bacteria was determined by DAPI staining (4',6-diamidino-2-phenylindole) and live-dead staining (BacLight). Additionally, determination of colony forming units was performed after desorption of the bacteria. TEM evaluation was carried out after application of the rinses. RESULTS: The number of adherent bacteria on control samples was 6.1 ± 8.1 × 10(5)/cm(2) after 8 h (DAPI). Fluorescence microscopic data from DAPI staining and live-dead staining as well as from the determination of CFU revealed no significant effects of rinsing with oils on the amount of adherent bacteria compared to the non-rinsed control samples. However, with chlorhexidine a significant reduction in the number of bacteria by more than 85 % was achieved (DAPI, chlorhexidine: 8.2 ± 17.1 × 10(4)/cm(2)). The ratio of viable to dead bacteria was almost equal (1:1) irrespective of the rinse adopted as recorded with BacLight. TEM indicated accumulation of oil micelles at the pellicle's surface and modification of its ultrastructure. CONCLUSION: Rinses with edible oils have no significant impact on the initial pattern and amount of bacterial colonization on enamel over 8 h. CLINICAL RELEVANCE: Rinses with edible oils cannot be recommended for efficient reduction of oral biofilm formation.

Activation of rat intestinal mucosal mast cells by fat absorption.

Previous studies have linked certain types of gut mucosal immune cells with fat intake. We determined whether fat absorption activates intestinal mucosal mast cells (MMC), a key component of the gut mucosal immune system. Conscious intestinal lymph fistula rats were used. The mesenteric lymph ducts were cannulated, and the intraduodenal (i.d.) tubes were installed for the infusion of Liposyn II 20% (an intralipid emulsion). Lymphatic concentrations of histamine, rat MMC protease II (RMCPII), a specific marker of rat intestinal MMC degranulation, and prostaglandin D(2) (PGD(2)) were measured by ELISA. Intestinal MMC degranulation was visualized by immunofluorescent microscopy of jejunum sections taken at 1 h after Liposyn II gavage. Intraduodenal bolus infusion of Liposyn II 20% (4.4 kcal/3 ml) induced approximately a onefold increase in lymphatic histamine and PGD(2), ∼20-fold increase in lymphatic RMCPII, but only onefold increase in peripheral serum RMCPII concentrations. Release of RMCPII into lymph increased dose dependently with the amount of lipid fed. In addition, i.d. infusion of long-chain triacylglycerol trilinolein (C18:2 n-6, the major composite in Liposyn II) significantly increased the lymphatic RMCPII concentration, whereas medium-chain triacylglycerol tricaprylin (C8:0) did not alter lymph RMCPII secretion. Immunohistochemistry image revealed the degranulation of MMC into lamina propria after lipid feeding. These novel findings indicate that intestinal MMC are activated and degranulate to release MMC mediators to the circulation during fat absorption. This action of fatty acid is dose and chain length dependent.

Effect of safflower oil on the protective properties of the in situ formed salivary pellicle.

AIM: The prevalence of dental erosion is still increasing. A possible preventive approach might be rinsing with edible oils to improve the protective properties of the pellicle layer. This was tested in the present in situ study using safflower oil. METHODS: Pellicle formation was carried out in situ on bovine enamel slabs fixed buccally to individual upper jaw splints (6 subjects). After 1 min of pellicle formation subjects rinsed with safflower oil for 10 min, subsequently the samples were exposed in the oral cavity for another 19 min. Enamel slabs without oral exposure and slabs exposed to the oral cavity for 30 min without any rinse served as controls. After pellicle formation in situ, slabs were incubated in HCl (pH 2; 2.3; 3) for 120 s, and kinetics of calcium and phosphate release were measured photometrically (arsenazo III, malachite green). Furthermore, the ultrastructure of the pellicles was evaluated by transmission electron microscopy (TEM). RESULTS: Pellicle alone reduced erosive calcium and phosphate release significantly at all pH values. Pellicle modification by safflower oil resulted in an enhanced calcium loss at all pH values and caused an enhanced phosphate loss at pH 2.3. TEM indicated scattered accumulation of lipid micelles and irregular vesicle-like structures attached to the oil-treated pellicle layer. Acid etching affected the ultrastructure of the pellicle irrespective of oil rinsing. CONCLUSION: The protective properties of the pellicle layer against extensive erosive attacks are limited and mainly determined by pH. The protective effects are modified and reduced by rinses with safflower oil.

Maternal safflower oil consumption improve reflex maturation, memory and reduces hippocampal oxidative stress in the offspring rats treated during pregnancy and lactation.

OBJECTIVE: Evaluate the influence of maternal consumption of safflower oil on reflex maturation, memory and offspring hippocampal oxidative stress. METHODOLOGY: Two groups were formed: control group (C), whose mothers received a standard diet, and Safflower group (SF), whose mothers received a normolipidic diet with safflower oil as lipid source. Treatment was given from the 14th day of gestation and throughout lactation. To evaluate newborn development, the reflex ontogeny indicators between the 1st and the 21st days of life were evaluated; to assess memory, from the 42nd day of life on these animals were examined on open field habituation and novel object recognition test. Following behavioral analysis, the animals were anesthetized and decapitated. Hippocampus was rapidly dissected. In the hippocampal tissues, we evaluated the levels of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione S transferase (GST) and reduced glutathione (GSH). RESULTS: SF offspring showed delayed maturation of reflexes and improvement of novel object recognition in short-term and long-term (p < 0.05). Safflower oil decreases lipid peroxidation evaluated by MDA levels (p < 0.001) and increases antioxidant defenses as shown by SOD, CAT, GST and GSH levels (p < 0.05). In our study, the composition of flavonoids present in the oil was not evaluated. Furthermore, in a future study, the effect of maternal consumption on female offspring should be verified. CONCLUSION: Maternal intake of safflower oil could: (1) change neonate reflex parameters, (2) promote improvement of cognitive development in adolescence (3) improve antioxidant enzymatic and non-enzymatic defenses in the hippocampus.

Effect of different dietary fats on inflammation and glucose intolerance in high fructose and high fat fed experimental animals.

OBJECTIVES: Diet is the major modifiable risk factor for the onset of insulin resistance and its progression into diabetes. In the present study the effect of various dietary fats on inflammatory homeostasis and glucose tolerance is investigated in high fat and high fructose fed mice model. METHODS: C57/BL6J mice were divided into four groups and fed a casein-based diet containing high fructose (45%) and high fat (24%) (clarified butter oil [CBO]; safflower oil [SFFO] and lard oil [LO]) for 120 days; oral glucose tolerance (OGTT), plasma lipid profile and plasma & adipose tissue cytokines levels were compared with the control diet (10% groundnut oil and 59.5% starch) fed animals. RESULTS: The total cholesterol and triglycerides were higher in CBO and LO fed animals with glucose intolerance and increased body weights; liver and white adipose tissue weights were higher in CBO and LO fed animals respectively. CBO feeding increased the plasma (IFN-γ) and adipose tissue cytokines (IFN-γ, IL-10, IL-6 & TNF-α). LO feeding increased plasma IFN-γ, TNF-α and IL-1ß and adipose tissue IL-6. SFFO feeding decreased body weight and tissue cytokines and increased plasma IFN-γ levels without causing impairment in the glucose tolerance. CONCLUSIONS: Consumption of a high fructose and high fat diet which mimic the present-day dietary pattern resulted in altered inflammatory homeostasis and impairment in glucose tolerance in 24% CBO and LO fed animals. The deleterious effects of high fructose feeding were reversed in SFFO fed mice possibly due to the presence of oleic and linoleic acids.

CLA does not impair endothelial function and decreases body weight as compared with safflower oil in overweight and obese male subjects.

OBJECTIVE: Conjugated linoleic acid (CLA) showed a wide range of beneficial biological effects with relevance for cardiovascular health in animal models and humans. Most human studies used olive oil as a reference. This study assessed the effect of CLA as compared with safflower oil on endothelial function and markers of cardiovascular risk in overweight and obese men. Heated safflower oil and olive oil were given for additional descriptive control. METHODS: Eighty-five overweight men (aged 45-68 years, body mass index 25-35 kg/m(2)) were randomized to receive 4.5 g/d of the CLA isomeric mixture, safflower oil, heated safflower oil, or olive oil in a 4-week double-blind study. Endothelial function was assessed by peripheral arterial tonometry (PAT) index determination in the fasting and postprandial state (i.e., 4 hours after consumption of a fat- and sucrose-rich meal). RESULTS: CLA as compared with safflower oil consumption did not impair fasting or postprandial PAT index but decreased body weight. CLA as compared with safflower oil did not change total, low-density lipoprotein (LDL), or high-density lipoprotein (HDL) cholesterol; triglycerides; insulin sensitivity indices; C-reactive protein; soluble adhesion molecules; oxidized LDL; lipoprotein a (Lp[a]); paraoxonase; or platelet-activating factor acetylhydrolase (PAF-AH) activity, but significantly reduced arylesterase activity and increased concentrations of the F(2)-isoprostane 8-iso-prostaglandin F (PGF)(2α). CONCLUSION: CLA did not impair endothelial function. Other parameters associated with metabolic syndrome and oxidative stress were not changed or were slightly improved. Results suggest that CLA does not increase cardiovascular risk. Increased F(2)-isoprostane concentrations in this context may not indicate increased oxidative stress.

Omega-3 polyunsaturated fatty acids prevent obesity by improving tricarboxylic acid cycle homeostasis.

The beneficial effects of omega-3 polyunsaturated fatty acids (n-3 PUFAs) on preventing obesity are well known; however, the underlying mechanism by which n-3 PUFAs influence tricarboxylic acid (TCA) cycle under obesity remains unclear. We randomly divided male C57BL/6 mice into 5 groups (n=10) and fed for 12 weeks as follows: mice fed a normal diet (Con, 10% kcal); mice fed a high-fat diet (HFD, lard, 60% kcal); and mice fed a high-fat diet (60% kcal) substituting half the lard with safflower oil (SO), safflower oil and fish oil (SF) and fish oil (FO), respectively. Then we treated HepG2 cells with palmitic acid and DHA for 24 h. We found that body weight in FO group was significantly lower than it in HFD and SO groups. N-3 PUFAs reduced the transcription and translation of TCA cycle enzymes, including IDH1, IDH2, SDHA, FH and MDH2, to enhance mitochondrial function in vivo and vitro. DHA significantly inhibited protein expression of the mTORC1 signaling pathway, increased p-AKT protein expression to alleviate insulin resistance and improved mitochondrial oxygen consumption rate and glycolysis ability in HepG2 cells. In addition, the expressions of IDH2 and SDHB were reduced by rapamycin. N-3 PUFAs could prevent obesity by improving TCA cycle homeostasis and mTORC1 signaling pathway may be upstream.

Safflower seed oil improves steroidogenesis and spermatogenesis in rats with type II diabetes mellitus by modulating the genes expression involved in steroidogenesis, inflammation and oxidative stress.

ETHNOPHARMACOLOGICAL RELEVANCE: Diabetes mellitus (DM), as a multiorgan syndrome, is an endocrine and metabolic disorder that is associated with male reproductive system dysfunction and infertility. Safflower (Carthamus tinctorius L.) as an herbal remedy improves DM and infertility-related disorders. The anti-hypercholesterolemic, anti-inflammatory, and antioxidative properties of this herb have been well documented, but its role in testosterone production, male reproductive system and zinc homeostasis has not been fully illustrated. AIM OF THE STUDY: This study aimed to investigate the preventive and therapeutic properties of different doses of safflower seed oil against reproductive damage caused by type II DM by investigating zinc element homeostasis, inflammation and oxidative damage in testis tissue and their relationship with testosterone production and sperm parameters. MATERIALS AND METHODS: Eighty adult male Sprague-Dawley rats were randomly divided into eight groups and treated daily for 12 and 24 weeks in protective and therapeutic studies, respectively. Type II DM was induced by a High Fat Diet (HFD) in normoglycemic rats for three months. At the end of each study, serum level of glucose, testosterone, gonadotropins, TNF-α, insulin, and leptin were measured. Moreover, antioxidant enzymes activity, lipid peroxidation, zinc and testosterone along with the expression of Nrf-2, NF-κB, TNF-α, StAR, P450scc, and 17ßHSD3 genes in the testis were detected. RESULTS: After the intervention, the activity of antioxidant enzymes and the level of testosterone and gonadotropins significantly decreased in the rats with DM in comparison to the others. However, lipid peroxidation and serum level of insulin, leptin and TNF-α increased and the testicular level of zinc significantly changed in the rats with DM compared to the control groups (p < 0.05). The gene expression of NF-κB and TNF-α were also significantly increased and the gene expression of Nrf2, StAR, P450scc and 17ßHSD3 were decreased in the testis of diabetic rats (p < 0.05). The results showed that pretreatment and treatment with safflower seed oil could improve these parameters in diabetic rats compared with untreated diabetic rats (p < 0.05). CONCLUSION: HFD could impair the production of testosterone and sperm, and reduce gonadotropin by increasing the serum level of leptin and inducing insulin resistance, oxidative stress and inflammation. However, safflower oil in a dose-dependent manner could improve testosterone level and sperm parameters by improving the level of leptin, zinc and insulin resistance, and the genes expression involved in testosterone synthesis, inflammation and oxidative stress.

Relative efficacy of casein or soya protein combined with palm or safflower-seed oil on hyperuricaemia in rats.

Diets that ameliorate the adverse effects of uric acid (UA) on renal damage deserve attention. The effects of casein or soya protein combined with palm or safflower-seed oil on various serum parameters and renal histology were investigated on hyperuricaemic rats. Male Wistar rats administered with oxonic acid and UA to induce hyperuricaemia were fed with casein or soya protein plus palm- or safflower-seed oil-supplemented diets. Normal rats and hyperuricaemic rats with or without allopurinol treatment (150 mg/l in drinking water) were fed with casein plus maize oil-supplemented diets. After 8 weeks, allopurinol treatment and soya protein plus safflower-seed oil-supplemented diet significantly decreased serum UA in hyperuricaemic rats (one-way ANOVA; P < 0.05). In addition, soya protein and casein attenuated hyperuricaemia-induced decreases in serum albumin and insulin, respectively (two-way ANOVA; P < 0.05). Safflower-seed oil significantly decreased serum TAG and UA, whereas palm oil significantly increased serum cholesterol, TAG, blood urea N and creatinine. However, soya protein significantly decreased renal NO and nitrotyrosine and palm oil significantly decreased renal nitrotyrosine, TNF-alpha and interferon-gamma and increased renal transforming growth factor-beta. Casein with safflower-seed oil significantly attenuated renal tubulointerstitial nephritis, crystals and fibrosis. Comparing casein v. soya protein combined with palm or safflower-seed oil, the results support that casein with safflower-seed oil may be effective in attenuating hyperuricaemia-associated renal damage, while soya protein with safflower-seed oil may be beneficial in lowering serum UA and TAG.

An Experimental Comparison of the Analgesic and Anti-Inflammatory Effects of Safflower Oil, Benzydamine HCl, and Naproxen Sodium.

The study aims to establish how feasible a natural therapy option (safflower oil) is in the treatment of postoperative pain. Naproxen sodium has already been experimentally proven to be effective for this purpose. Accordingly, the analgesic and anti-inflammatory effects of safflower oil were compared with those obtained with benzydamine HCl and naproxen sodium. Forty-two, healthy, adult female rats of Wistar albino species were divided at random into six groups of seven rats. The intervention allocation was as follows: Group No. 1-physiological saline 0.9%; Group No. 2-safflower oil 100 mg/kg; Group No. 3-safflower oil 300 mg/kg; Group No. 4-benzydamine HCl 30 mg/kg; Group No. 5-benzydamine HCl 100 mg/kg; and Group No. 6-naproxen sodium 10 mg/kg. Following allocation of treatment, pain was induced experimentally and tested in various ways (hot plate test, tail-pinching test, and writhing test) and the efficacy of each treatment in providing peripheral and central analgesia was evaluated. The second stage consisted of providing different treatments to four groups (groups 7-10) of seven rats each, chosen at random. The allocations were as follows: Group No. 7-physiological saline 0.9%; Group No. 8-safflower oil 300 mg/kg; Group No. 9-benzydamine HCl 100 mg/kg; and Group No. 10-naproxen sodium 10 mg/kg. To create experimental inflammation, 2% formaldehyde was injected into the experimental animal's paw and the resulting edema was measured and recorded for a 10-day period. Edema inhibition was calculated as a percentage. The rats were sacrificed and the paw and stomach dissected for histopathological examination. The data were used for statistical analysis, using the Shapiro-Wilk, Kruskal-Wallis H test, and two-way analysis of variance. In the tail-pinching test, it was determined that a 300 mg/kg dose of safflower oil shows central spinal analgesic efficacy and this effect is close in magnitude to 10 mg/kg of the reference material, naproxen sodium. In the squirming test, it was observed that the 100 and 300 mg/kg doses of safflower oil had a peripheral analgesic effect when compared with the serum physiological (placebo) group. The peripheral efficacy of 300 mg/kg safflower oil was found to approximate that of 10 mg/kg naproxen sodium. In rats treated with benzydamine HCl 100 mg/kg, similar peripheral analgesic efficacy to naproxen sodium 10 mg/kg was noted. In the hot plate test, no difference in the analgesic efficacy between the various agents was found. The change in inhibition of edema between the 1st and 10th days was most marked in rats receiving naproxen sodium 10 mg/kg. A significant difference was determined in the safflower oil 300 mg/kg and benzydamine HCl 100 mg/kg groups (P < .001). Regarding histopathology findings in the rat paw, significant differences were seen in venous congestion between placebo and safflower oil 300 mg/kg and in inflammation between the control and benzydamine HCl 100 mg/kg groups. Regarding the histopathology findings in the rat stomach, significant differences were observed in venous congestion between placebo and safflower oil 300 mg/kg; in damage to the epithelium between placebo and safflower oil 300 mg/kg and between naproxen sodium 10 mg/kg and safflower oil; and in cell infiltration and development of edema between placebo and safflower oil 300 mg/kg. It is predicted that further research into safflower oil and benzydamine HCl will create opportunities to develop analgesic-anti-inflammatory therapeutics of a novel kind for the treatment of postoperative pain and inflammation.

Differential Effect of Four-Week Feeding of Different Dietary Fats on the Accumulation of Fat and the Cholesterol and Triglyceride Contents in the Different Fat Depots.

The aim of the present study was to determine the effects of feeding of a high-fat diet containing different types of lipids for four weeks on the cholesterol and triglyceride contents of different fat depots and on body temperature in rats. Four groups of adult rats were fed 10% fat, containing either beef tallow, safflower oil, or fish oil, respectively, as well as a normal rodent diet with 4% fat, for four weeks. The rats on normal rodent diet consumed significantly more food and water than the rats in the other three groups. Rectal temperature increased only after four-week feeding with safflower oil fat. Increased fat deposition and adipocyte size were observed in rats fed safflower oil and beef tallow. In all fat pads of safflower oil-fed rats, cholesterol content was significantly higher than the other three groups. Feeding of beef tallow increased triglyceride depot without increasing cholesterol content. The rats fed fish oil had significantly less triglyceride and cholesterol deposition in adipose tissues than the rats fed safflower oil or beef tallow. These results clearly demonstrated the differences in fat deposition, adipocyte size and number, triglyceride and cholesterol accumulation in fat cells are dependent on the dietary lipid composition.

Safflower Seed Oil and Its Active Compound Acacetin Inhibit UVB-Induced Skin Photoaging.

Ultraviolet (UV) is one of the major factors harmful to skin health. Irradiation with ultraviolet accelerates the decline of skin function, causing the skin to have deep wrinkles, dryness, decreased procollagen production, and degradation of collagen. Novel materials are needed to prevent the aging of the skin by blocking the effects of UV. Safflower seed oil (Charthamus tinctorius L., SSO) contains significantly high levels of unsaturated fatty acids and phytochemicals. SSO has been traditionally used in China, Japan, and Korea to improve skin and hair. Our objective in this study was to determine the effect of SSO and its active compound acacetin on UVB-induced skin photoaging in HaCaT cells and human dermal fibroblasts (HDF). SSO inhibited UVB-induced matrix metalloproteinase-1 (MMP-1) at both protein and mRNA levels in HaCaT cells and HDF. MMP-1 is known to play important roles in collagen degradation and wrinkle formation. Acacetin, a type of flavonoid, is present in SSO. Similar to SSO, acacetin also inhibited UVB-induced MMP-1 protein and mRNA levels in HaCaT cells and HDF. MMP-1 mRNA is primarily regulated by the mitogen-activated kinase (MAPK) signaling pathway. Acacetin regulated the phosphorylation of JNK1/2 and c-jun, but did not inhibit the phosphorylation of ERK1/2, p38 and AKT. Taken together, these results indicate that SSO and its active compound acacetin can prevent UVB-induced MMP-1 expression, which leads to skin photoaging, and may therefore have therapeutic potential as an anti-wrinkle agent to improve skin health.