METHODS: A non-blinded, randomised controlled trial will be conducted. A total of sixty-six patients who fulfil the inclusion criteria will be recruited. The participants will be randomly allocated into intervention (traditional Malay massage) and control (relaxation position) groups. Blood and saliva samples will be collected before and immediately after intervention. All collected samples will be analysed. The primary outcomes are the changes in the level of substance P in both saliva and blood samples between both groups. The secondary outcomes include the levels of inflammatory mediators [i.e. TNF-α, IL-1β, IL-8, monocyte chemotactic protein-1, IL-6 and IL-10, and the soluble form of the intercellular adhesion molecule], the pain intensity as measured by a visual analogous scale and functional outcomes using the Roland-Morris Disability Questionnaire.
DISCUSSION: Massage is a type of physical therapy that has been proven to be potentially capable of reducing unpleasant pain sensations by a complex sensory response and chemical mediators such as substance P and various inflammatory mediators. Previous studies conducted using Thai, Swedish, or other forms of massage therapies, have showed inconsistent findings on substance P levels pre and post the interventions. Each massage genre varies in terms of massage and joint mobilization points, as well as the lumbar spinous process. Traditional Malay massage, known locally as "Urut Melayu", involves soft-tissue manipulation of the whole body applied using the hands and fingers. This massage technique combines both deep muscular tissue massage and spiritual rituals. This trial is expected to give rise to new knowledge underlying the mechanisms for pain and inflammation relief that are activated by traditional Malay massage.
TRIAL REGISTRATION: Australian New Zealand Clinical Trials ACTRN12615000537550 .
METHODS: Forty female rats were randomly assigned into five groups (n = 8/group) i.e. non-DM (non-diabetes), DM (diabetes), DM + Propolis (diabetes on propolis orally); DM + Insulin (diabetes on insulin subcutaneously) and DM + Combined (diabetes on propolis and insulin) groups. Propolis and insulin were given at 300 mg/kg/day orally and 5.0 IU/kg/day subcutaneously, respectively, for 4 weeks.
RESULTS: Fasting blood glucose, conception period, implantation losses, foetal blood glucose and placental oxidative stress markers such as malonaldehyde and protein carbonyl were significantly higher while maternal weight gain, foetal body weight and total antioxidant capacity were significantly lower in DM group compared with non-DM group. These changes were significantly improved in rats treated with propolis or insulin alone with greater significant effects in rats treated with both propolis and insulin.
CONCLUSION: This study may suggest the protective effects of propolis against DM-induced impaired pregnancy outcomes and placental oxidative stress with greater effects when combined with insulin.
METHODS: A WEHI-3 cell line was used to evaluate the cytotoxicity of BM by MTT. AO/PI and Hoechst 33342 dyes, Annexin V, multiparametric cytotoxicity 3 by high content screening (HCS); cell cycle tests were used to estimate the features of apoptosis and BM effects. Caspase 3 and 9 activities, ROS, western blot for Bcl2, and Bax were detected to study the mechanism of apoptosis. BALB/c mice injected with WEHI-3 cells were used to assess the apoptotic effect of BM in vivo.
RESULTS: BM suppressed the growth of WEHI-3 cells at an IC50value of 14 ± 3 μg/mL in 24 h. The ROS production was increased inside the cells in the treated doses. Both caspases (9 and 3) were activated in treating WEHI-3 cells at 24, 48 and 72 h. Different signs of apoptosis were detected, such as cell membrane blebbing, DNA segmentation and changes in the asymmetry of the cell membrane. Another action by which BM could inhibit WEHI-3 cells is to restrain the cell cycle at the G1/G0 phase. In the in vivo study, BM reduced the destructive effects of leukaemia on the spleen and liver by inducing apoptosis in leukaemic cells.
CONCLUSION: BM exerts anti-leukaemic properties in vitro and in vivo.
METHODS: Mice were initiated with single dose of 7,12-dimethylbenz[α]anthracene (DMBA) (390 nmol/100 μL) followed by, in subsequent week, repeated promotion (twice weekly; 22 weeks) with 12-O-tetradecanoylphorbol-13-acetate (TPA) (1.7 nmol/100 μL). Annonacin (85 nM) and curcumin (10 mg/kg; reference) were, respectively, applied topically to DMBA/TPA-induced mice 30 min before each TPA application for 22 weeks. Upon termination, histopathological examination of skin, liver and kidney as well as genes and proteins expression analysis were conducted to elucidate the potential mechanism of annonacin.
RESULTS: With comparison to the carcinogen control, Annonacin significantly increased the tumor latency period and reduced the tumor incidence, tumor burden and tumor volume, respectively. In addition, it also suppressed tumorigenesis manifested by significant reduction of hyperkeratosis, dermal papillae and number of keratin pearls on skin tissues. Annonacin also appeared to be non-toxic to liver and kidney. Significant modulation of both AKT, ERK, mTOR, p38, PTEN and Src genes and proteins were also observed in annonacin-targeted signaling pathway(s) against tumorigenesis.
CONCLUSIONS: Collectively, results of this study indicate that annonacin is a potential therapeutic compound targeting tumor promoting stage in skin tumorigenesis by modulating multiple gene and protein in cancer signaling pathways without apparent toxicity.
METHODS: Well diffusion, minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC) assays were used to test antibacterial activity against four pathogenic bacteria namely Staphylococcus aureus, Escherichia coli, Bacillus cereus, and Pseudomonas aeruginosa. DPPH (2, 2-diphenyl-1- picrylhydrazyl) and superoxide dismutase (SOD) assays were used to evaluate antioxidant activity. HPLC and gel filtration were used for purification of the peptides. Scanning electron microscope was applied to investigate the mode of attachment of the peptides on target microbial membranes.
RESULTS: Aqueous extraction of the mixture showed no inhibition zones against all the test bacteria. Mean diameter of inhibition zones for ethanol extraction of this mixture attained 8.33 mm, 7.33 mm, and 6.33 mm against S. aureus at corresponding concentrations of 500, 250 and 125 mg/ml while E .coli showed inhibition zones of 9.33 mm, 8.00 mm and 6.66 mm at the same concentrations. B. cereus exhibited inhibition zones of 11.33 mm, 10.33 mm and 10.00 mm at concentrations of 500, 250 and 125 mg/ml respectively. The peptide extract demonstrated antibacterial activity against S. aureus, E. coli and B. cereus. The MIC and MBC values for ethanol extracts were determined at 125 mg/ml concentration against S. aureus and E. coli and B. cereus value was 31.5 mg/ml. MIC and MBC values showed that the peptide extract was significantly effective at low concentration of the Australian plant mixture (APM). Phenolic compounds were detected in hot aqueous and ethanolic extracts of the plant mixture. Hot aqueous, ethanol and peptides extracts also exhibited antioxidant activities.
CONCLUSIONS: It was concluded that APM possessed good antibacterial and antioxidant activities following extraction with different solvents. The results suggest that APM provide a new source with antibacterial agents and antioxidant activity for nutraceutical or medical applications.