The purpose of this study is to investigate the effectiveness of Ficus deltoidea (F. deltoidea) as an antioral ulcer on animal models. Adult male Sprague Dawley rats were sedated with Nembutal through intraperitoneal route; oral ulcer models were made by applying 99.5% of glacial acetic acid moistened paper disc on rat buccal mucosa. Four groups of these rats were treated respectively with: no treatment (group 1: negative control); Triamcinolone acetonide (group 2: positive control); 250 mg kg-1 F. deltoidea extract (group 3: experimental); 500 mg kg-1 F. deltoidea extract (group 4: experimental) for 10 consecutive days, respectively. On days 2, 4, 6, 8 and 10, the ulcers size was assessed. Data was analysed statistically by using SPSS. The negative control rats exhibited buccal mucosa injury whereas treatment with F. deltoidea and Triamcinolone acetonide resulted in significantly reduced size of oral ulcer. The percentage of inhibitory area of oral ulcer was more prominent in 500 mg kg-1 F. deltoidea extract than 250 mg kg-1. Meanwhile, in vivo study showed that F. deltoidea extract not toxic up to 1000 mg kg-1. The present findings suggest that F. deltoidea extract effectively accelerates oral ulcer healing process, and could therefore be developed as a therapeutic agent for healing oral ulcer.
Studies have found the association between hypercholesterolemia with oxidative stress and atherogenesis. Atherosclerosis has become one of the leading causes of mortality among industrial countries due to abnormal cholesterol metabolism, inflammation of arterial wall and build-up of atherosclerotic plaque. This disease has been recently linked with alpha lipoic acid (ALA), a mitochondrial compound with antioxidative effects in water- and fat-soluble mediums, in both oxidized and reduced forms: lipoic acid (LA) and dihydrolipoic acid (DHLA), respectively. This article provides a comprehensive review of the development and progression of atherosclerosis and the roles and regulations of ALA as a potent antioxidant against atherosclerosis.
The objective of this research is to investigate the regulation of apoptotic associated-genes and proteins expression of aloe emodin on oestrogen receptor (ER)-positive (MCF-7). Oestrogen receptor (ER)-positive (MCF-7) cells were cultured in complete RPMI media. Cells were treated with aloe emodin at its IC50 of 80uM. Maximum treatment time was set for 72 hours in all assays. Both genes and proteins involved in the regulation of apoptosis (Fas, FADD, Caspase-3, Caspase-8, Caspase-9, Bax, Bcl-2, and Cytochrome c) in aloe emodin-treated MCF-7 were determined using Quantigene 2.0 Plex and protein ELISA assays respectively. Aloe emodin, previously reported as anti-cancer agent, was found to act as an apoptotic inducer on MCF-7 cells. In intrinsic apoptosis signalling, Bax, Cytochrome c and Caspase-9 proteins were upregulated (54.11% ± 4.51, 25.17% ± 4.13 and 36.05% ±11.75); while no change was observed in Bcl-2 protein. Except for Caspase-9, these results are in accordance with gene expression. In extrinsic apoptosis, Fas and Caspase-8 were upregulated (133.82% ± 2.85 and 26.44% ± 2.48), contrary to gene expression. These findings indicate that aloe emodin activates both extrinsic and intrinsic apoptosis pathways. The data suggests (i) aloe emodin has the potential to be a selective apoptotic inducer in ER+-breast cancer management; and (ii) the present study could be used as a basis for in vivo experiment.
Two-third of breast cancer patients expressed estrogen receptors (ER)s and received endocrine treatment with established anti-estrogens such as tamoxifen. But the action and acquired resistance during treatment are largely unknown. In contrary, phytochemicals are more selective and less cytotoxic to normal cells. Accordingly, we found aloe emodin, an anthraquinone to inhibit the proliferation of ER+-breast cancer cells, MCF-7 with IC50 of 80 µM, but not affecting control breast cells, MCF-10A. Tamoxifen was non-selective to both cells with IC50 of 27 and 38 μM, respectively. Thus, we aimed to investigate the anti-proliferative mechanism of aloe emodin on MCF-7 and its underlying signalling compared to tamoxifen. Cells were treated separately with aloe emodin and tamoxifen at respective IC50 for 72 h. Apoptosis was determined using Annexin V-FITC/PI staining. The expression of insulin-like growth factor-1 receptor (IGF-1R), insulin like growth factor binding protein (IGFBP)-2 and B-raf gene was investigated using QuantiGene 2.0 Plex assay. Pairedstudent t-test and ANOVA test were used to compare between untreated and treated cells on the measured parameters. Each treatment was conducted in triplicate and repeated three times. Significance was set at p<0.05. The presences of early and late apoptosis in MCF-7 were seen in both treatments. All target genes were down regulated. The anti-proliferation effect of aloe emodin on MCF-7 is similar with tamoxifen which mediates inhibition of IGF-1R signalling pathway. This suggests aloe emodin as a potential anti-cancer agent to be used in combined anti-estrogen therapy to enhance its efficacy in ER+-breast cancer treatment.