Single or Daily Application of Topical Curcumin Prevents Ultraviolet B-Induced Apoptosis in Mice.

Curcumin is a natural ingredient with antioxidant effects, widely studied as a treatment for various types of cancer. However, its effects on ultraviolet radiation have not been fully explored. The effects of single or daily application of 0.1-100 µM curcumin on cell apoptosis in ultraviolet B (UVB)-induced mice were tested using an experimental double-blind posttest design with a control group and two research models: a single application of curcumin before a single UVB exposure and daily application of curcumin for 7 days before a single UVB exposure on the seventh day. Apoptotic cells were counted using a tunnel system kit. The number of apoptotic cells under a single or daily application of curcumin for 7 days was significantly lower than that of the UVB controls (p ≤ 0.05). The number of apoptotic cells decreased with the increasing concentration of curcumin, and the maximum effect was observed at 100 µM. Daily application of topical curcumin was superior in preventing apoptosis (mean apoptotic cell count of 14.86 ± 1.68) compared with a single application (17.46 ± 0.60; p = 0.011). Topical curcumin can act as a potential photoprotective agent in preventing cutaneous malignancies due to UVB radiation. Further studies are warranted, especially in humans.

Effect of erythropoietin administration on expression of mRNA brain-derived Neutrophic factor, levels of stromal cell-derived Factor-1, and neuron specific enolase in brain injury model Sprague Dawley.

BACKGROUND: Traumatic brain injury (TBI) is a complicated condition that is the primary cause of death and disability in children and young adults in developed countries. Various kinds of therapy have been carried out in the management of brain injury, one of which is the administration of erythropoietin (EPO). There are not many studies in Indonesia have proven that EPO administration is effective on parameters such as stromal cell-derived factor 1 (SDF-1), brain-derived neurotrophic factor (BDNF mRNA), and neuron-specific enolase (NSE) in brain injury patients. The purpose of this study was to see how EPO affected BDNF mRNA expression, SDF-1 serum levels, and NSE levels in experimental rats with TBI. METHODS: This study was conducted using a rat head injury model. Fifteen rats were randomly assigned to one of three groups: A, B, or C. EPO was administered subcutis with a dose of 30.000 U/kg. Blood samples were taken after brain injury (H0), 12 h (H12), and 24 h (H24) after brain injury. Serum level of SDF-1 and NSE were measured using mRNA BDNF gene expression was measured with Real-Time-PCR, and ELISA. RESULTS: This study found EPO increase BDNF mRNA expression in group C at H-12 (7,92 ± 0.51 vs 6.45 ± 0.33) compared to group B, and at H-24 (9.20 ± 0.56 vs 7.22 ± 0.19); increase SDF-1 levels in group C at H-12 (7,56 ± 0,54) vs 4,62 ± 0,58) compared to group B, and at H-24 (11,32 ± 4,55 vs 2,55 ± 0,70); decrease serum NSE levels in group C at H-12 (17,25 ± 2,02 vs 29,65 ± 2,33) compare to group B and at H-24 (12,14 ± 2,61 vs 37,31 ± 2,76); the values are significantly different with p < 0,05. CONCLUSION: EPO may have neuroprotective and anti-inflammatory properties in TBI by increasing mRNA BDNF expression and serum SDF-1 levels, and decrease serum NSE levels.

Combination of platelet rich plasma and stromal vascular fraction on the level of vascular endothelial growth factor in rat subjects experiencing deep dermal burn injury.

BACKGROUND: The healing process of burns includes coagulation, inflammation, and remodeling. Vascular endothelial growth factor (VEGF) is involved throughout this healing process. Stem cells from the platelet-rich plasma (PRP) with stromal vascular fraction (SVF) can increase concentrations of growth factors, including VEGF. This is expected to accelerate burn healing. The aim of this study was to determine the effect of a combination of PRP and SVF on VEGF levels in a rats model of deep dermal burn wound healing. MATERIALS AND METHODS: This is an experimental research study in rats using a post-test control group design with 4 groups: A) control, B) Vaseline, C) topical PRP and SVF, and D) PRP and SVF injection. Burn wounds were induced according to the modified Guo method. RESULTS: In a rats model of deep dermal wound healing, topical Vaseline significantly increased serum VEGF compared to control. Topical application and injection of stem cells also significantly increased serum VEGF compared to control and Vaseline. The VEGF concentration was significantly higher following injection of PRP and SVF, suggesting that the injection route is more effective at increasing VEGF levels compared to the topical application of stem cells. CONCLUSION: The combination of PRP and SVF, either by injection or topical application, can increase VEGF levels during the healing process from deep dermal burns.

Effects of hyperbaric oxygen therapy on the healing of thermal burns and its relationship with ICAM-1: A case-control study.

BACKGROUND: The damaging effects of thermal burns need to be managed holistically in order to create a suitable environment for wound healing. The purpose of our study was to investigate the effects of hyperbaric oxygen therapy (HBOT) on the healing of thermal burns and its relationship with intercellular adhesion molecule 1 (ICAM-1). METHODS: Twenty patients with thermal burns were randomly divided into two groups: the group to receive HBOT and the control group. Levels of the ICAM-1 mRNA gene and ICAM-1 serum along with the degree of wound epithelialization were examined before and after treatment. Laboratory and physical findings between the groups were compared. RESULTS: In the HBOT group compared with the control group, thermal wound complications were significantly reduced (p = .006), while length of stay in hospital was substantially reduced (p = .001). ICAM-1 serum levels strongly correlated with ICAM-1 mRNA gene expression (R 2 = 0.909, p < .001). The expression of the ICAM-1 mRNA gene (12.32 ± 1.31 vs. 10.79 ± 1.38) and ICAM-1 serum level (231.46 ± 37.20 vs. 158.23 ± 68.30) in patients with at least a 50% burn area exceeded those of patients with a smaller burn area. HBOT significantly decreased (p < .05) the expression of the ICAM-1 mRNA gene and ICAM-1 serum level (p = .004). The number of HBOT sessions strongly correlated with ICAM-1 serum level (p = .043) but poorly correlated with ICAM-1 mRNA gene expression (p = .22). The expression of the gene, however, strongly correlated with ICAM-1 serum level (r = -0.988, p < .001). CONCLUSION: HBOT can reduce thermal wound complications, length of stay in hospitals due to thermal burns, ICAM-1 mRNA gene expression, and ICAM-1 serum level.

The association between metabolic syndrome components, low-grade systemic inflammation and insulin resistance in non-diabetic Indonesian adolescent male.

BACKGROUND AND AIMS: Millions of people in Indonesia have diabetes. The cluster of metabolic abnormalities has long been identified as the risk factors for type 2 diabetes and is now commonly described as metabolic syndrome/MetS. Insulin resistance takes a key role in the process of the MetS and has even been hypothesized as its underlying cause. Clinical and epidemiologic studies also indicate that inflammatory factors might be correlated with IR. Prospective studies have proved that metabolic syndrome grows during childhood/adolescence and progresses to adulthood T2DM. The purpose of this study was to investigate relationships between metabolic syndrome components and low-grade systemic inflammation with insulin resistance in non-diabetic Indonesian adolescent male. METHODS: This was a cross-sectional analysis of non-diabetic adolescent male in Indonesian population (n = 128) aged between 18 and 22 years old. MetS components are based on NCEP ATP III (2004) modification for Asia Pacific population. Marker for low-grade systemic inflammation is hsCRP and insulin resistance was determined by HOMA-IR formula. Relevant measures were anthropometry, blood pressure, fasting insulin, serum glucose, lipid profiles and hsCRP. RESULTS: Of the 128 adolescent male, we found that 16 subjects (12.5%) have central obesity; 3 subjects (2.3%) have hyperglycemia; 26 subjects (20.3%) have low HDL-c; 19 subjects (14.8%) have high triacylglycerol; 45 subjects (35.2%) have hsCRP ≥1.0 mg/dL; 4 subjects (3.1%) have high blood pressure and 39 subjects (30.5%) have insulin resistance. The association of MetS components with the risk of insulin resistance is central obesity and high triacylglycerol with OR of 24.4 (95%CI: 5.19-114.42) and 9.4 (95%CI: 3.09-28.68) consecutively. We also found that low-grade systemic inflammation (hsCRP ≥1.0 mg/dL) was strongly associated with incident of insulin resistance with OR 5.2 (95%CI: 2.31-11.64). Meanwhile, we found that high triacylglycerol level is the solely one of five MetS components which has contribution to the incident of systemic low-grade inflammation with OR 3.9 (95%CI: 1.43-10.92). CONCLUSION: Central obesity and high triacylglycerol level are the important MetS components associated with IR. Systemic low-grade inflammation has been associated with insulin resistance. Identification of obesity, high triacylglycerol and high hsCRP should be focused for prevention of type 2 diabetes in non-diabetic Indonesian adolescent male.