METHODS: Purification and structure elucidation were carried out by chromatographic and spectroscopic techniques, respectively. MTT and trypan blue exclusion methods were performed to study the cytotoxic activity. Antibacterial activity was conducted by disc diffusion and microdilution methods, whereas antioxidant activities were done by ferric thiocyanate method and DPPH radical scavenging.

RESULTS: The phytochemical study led to the isolation of α,β-mangostin and cycloart-24-en-3β-ol. α-Mangostin exhibited cytotoxic activity against HSC-3 cells with an IC(50) of 0.33 μM. β- and α-mangostin showed activity against K562 cells with IC(50) of 0.40 μM and 0.48 μM, respectively. α-Mangostin was active against Gram-positive bacteria, Staphylococcus aureus (S. aureus) and Bacillus anthracis (B. anthracis) with inhibition zone and MIC value of (19 mm; 0.025 mg/mL) and (20 mm; 0.013 mg/mL), respectively. In antioxidant assay, α-mangostin exhibited activity as an inhibitor of lipid peroxidation.

METHODS: Observing anti-urolithiathic activity via in vitro nucleation and aggregation assay using a spectrophotometer followed by microscopic observation. A total of 12 methanolic extracts were tested to determine the potential extracts in anti-urolithiasis activities. Cystone was used as a positive control.

RESULTS: The results manifested an inhibition of nucleation activity (0.11 ± 2.32% to 55.39 ± 1.01%) and an aggregation activity (4.34 ± 0.68% to 58.78 ± 1.81%) at 360 min of incubation time. The highest inhibition percentage in nucleation assay was obtained by the Musa acuminate x balbiciana Colla cv "Awak Legor" methanolic pseudo-stem extract (2D) which was 55.39 ± 1.01%at 60 min of incubation time compared to the cystone at 30.87 ± 0.74%. On the other hand,the Musa acuminate x balbiciana Colla cv "Awak Legor" methanolic bagasse extract (3D) had the highest inhibition percentage in the aggregation assay incubated at 360 min which was obtained at 58.78 ± 1.8%; 5.53% higher than the cystone (53.25%).The microscopic image showed a great reduction in the calcium oxalate (CaOx) crystals formation and the size of crystals in 2D and 3D extracts, respectively, as compared to negative control.

METHODS: Release of interleukin (IL)-1β and tumor necrosis factor (TNF)-α, and production of prostaglandin E2 (PGE2) were determined by using enzyme-linked immunosorbent assay (ELISA). Immunoblot technique was executed to determine the activation of MAPKs molecules, NF-κB, PI3K-Akt and cyclooxygenase-2 (COX-2) protein. Determination of pro-inflammatory cytokines and COX-2 relative gene expression levels was by performing the real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR). A reversed-phase HPLC method was developed and validated to standardize the T. crispa extract and chemical profiling of its secondary metabolites was performed by LC-MS/MS.

RESULTS: Qualitative and quantitative analyses of chromatographic data indicated that syringin and magnoflorine were found as the major components of the extract. T. crispa-treatment prompted activation of NF-κB by enhancing IKKα/β and NF-κB (p65) phosphorylation, and degradation of IκBα. The extract upregulated COX-2 protein expression, release of pro-inflammatory mediators and MAPKs (ERK, p38 and JNK) phosphorylation as well as Akt dose-dependently. T. crispa extract also upregulated the upstream signaling adaptor molecules, toll-like receptor 4 (TLR4) and MyD88. T. crispa-treatment also upregulated the pro-inflammatory markers mRNA expression.

METHODS: The antinociceptive potential of orally administered PECN (100, 250, 500 mg/kg) was studied using the abdominal constriction-, hot plate- and formalin-induced paw licking-test in mice (n = 6). The effect of PECN on locomotor activity was also evaluated using the rota rod assay. The role of opioid receptors was determined by pre-challenging 500 mg/kg PECN (p.o.) with antagonist of opioid receptor subtypes, namely β-funaltrexamine (β-FNA; 10 mg/kg; a μ-opioid antagonist), naltrindole (NALT; 1 mg/kg; a δ-opioid antagonist) or nor-binaltorphimine (nor-BNI; 1 mg/kg; a κ-opioid antagonist) followed by subjection to the abdominal constriction test. In addition, the role of L-arg/NO/cGMP pathway was determined by prechallenging 500 mg/kg PECN (p.o.) with L-arg (20 mg/kg; a NO precursor), 1H-[1, 2, 4] oxadiazolo [4,3-a]quinoxalin-1-one (ODQ; 2 mg/kg; a specific soluble guanylyl cyclase inhibitor), or the combinations thereof (L-arg + ODQ) for 5 mins before subjection to the abdominal constriction test. PECN was also subjected to phytoconstituents analyses.

RESULTS: PECN significantly (p  0.05) affect the locomotor activity of treated mice. The antinociceptive activity of PECN was significantly (p  0.05) affected by ODQ. HPLC analysis revealed the presence of at least cinnamic acid in PECN.

OBJECTIVE: This study aimed to investigate the effect of turmeric (20mg/kg) on learning and memory and cholinergic system in a mouse model of stress along with cholinergic blockade.

METHODS: Restrained stress was induced and cholinergic receptors were blocked using scopolamine in mice. Animals were treated with turmeric (turmeric rhizome powder which was also subjected to NMR analyses) and learning and social behavior was examined. Effect of turmeric on cholinergic muscarinic receptors (mAChR; M1, M3 and M5) gene expression was assessed by RT-PCR in both pre-frontal cortex and hippocampus.

RESULTS: Ar-turmerone, curcuminoids and α-linolenic acid were the lead compounds present in turmeric extract. Increased serum corticosterone levels were observed in stressed mice when compared to the control group, while turmeric treatment significantly reduced serum corticosterone level. Turmeric treatment caused an improved learning and memory in Morris water maze test in stressed animals. Social novelty preference was also restored in turmeric treated animals. Following turmeric treatment, M5 expression was improved in the cortex and M3 expression was improved in the hippocampus of stress + scopolamine + turmeric treated group.