Fermented barley bran water-soluble extracts inhibit the expression of adipogenic and lipogenic regulators in 3T3-L1 adipocytes.

PMID: 

Food Sci Biotechnol. 2016 ;25(6):1727-1735. Epub 2016 Dec 31. PMID: 30263468

Abstract Title: 

(fermented barley bran) water-soluble extracts inhibit the expression of adipogenic and lipogenic regulators in 3T3-L1 adipocytes.

Abstract: 

prepared from fermented barley bran is a traditional fermented food found only in the Gyeongsang-do area of South Korea. There have been no studies reported to date despite the potential bioactivities of. In this study, the anti-obesity activities ofextracts (SEs) during 3T3-L1 differentiation into adipocytes were investigated. SEs inhibited adipocyte differentiation by suppressing the CCAAT/enhancer binding protein-β and sterol regulatory element binding protein-1c expression in the early stage of differentiation, followed by the suppression of the peroxisome proliferator-activated receptor-γ, CCAAT/enhancer binding protein-α, and adiponectin. These changes in adipogenic markers induced inhibition of lipogenesis via down-regulation of mainly fatty acid synthase, acetyl-CoA carboxylase, fatty acid binding protein 4, and perilipin. These results were more significant in the extract offermented with isolatedMFST compared to naturally fermentedgroup. SEs can be considered as a useful material for developing food with health benefits and anti-obesity properties.

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Barley grass extract causes apoptosis of cancer cells by increasing intracellular reactive oxygen species production.

PMID: 

Biomed Rep. 2017 Jun ;6(6):681-685. Epub 2017 May 3. PMID: 28584641

Abstract Title: 

Barley grass extract causes apoptosis of cancer cells by increasing intracellular reactive oxygen species production.

Abstract: 

Cancer remains a leading cause of mortality worldwide, therefore food products are being investigated for potential prevention or treatment strategies. The ingredient, barley grass extract (L.; Bex) is used to prevent or ameliorate various types of disease. In cancer, Bex has been revealed to inhibit tumor growth. However, its effect on cancer cells is yet to be clearly defined. In the present study, the effect of Bex on cancer cell growth was investigated. Bex inhibited the viabilities of breast and prostate cancer cells according to the results of MTT assays. Accordingly, Bex caused apoptosis, which was confirmed by Annexin V staining and western blot analysis for poly (ADP-ribose) polymerase and caspases. Furthermore, Bex increased the intracellular levels of reactive oxygen species (ROS), and-acetyl-L-cystein blocked Bex-induced apoptosis. Therefore, the study demonstrated that Bex causes apoptosis of breast and prostate cancer cells by increasing intracellular ROS levels.

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Barley sprout extracts reduce hepatic lipid accumulation in ethanol-fed mice by activating hepatic AMP-activated protein kinase.

PMID: 

Food Res Int. 2017 11 ;101:209-217. Epub 2017 Sep 12. PMID: 28941686

Abstract Title: 

Barley sprout extracts reduce hepatic lipid accumulation in ethanol-fed mice by activating hepatic AMP-activated protein kinase.

Abstract: 

Chronic alcohol consumption leads to hepatic lipid accumulation and alcoholic fatty liver disease. Previously, we demonstrated that barley sprout extract, which contains saponarin as an active compound, reduces hepatic steatosis. In this study, we investigated the effect of barley sprout extracts (BSE) on hepatic lipid accumulation in a mouse model of alcoholic fatty liver disease. Seven-week-old C57BL/6 mice were fed an alcohol-containing diet (5% ethanol) and a low or high dose of BSE (100 or 200mg/kg body weight, respectively) for 10days. The high dose of BSE significantly decreased hepatic lipid accumulation compared with the ethanol-only control group. In the second animal study, mice were fed an alcohol-containing diet for 10days, followed by a 45% high-fat diet with oral administration of BSE (100 or 200mg/day/kg body weight) for 4weeks. Mice in both BSE-fed groups showed reduced hepatic steatosis. In the livers of mice fed BSE, phosphorylation of AMP-activated protein kinase (AMPK) was increased, and expression of hepatic autophagy markers was elevated. In cultured hepatocytes, BSE (200μg/mL) increased the rate of fatty acid oxidation and reduced that of fatty acid synthesis. Taken together, these findings suggest that BSE promotes degradation of lipid droplets and subsequent activation of fat oxidation by activating AMPK in the liver, thus protecting against development of hepatic steatosis in alcohol-fed mice. Saponarin, a major flavonoid in BSE and an activator of AMPK, increased the activity of microsomal triglyceride transfer protein, which suggests that the reduction in hepatic triglyceride levels was mediated by this component of BSE. In conclusion, BSE ameliorated hepatic steatosis in a mouse model of ethanol-induced fatty liver by activating AMPK, an effect possibly mediated by the saponarin component.

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White sesame seed oil may play an important role in GLU regulation and against deleterious effects of diabetes in humans with type 2 diabetes.

PMID: 

J Am Coll Nutr. 2019 Mar-Apr;38(3):235-246. Epub 2018 Sep 27. PMID: 30260748

Abstract Title: 

White Sesame Seed Oil Mitigates Blood Glucose Level, Reduces Oxidative Stress, and Improves Biomarkers of Hepatic and Renal Function in Participants with Type 2 Diabetes Mellitus.

Abstract: 

OBJECTIVES: The study was designed to investigate the impact of white sesame seed oil (WSSO) consumption on fasting blood glucose (GLU), insulin (INS), glycosylated hemoglobin (HbA1c), and hepatic antioxidant enzymes. A secondary aim was to check the influence on serum biochemistry, hepatic, cardiac, and renal functions.METHODS: Forty-six participants with type 2 diabetes were recruited and randomly divided into two equal groups: diabetic control (DCON) and diabetic sesame oil (DSO). At baseline and 30, 60, and 90 days, blood samples were drawn and analyzed. Two-way repeated-measures analysis of variance was used to evaluate the difference between groups and across time.RESULTS: In both groups, GLU, INS, and HbA1c were not significantly different at baseline (mean 187.07 ± 5.63 mg/dl, mean 12.12 ± 1.03 μU/ml, and mean 7.55 ± 0.37%, respectively). At 90 days, GLU was significantly (p 

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Application of massage with sesame oil as a complementary method is effective in reducing the pain severity of patients with CIP.

PMID: 

Complement Ther Clin Pract. 2019 May ;35:78-85. Epub 2019 Feb 2. PMID: 31003690

Abstract Title: 

Effects of topical sesame (Sesamum indicum) oil on the pain severity of chemotherapy-induced phlebitis in patients with colorectal cancer: A randomized controlled trial.

Abstract: 

BACKGROUND AND PURPOSE: Chemotherapy-induced phlebitis (CIP) is one of the most important and common complications in patients with cancer. Currently, the use of complementary methods to prevent or alleviate phlebitis symptoms has attracted great attention. In this study, we aimed to assess the effects of topical sesame oil in reducing the pain severity of CIP.MATERIALS AND METHODS: This randomized clinical trial was conducted on 60 patients with colorectal cancer afflicted with CIP. Patients received, twice a day for seven consecutive days, a 5-min massage solely (as the control group) or with 10 drops of sesame oil (as the experimental group) within the 10 cm radius of the affected site. The pain severity was evaluated by the visual analog scale on the first, third, fifth, and seventh days of the intervention.RESULTS: Mean changes of the pain severity compared to the baseline were significant on the third (P = 0.009), fifth (P 

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Sesame oil and vitamin E co-administration may improve cardiometabolic risk factors in patients with metabolic syndrome.

PMID: 

Eur J Clin Nutr. 2019 Oct ;73(10):1403-1411. Epub 2019 May 14. PMID: 31089253

Abstract Title: 

Sesame oil and vitamin E co-administration may improve cardiometabolic risk factors in patients with metabolic syndrome: a randomized clinical trial.

Abstract: 

OBJECTIVES: Metabolic syndrome (MetS) represents a clustering of metabolic abnormalities that are associated with an increased risk of type 2 diabetes and cardiovascular disease. We aimed to evaluate the effects of sesame oil enriched with vitamin E (vit E), sesame oil alone and sunflower oil on lipid profile, fasting blood glucose (FBG), malondialdehyde (MDA), high-sensitivity C-reactive protein (Hs-CRP), homeostatic model assessment (HOMA-IR), and blood pressure (BP) in patients with MetS.SUBJECTS: Overall, 75 individuals with MetS (aged 30-70 years) participated in this randomized, single-blind controlled trial. Patients were randomly allocated to: (1) Group A (n = 25): sesame oil (30 ml/day) enriched with vit E (400 mg/day), (2) Group B (n = 25): sesame oil (30 ml/day), (3) Group C (n = 25): sunflower oil (30 ml/day). Anthropometric data, dietary intake, blood pressure, and biochemical markers, including fasting serum lipids, FBG, seruminsulin, MDA, and hs-CRP were measured at baseline and at week 8.RESULTS: In individuals in the sesame oil enriched with vit E group (Group A), there were significant reductions in serum total cholesterol (TC), triglycerides (TG), FBG, HOMA-IR, MDA, hs-CRP, high-density lipoprotein (HDL-C) systolic and diastolic BP (for all the comparison p 

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Topical sesame oil was non-inferior to diclofenac gel on the reduction of the knee osteoarthritis pain.

PMID: 

Complement Ther Med. 2019 Dec ;47:102183. Epub 2019 Aug 22. PMID: 31780006

Abstract Title: 

The efficacy of topical sesame oil in patients with knee osteoarthritis: A randomized double-blinded active-controlled non-inferiority clinical trial.

Abstract: 

OBJECTIVE: Sesame oil is an herbal product that has been used to treat the joints pain in several traditional medicines. In this study, we evaluated the efficacy of topical sesame oil versus diclofenac gel in patients with knee osteoarthritis (OA).METHODS: One hundred and four patients were randomly enrolled in two arms of the trial. Patients were treated by topical sesame oil or diclofenac (three times a day) for 4 weeks. Outcome measures were knee pain via visual analogue scale (VAS), Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) questionnaire, knee joint's flexion angle, 8-meter walk test and number of used analgesics. Patients were evaluated at baseline, 2 and then 4 weeks after the intervention.RESULTS: At the follow-up visits, sesame oil was not inferior to diclofenac regarding scores of WOMAC pain, 8-meter walk test, and knee flexion angle. Although, its non-inferiority was not proved regarding scores of VAS, WOMAC stiffness, and WOMAC total at the 4week. Moreover, sesame oil was not inferior to diclofenac regarding consumed analgesics.CONCLUSION: It seems that the topical sesame oil was non-inferior to diclofenac gel on the reduction of the knee OA pain and improvement of some indicators of its function.

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Sesamin promotes angiogenesis and accelerates wound healing.

PMID: 

Biosci Biotechnol Biochem. 2020 Jan 21:1-11. Epub 2020 Jan 21. PMID: 31964241

Abstract Title: 

Sesamin promotes angiogenesis and accelerates wound healing in rats via alleviates TBHP-induced apoptosis in human umbilical vein endothelial cells.

Abstract: 

Acute stress induces tissue damage through excessive cellular apoptosis. In our study, the effects of sesamin on apoptosis and wound healing were investigated. The angiogenesis effect of sesamin was evaluated by the abilities of adherence, migration and tube formation in human umbilical vein endothelial cells (HUVECs). Our data demonstrated that treatment with sesamin dose-dependently promoted the proliferation, adherence, migration and enhanced their angiogenic ability. Moreover, the increased apoptosis in HUVECs, which stimulated by tert-butyl hydroperoxide (TBHP) was significantly attenuated by the sesamin treatment. Furthermore, we revealed that neogenesis of granulation tissue and deposition and remodeling of the collagen matrix were accelerated by the administration of sesamin in ourstudy. These results confirm that sesamin accelerates wound healing at least partly through its antiapoptotic effects on endothelial cells at the injury site. Thus, sesamin represents a potential therapeutic medicine for vessel injury-related wounds.

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Ameliorating effect of sesamin on insulin resistance of hepatic L02 cells induced by high glucose/high insulin.

PMID: 

Pak J Pharm Sci. 2019 Nov ;32(6):2733-2739. PMID: 31969308

Abstract Title: 

Ameliorating effect of sesamin on insulin resistance of hepatic L02 cells induced by high glucose/high insulin.

Abstract: 

Sesamin (SES) has the ameliorating effect on L02 hepatocyte model of insulin resistance induced by high glucose and high insulin, based on insulin receptor signaling pathway IRS/PI3K/Akt. Treatment with SES (200, 100μg/ml) increased glucose consumption, glucose uptake and the intracellular glycogen synthesis of L02 hepatocyte model of insulin resistance significantly. Moreover, treatment with SES promoted the gene and protein expression levels of insulin receptor (InsR) and the post-receptor associated proteins, such as insulin receptor substrate 1 (IRS1), insulin receptor substrate 2 (IRS2), PI3K (phosphatidylinositol 3-kinase), GLUT4 (glucose transporter 4) significantly, which were determined by RT-PCR and immunoblot analysis. In conclusion, SES has the ameliorating effect on L02 hepatocyte model of insulin resistance induced by high glucose/high insulin, which might be related to its effect on promoting expression of insulin receptor and its associated proteins of IRS-PI3K-Akt passway, and thus promoting insulin sensitivity.

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Sesamol alleviates obesity-related hepatic steatosis via activating hepatic PKA pathway.

PMID: 

Nutrients. 2020 Jan 26 ;12(2). Epub 2020 Jan 26. PMID: 31991934

Abstract Title: 

Sesamol Alleviates Obesity-Related Hepatic Steatosis via Activating Hepatic PKA Pathway.

Abstract: 

This study aimed to investigate the effect of sesamol (SEM) on the protein kinase A (PKA) pathway in obesity-related hepatic steatosis treatment by using high-fat diet (HFD)-induced obese mice and a palmitic acid (PA)-treated HepG2 cell line. SEM reduced the body weight gain of obese mice and alleviated related metabolic disorders such as insulin resistance, hyperlipidemia, and systemic inflammation. Furthermore, lipid accumulation in the liver and HepG2 cells was reduced by SEM. SEM downregulated the gene and protein levels of lipogenic regulator factors, and upregulated the gene and protein levels of the regulator factors responsible for lipolysis and fatty acidβ-oxidation. Meanwhile, SEM activated AMP-activated protein kinase (AMPK), which might explain the regulatory effect of SEM on fatty acid β-oxidation and lipogenesis. Additionally, the PKA-C and phospho-PKA substrate levels were higher after SEM treatment. Further research found that after pretreatment with the PKA inhibitor, H89, lipid accumulation was increased even with SEM administration in HepG2 cells, and the effect of SEM on lipid metabolism-related regulator factors was abolished by H89. In conclusion, SEM has a positive therapeutic effect on obesity and obesity-related hepatic steatosis by regulating the hepatic lipid metabolism mediated by the PKA pathway.

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