Background: An experimental study was undertaken to determine the efficacy of the epidermal growth factor (EGF) with tocotrienol-rich fraction (TRF) cream in the wound-healing process on skin with deep partial-thickness burn in rats. Methods: A total of 180 Sprague-Dawley rats were randomly divided into six groups of six each and were: untreated control, treated with Silverdin® cream, base cream, base cream with c% EGF, base cream with 3% TRF or base cream with c% EGF and 3% TRF, respectively. Creams were applied once daily for 21 consecutive days. Six animals from each group were sacrificed using anaesthetic overdose on the third, seventh, 11th, 14th and 21st day post-burn. Skin tissues with the wound to be examined were excised for macroscopic and microscopic evaluation and biochemical analyses. Results: EGF + TRF formulation decreased the number of neutrophils, lymphocytes and myofibroblasts post-burn. However, no effects on the number of adipose cells in the healing process were recorded. In addition, lipid peroxidation and nitrite production were found to be reduced post-burn, reducing oxidative stress. Conclusions: Results of the present study indicate that the addition of EGF with TRF have ameliorating effects on deep-partial thickness burn healing parameters.

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Background: Burns are injuries that lie on the skin or other organic tissues caused by exposures to the heat, electricity, chemicals or ionizing radiation. The present study was carried out to record temporal changes in the cell population and wound healing-related gene expression in rats with deep partial-thickness burn. Methods: Burn wound was induced on the dorsal part of Sprague-Dawley rats using temperature-regulated 20-mm wide aluminum head heating device. Animals were then sacrificed on days three, seven, 11, 14 and 21 post-burn, respectively. Half of the wounded skin tissues were dissected and fixed in buffered neutral formalin for Hematoxylin & Eosin (H&E) staining, and the other half were cut off and stored in − 20°C for real-time PCR analyses. Results: The number of adipose cells was found to be maximal on the 3rd day post-burn, and it gradually decreased over time and completely disappeared on day 11 post-burn. The maximum number of neutrophils were found to be on the 3rd and 14th day post-burn, while the maximum number of myofibroblasts were found on the 11th day post-burn. The number of lymphocytes did not change too much during the whole healing process. At the gene expression level, the expression pattern of inflammation-related genes including IL-6, TNF-α and iNOS were similar, which was found to be increased from day 3 to day 11 and decreased thereafter. Angiogenesis related genes including both VEGF-A and TGF-β1 showed a same expression pattern, both of which were slightly increased from day 3 to day 14 and smoothly decreased on day 21 post-burn. Matrix re-modeling related genes including MMP-2, TIMP-2 and Collagen-1 changed over time synchronously, where they all persistently increased from day 3 till day 14, then slightly declined on day 21 post-burn. Conclusion: The present study revealed the changes in the cell population and expression profile of wound healing-related genes in deep partial-thickness burn, which could provide a cellular and genomic basis for the future research of burn injuries.

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.

The burden of cancer continues to grow in developed and developing countries, with about 70% of all cancer mortality in low- and middle-income countries. Among different cancer types, breast cancer is recognized as one of the five most common causes of death in cancer in women worldwide, right after lung cancer. Histological classification divides breast tumors into different categories based on their behavior and clinical outcome. However, the histological classification system has some limitations, thus molecular subtype classification has been studied extensively to improve the classification system for breast cancer. Like any other cancers, several signaling pathways that enhance the proliferation, survival, invasion, and metastasis capability of tumor cells have been observed in breast cancer. These crucial signaling pathways contributing to the etiology of breast cancer include breast tumor kinase (BRK) pathway, Notch signaling, Nuclear Factor-kappaB (NF-κB) pathway, and human epidermal growth factor receptor (HER) pathway. In the present review article, we summarize our current understanding of breast cancer and its signaling pathways, which serve as basic information on tumor formation, maintenance, and expansion that could help form better breast cancer management in patients.