tocotrienol rich fraction
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Author(s):  
Sitti Rahma Abd Hafid ◽  
Maliya Azilah Mohammad Aini ◽  
Nabiha Iran ◽  
Irmaliayana Norisam ◽  
Khairul Adzfa Radzun ◽  
...  

Background: Inflammation plays a vital role in the pathogenesis of chronic non-communicable diseases (NCDs), the leading health issue worldwide. An earlier study reported that tocotrienol-rich fraction (TRF) showed better anti-inflammation effects in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages. Aim: This study aimed to investigate the anti-inflammatory effects of tocotrienol-rich fraction at the molecular level by looking at the genes that were differentially regulated and pathways affected in LPS-stimulated macrophages exposed to TRF using the microarray approach. Methods: A microarray study was carried out in LPS-stimulated RAW 264.7 macrophages. Total ribonucleic acid (RNA) was extracted from the RAW 264.7 cells treated with TRF (10µg/mL), alpha-tocopherol (10 µg/mL) or LPS (10 ng/mL). Untreated cells served as control. Enrichment analyses, such as Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes pathway (KEGG), were conducted for genes listed in the differentially expressed genes (DEGs).  Results: The microarray analysis showed that the expression of five genes [Hamp, Interleukin-1a (IL-1a), IL-b, C-X-C motif chemokine ligand 2 (CXCL2) and colony-stimulating factor 3 (CSF3)] and one gene (SLC1A4), an amino acid transporter, was modulated (fold change 2, P< 0.05) in the TRF-treated cells. With a more stringent analysis (fold change 3, P < 0.05), only one gene (CSF3) was downregulated in the TRF-treated in RAW 264.7 cells. Analysis using the GO and KEGG pathways revealed interactions between pro-inflammatory agents such as tumor necrosis factor-alpha (TNFα) and nuclear factor kappa-light-chain-enhancer of activated B-cells (NF-B), as well as signaling pathways of interleukin (IL)-1 and IL-17. Conclusion: TRF modulated the expression of genes responsible for acute and chronic inflammation that were part of the lipoxygenase (LOX) and cyclooxygenase (COX) inflammatory pathways. Further investigation on the effects of TRF in different cell lines and in vivo studies should be conducted in the future.


2021 ◽  
Vol 11 (20) ◽  
pp. 9643
Author(s):  
Kok-Lun Pang ◽  
Norzana Abd Ghafar ◽  
Ima Nirwana Soelaiman ◽  
Kok-Yong Chin

Background: This study aimed to compare the chondroprotective efficacy and mechanism of annatto tocotrienol (AnTT) and palm tocotrienol-rich fraction (PT3) using SW1353 chondrocytes treated with monosodium iodoacetate (MIA). Methods: The chondrocytes were incubated with AnTT or PT3 in advance or concurrently with MIA for 24 h. The viability of the cells was tested with an MTT assay. The 8-isoprostane F2-α, extracellular matrix proteins, metalloproteinase and sex-determining region Y box protein 9 (SOX9) levels were determined using immunoassays. Results: AnTT and PT3 reversed an MIA-induced decrease in chondrocyte viability when incubated together with MIA (p < 0.05). Prior incubation with both mixtures did not produce the same effects. AnTT and PT3 cotreatment could suppress 8-isoprostane F2-α level in chondrocytes exposed to MIA (p < 0.01). Co-exposure to tocotrienols and MIA increased the type II collagen/type I collagen ratio in chondrocytes (p < 0.01). In addition, the co-exposure of AnTT and MIA for 24 h significantly upregulated SOX9, type II collagen and aggrecan levels (p < 0.05), which was not observed with co-exposure of PT3 and MIA, AnTT or PT3 exposure alone. Conclusion: AnTT and PT3 could prevent a reduction in chondrocyte viability following MIA exposure by reducing oxidative stress. In addition, AnTT might induce self-repair and anabolic activities in chondrocytes challenged with MIA.


2021 ◽  
Vol 11 (18) ◽  
pp. 8577
Author(s):  
Hiba Murtadha Al-Saadi ◽  
Kok-Yong Chin ◽  
Fairus Ahmad ◽  
Elvy Suhana Mohd Ramli ◽  
Azlan Mohd Arlamsyah ◽  
...  

Background: Osteoarthritis is a degenerative joint disease lacking disease-modifying therapeutic agents. This study aimed to compare the effects of palm tocotrienol-rich fraction (TRF), glucosamine sulphate, and both agents combined in rats with osteoarthritis induced by monosodium iodoacetate (MIA). Methods: Thirty adult male rats were randomized into normal control, and osteoarthritis groups were treated orally daily with vehicle, palm TRF (100 mg/kg), glucosamine sulphate (250 mg/kg), and both agents combined for 4 weeks. Body weight and grip strength were measured weekly. After being sacrificed, the joints and blood were harvested for histology and serum cartilage oligomeric matrix protein (COMP) levels. Results: The body weight of the rats receiving treatment rebounded significantly after an initial reduction (vs osteoarthritic control, p < 0.05). The rats receiving combined treatments showed significantly better grip strength than the osteoarthritic control and individual treatment groups (p < 0.05). The serum COMP level was lower in all the treated groups (vs osteoarthritic control, p < 0.05). Cartilage histology of the treated rats was not significantly improved (vs osteoarthritic control, p > 0.05). Conclusion: The combination of palm TRF and glucosamine sulphate was more effective than individual agents in improving the grip strength of the rats, but the cartilage damage might need more time to heal.


2021 ◽  
Vol 50 (5) ◽  
pp. 1457-1466
Author(s):  
Noor Shareena Aisha Abdul Khalid ◽  
Khuzaidatul Azidah Ahmad Nazri ◽  
Zakiah Jubri

Oxidative stress plays an important role in the pathogenesis of heart disease. Tocotrienol-rich fraction (TRF) is an antioxidant and that has the potential to reduce the risk of heart disease. This study is to determine the protective effects of palm TRF against H2O2-induced oxidative damage in neonatal rat cardiomyocytes (NRCM). The NRCM were divided into control, treated with TRF (10 µg/mL), H2O2 (0.5 mM) and treated with TRF prior to H2O2 induction (pre-treatment). Cell viability was determined by the MTS assay,while the presence of reactive oxygen species (ROS) was determined using fluorescent dihydroethidium (DHE) and 5-(and-6)-carboxy-2′,7′-dichlorodihydrofluorescein diacetate (carboxy-H2DCFDA) dye. Mitochondrial integrity and cell death were determined using JC-1 and Annexin V-FITC staining, respectively. Lactate dehydrogenase (LDH) and superoxide dismutase (SOD) activity were determined by colorimetric assay kit. The concentration of H2O2 from 0.5 to 5 mM reduced the cell viability and the H2O2 IC50 value of 0.5 mM was used in the experiment. H2O2 induction increased the intensity of carboxy-H2DCFDA and DHE-stains; and also the intensity of green fluorescence of J-monomers in JC-1 staining compared to the control group. The activity of LDH increased while the activity of SOD decreased in the H2O2 group. Pre-treatment with TRF reduced the intensities of carboxy-H2DCFDA and DHE-stains, as well as the green fluorescence of J-monomers in JC-1. Meanwhile, the LDH activity was reduced in the pre-treatment group but no changes were recorded in SOD activity compared to the H2O2 group. Palm TRF protects cardiomyocytes from oxidative damage by reducing ROS production and maintaining the mitochondrial membrane integrity thus reducing cell death.


2021 ◽  
Vol 50 (2) ◽  
pp. 429-436
Author(s):  
Tzer Sien Tan ◽  
Muhammad Firdaus Sathik Rahman ◽  
Siti Sara Ismail ◽  
Nur Najihah Mohamad ◽  
Ahmad Hazim Mustaffa ◽  
...  

Vitamin E is an established antioxidant. However, the effect of vitamin E on healthspan, which deteriorates during ageing, has not been determined because most related studies have emphasized its effects on lifespan. Therefore, the purpose of this study was to determine the effect of palm tocotrienol-rich fraction (TRF) on the lifespan, locomotion and thermotolerance of Caenorhabditis elegans, which share many common gene sequences with humans. The nematodes were treated with different concentrations of TRF (0 - 200 μg/mL), and the number of surviving nematodes at each concentration (N=30, duplicate) was counted daily under a light microscope to determine the optimal dose of treatment. The nematodes were divided into 3 groups, namely; control, Tween-80 (vehicle) and TRF-treated. Locomotion and thermotolerance were determined on day 4 and 12 of treatment in adult nematodes. ImageJ was used for locomotion analysis, and thermotolerance was determined based on nematode survivals after exposure to 37 °C. TRF-treated C. elegans had significantly longer lifespans compared to controls (P = 0.003). The TRF group (50 μg/mL) had the longest mean lifespan (23.5 days), which was significantly longer compared to controls, (18.5 days; (P = 0.002). However, locomotion was similar between all groups. In the thermotolerance assay, the survival determined on day 4 and day 12 of TRF-treatment was higher compared to controls (P= 0.046). Interestingly, the Tween- 80-treated group showed similar results as the TRF-treated group compared to controls. The findings indicate that TRF prolongs the lifespan and increases the thermotolerance of C. elegans but does not improve the locomotion of the worms as they age.


2021 ◽  
Vol 0 ◽  
pp. 0-0
Author(s):  
Mohd Danial Mohd Efendy Goon ◽  
Nur Izzati Zulkanain ◽  
Siti Hamimah Sheikh Abdul Kadir ◽  
Sharaniza Ab Rahim ◽  
Musalmah Mazlan ◽  
...  

Author(s):  
Hui-Fang Guo ◽  
Razana Mohd Ali ◽  
Roslida Abd Hamid ◽  
Sui Kiat Chang ◽  
Mohammed Habibur Rahman ◽  
...  

Our previous study has demonstrated that epidermal growth factor (EGF) with tocotrienol-rich fraction (TRF) cream formulation accelerating postburn wound healing with deep partial-thickness burn in rats. Current study was conducted to determine the gene expression levels related to burn wound healing process. A total of 180 Sprague-Dawley rats were randomly divided into 6 groups: untreated control, treated with Silverdin cream, base cream, base cream with 0.00075% EGF, base cream with 3% TRF or base cream with 0.00075% EGF, and 3% TRF, respectively. Burn wounds were created and the above-mentioned creams were applied once daily. Six animals from each group were sacrificed on days 3, 7, 11, 14, and 21 postburn. RNA was extracted from wound tissues and quantitative real-time polymerase chain reaction was performed to analyze the 9 wound healing-related genes against time postburn. Results demonstrated that topically applied EGF + TRF formulation downregulated the expression levels of IL-6 ( interluekin-6), TNF-α ( tumor necrosis factor-α) and iNOS ( inducible nitric oxide synthase) throughout the whole healing process. TGF-β1 ( transforming growth factor-β) and VEGF-A ( vascular endothelial growth factor-A) were reduced on day 14 postburn. On the contrary, increased expression of Collagen-1 in the early stage of wound healing was observed with no effects on epidemal growth factor receptor (EGFR). The results showed beneficial application of EGF + TRF cream in the treatment of burn wound since it accelerated wound healing by relieving oxidative stress, decreasing inflammation, and promoting proper tissue modelling in the burn wound.


PLoS ONE ◽  
2020 ◽  
Vol 15 (11) ◽  
pp. e0241112
Author(s):  
Aishatu Ali Chiroma ◽  
Huzwah Khaza’ai ◽  
Roslida Abd. Hamid ◽  
Sui Kiat Chang ◽  
Zainul Amiruddin Zakaria ◽  
...  

Natural α-tocopherol (α-TCP), but not tocotrienol, is preferentially retained in the human body. α-Tocopherol transfer protein (α-TTP) is responsible for binding α-TCP for cellular uptake and has high affinity and specificity for α-TCP but not α-tocotrienol. The purpose of this study was to examine the modification of α-TTP together with other related vitamin E-binding genes (i.e., TTPA, SEC14L2, and PI-TPNA) in regulating vitamin E uptake in neuronal cells at rest and under oxidative stress. Oxidative stress was induced with H2O2 for an hour which was followed by supplementation with different ratios of α-TCP and tocotrienol-rich fraction (TRF) for four hours. The cellular levels of vitamin E were quantified to determine bioavailability at cellular levels. The expression levels of TTPA, SEC14L2, and PI-TPNA genes in 0% α-TCP were found to be positively correlated with the levels of vitamin E in resting neuronal cells. In addition, the regulation of all the above-mentioned genes affect the distribution of vitamin E in the neuronal cells. It was observed that, increased levels of α-TCP secretion occur under oxidative stress. Thus, our results showed that in conclusion vitamin E-binding proteins may be modified in the absence of α-TCP to produce tocotrienols (TCT), as a source of vitamin E. The current study suggests that the expression levels of vitamin E transport proteins may influence the cellular concentrations of vitamin E levels in the neuronal cells.


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