15 research outputs found

    Physicochemical properties of nanostructured lipid carriers as colloidal carrier system stabilized with polysorbate 20 and polysorbate 80

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    Nanostructured lipid carriers (NLC), a colloidal carrier system offer many advantages as drug carrier. Incorporation of liquid lipid can improve the loading capacity of drugs in the NLCs. The NLC20 and NLC80 were produced by high-pressure homogenization technique, stabilized with polysorbate 20 and polysorbate 80, respectively. Transmission electron microscopy showed that these NLCs were spherical. Photon correlation spectroscopy showed that the average size of NLC80 and NLC20 were102.8 ± 0.1 and 261.63 ± 8.56 nm, respectively, and their zeta potentials were -23.93 ± 0.75 and -30.57 ±0.06 mV, respectively. The results suggest that NLC80 is a more stable formulation. X-ray diffractometryand differential scanning calorimetry showed that NCLs were less crystalline than the bulk lipid. The melting point depression of NLC80 was 5.71°C below bulk lipid’s melting point (61.56°C), while NLC20 exhibited two melting points at 54.80 and 59.10°C. These findings suggest that polysorbate 80 was a better dispersing agent for NLC than polysorbate 20. The physicochemistry properties of the NLCs are greatly influenced by the type of surfactant used. The small size and superior particle surface to volume ratio would increase loading efficiency and bioavailability of drugs, thus making NLC a promising drug delivery system.Key words: Nanostructured lipid carriers, colloidal delivery system,   polysorbate 80, polysorbate 20, highpressure homogenization,   physicochemical properties

    Induction of mammary gland tumor in female Sprague- Dawley rats with LA7 cells

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    The current methods for tumor induction in breast cancer research animal models are time-consuming, hazardous, expensive, sometimes irreproducible and inconvenient. We successfully developed a new, simple and cost-effective method in developing solid mammary gland tumor in female Sprague-Dawley rat using LA7 rat mammary tumor cells. Tumors developed in 7- 8 weeks old rats within 6 to 8 days of subcutaneous injection of LA7 cells into the mammary gland pad. Tumor size increased exponentially for four weeks. Histopathology examination confirmed that the induced tumors were adenocarcinomas. Evaluation of blood enzymes showed significantly higher (P < 0.005) serum alkaline phosphatase (ALP) and lactate dehydrogenase (LDH) in tumor-bearing than in normal rats. This LA7 cell-induced rat mammary gland tumor model may be useful for studies in breast cancer drug or nutraceutical research and development

    In Vitro Evaluation of the Effects of Tamoxifen on Prostate Cancer Cells

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    BACKGROUND AND OBJECTIVE: Considering the high prevalence of prostate cancer and the effect of androgens on its progression, this study was conducted to investigate the inhibitory effects of tamoxifen as an anti-androgen on prostate cancer. METHODS: In this experimental study, the human cell line (PC3) was purchased from the Pasteur Institute. The effect of tamoxifen at concentrations of 0, 3.25, 7.5, 15, 30 and 60 μM on cells was evaluated, and the tests of viability, migration, colonization and cell morphological changes were respectively performed using MTT, wound healing, colonization, and giemsa staining methods. FINDINGS: IC50 dosage of tamoxifen of 15 μM with a regression coefficient of 0.90 was obtained within 24 hours. The results showed that tamoxifen significantly inhibited proliferation with 7.3±0.6 colonies compared with 100 colonies of control (p<0.03) and migration with 278.4±1.5 μm groove diameter compared with 89.68 ± 0.9 μm of control (p<0.01) at the dose of 15 μM. Treatment of cells with a dose of 15 μM also causes changes in the nucleus and cytoplasm and causes apoptosis in comparison with the control group. CONCLUSION: The results of this study showed that tamoxifen has significant inhibitory effects on PC3 prostate cell and can be considered as an appropriate way for the treatment of prostate cancer

    Effect of gastric bypass surgery on the oxidative stress status in morbidly obese patients

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    in the present study, the effect of gastric bypass surgery on the oxidative and antioxidant status of morbidly obese people was investigated

    The anti-inflammatory effect of omega-3 polyunsaturated fatty acids dramatically decreases by iron in the hippocampus of diabetic rats

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    Aims: Receptor for advanced glycation end products (RAGE) production is induced by diabetes. Microglial cells are activated by RAGE and produce inflammatory cytokines such as tumor necrosis factor-α (TNF-α) and oxidative stress markers. Persistent production of TNF-α can provide a link between diabetes and Alzheimer's disease (AD). The purpose of this study was to investigate the effect of concomitant use of omega-3 polyunsaturated fatty acids (�-3 PUFAs) with iron supplements on microglial cell activation and inflammatory conditions in the hippocampus of type 2 diabetic rats. Main methods: Diabetic and normal Wistar rats were divided into six groups. Oxidative stress markers (total oxidant status (TOS), total antioxidant capacity (TAC), and malondialdehyde (MDA)), mRNA expression and protein levels of RAGE and TNF-α were evaluated in the hippocampus of the controls and supplemented with ferrous sulfate and �-3 PUFAs alone and together rats. Also, the entry of microglia cells into the hippocampus was evaluated by immunohistochemistry technique. Key findings: Levels of the microglial activation (2.4 fold, p < 0.0001), MDA (84, p < 0.0001) and oxidative stress index (OSI) (11, p = 0.0094), mRNA expression and protein contents of RAGE (1.83 fold and 82 respectively) and TNF-α (2.25 fold and 86 respectively) were strongly influenced by negative effect of iron compared to the group receiving only �-3 PUFAs which was dramatically improved by vitamin E. Significance: These observations indicated that the co-supplementation of ferrous sulfate with �-3 PUFAs decreases the anti-inflammatory ability of �-3 PUFAs in the hippocampus of diabetic rats via RAGE/TNF-α-induced oxidative stress pathway up-regulation. © 2020 Elsevier Inc
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