Strycnos spinosa decreases the blood glucose and lipid levels of diabetic albino rats

Diabetes mellitus has reached epidemic levels with an estimate of 451 million cases worldwide in 2017. Diabetes is a chronic disease that occurs when the pancreas does not produce enough insulin or when the body cannot effectively use the insulin. Strychnos spinosa has been used in folk medicine as a remedy for various diseases including diabetes but the exact mechanism of action is still unknown. The present study aimed to evaluate the hypoglycaemic and hypolipidemic effects of the methanolic extract of the Strychnos spinosa leaves on alloxan-induced diabetic albino rats. Diabetes mellitus was experimentally induced in rats by intraperitoneal injection of alloxan monohydrate at a dose of 150 mg/kg. The pure extract of S. spinosa leaf was given orally once daily for 2 weeks in three graded doses of 150, 300 and 500 mg/kg and glibenclamide was used to treat the positive control group. Following treatments, the glucose level and lipid profile assay were carried out using colorimetric methods. The extracts significantly reduced (p<0.05) the fasting blood glucose, TAG and cholesterol levels of the diabetic and non-diabetic rats. Treatment with the extract also decreased mortalities of the diabetic rats. These findings provides evidence to the increased use of the plant in folk medicine

Nutrient and Anti-Nutritional Composition of Jam Prepared from Pineapple Ananas Comosus

An investigation was conducted to evaluate the nutrient and anti-nutritional composition of jam prepared from Pineapple (Ananas comosus). The result of the proximate analysis indicated that processing caused a reduction in the moisture (30.0 + 0.08) protein content (0.8 + 0.008). However, processing  pineapple to jam caused an increase in the crude lipid (3.4 + 0.26), Carbohydrate (58.6 + 0.30), Ash content (5.0 + 0.8) and crude fibre (2.2 + 0.08). The result obtained for the anti-nutritional factors showed that processing caused a reduction in phytate content (0.67 + 0.004), Tannin (0.19 + 0.004) and Oxalate (8.64 + 0.008). Keywords: Ananas comosus, Processing, Jam, Tannin, Crude Fat, Oxalate

Isolation and Estimation of DNA Level in Coconut Leaf (Coccos Nucifera)

The DNA Level of Coconut leaf was determined using agarose gel electrophoresis and UV-double beam spectrophotometer. 30?g leaf sample was weighed; chemical homogenization using mortar and pestle was done using lyses buffer and “Morning fresh” detergent. Whole sample was centrifuged at 10,000 rpm for 20 minutes; the supernatant was decamped into clean microcentruifuge tubes. Ethanol (500ml) was added and mixed thoroughly and incubated at room temperature for 30 minutes. DNA is insoluble in ethanol and so will appear as white precipitate at the bottom of the tube. Sample was centrifuged at 10,000 rpm for 5 minutes, thereafter the content was exposed to the atmosphere for 10 minutes to rid off remaining solvent (Ethanol). The pellets were dissolved in 50ml of TE (Tris-EDTA) buffer. The DNA (25ml) was taken and diluted in 1.75ml of TE Buffer and absorbance read at 260nm and 280nm with purity of DNA calculated followed by Electrophoresis. 25ml of the DNA sample was taken and ran on 0.8% agarose gel electrophoresis using a standard marker for 60 minutes. The analysis was done in triplicate with the ratio of absorbance at 260 and 280nm (1.79, 1.76 and 1.84) showing the purity of the DNA sample. Keywords: Coccos nucifera, Percentage Purity, DNA Sample, TE Buffer, Agarose Gel Electrophoresis

Clausenidin from Clausena excavata induces apoptosis in hepG2 cells via the mitochondrial pathway

Ethnopharmacological relevance: Clausena excavata Burm.f. is used locally in folk medicine for the treatment of cancer in South East Asia. Aim of the study: To determine the mechanism of action of pure clausenidin crystals in the induction of hepatocellular carcinoma (hepG2) cells apoptosis. Materials and methods: Pure clausenidin was isolated from Clausena excavata Burm.f. and characterized using 1H and 13C NMR spectra. Clausenidin-induced cytotoxicity was determined by MTT assay. The morphology of hepG2 after treatment with clausenidin was determined by fluorescence and Scanning Electron Microscopy. The effect of clausenidin on the apoptotic genes and proteins were determined by real-time qPCR and protein array profiling, respectively. The involvement of the mitochondria in clausenidin-induced apoptosis was investigated using MMP, caspase 3 and 9 assays. Results: Clausenidin induced significant (p<0.05) and dose-dependent apoptosis of hepG2 cells. Cell cycle assay showed that clausenidin induced a G2/M phase arrest, caused mitochondrial membrane depolarization and significantly (p<0.05) increased expression of caspases 3 and 9, which suggest the involvement of the mitochondria in the apoptotic signals. In addition, clausenidin caused decreased expression of the anti-apoptotic protein, Bcl 2 and increased expression of the pro-apoptotic protein, Bax. This finding was confirmed by the downregulation of Bcl-2 gene and upregulation of the Bax gene in the treated hepG2 cells. Conclusion: Clausenidin extracted from Clausena excavata Burm.f. is an anti-hepG2 cell compound as shown by its ability to induce apoptosis through the mitochondrial pathway of apoptosis. Clausenidin can potentially be developed into an anticancer compound

Cytotoxic prenylated xanthone and coumarin derivatives from Malaysian Mesua beccariana

Our recent research on the phytochemical constituents of the stem bark of Mesua beccariana gave one new xanthone, beccarixanthone T (1) and one new coumarin, beccamarin T (2) together with three known xanthones mesuarianone (3), mesuasinone (4), 1,5-dihydroxyxanthone (5) and four known terpenoids, friedelin (6), stigmasterol (7), beta-sitosterol (8) and gamma-sitosterol (9). The structures of these compounds were elucidated and determined using spectroscopic techniques such as NMR and MS. The cytotoxic activities of compounds 1-4 as well as the crude extracts were tested against two cancer cell lines, Hep G2 (liver cancer cell line) and HT-29 (colon cancer cell line) using MTT assays. Mesuarianone (3) gave a significant activity on the HT-29 cell line while mesuasinone (4) gave moderate activity against HT-29 cell line

Carbapenem resistance expressed by Gram-negative bacilli isolated from a cohort of Libyan patients

Background and objectives: Carbapenem-resistant Enterobacteriaceae (CRE) and other Gram-negative bacteria are among the most common pathogens responsible for both community and hospital acquired infection. The global spread of cephalosporinases in Enterobacteriaceae has led to the increased use of carbapenems resulting in the emergence and rapid spread of CRE. This has become an alarming public health concern, yet the condition in Libya remains unclear. The aim of this study was to obtain a better understanding of CRE strains prevalent in Libyan patients by investigating their phenotypic characteristics and antibiograms. Methods: Gram-negative bacterial species were collected from Misrata Central Hospital, Misrata Cancer Centre and Privet Pathology Laboratories. Clinical samples and swabs were obtained from hospitalised and non-hospitalised patients and from mechanical ventilation and suction machines. Patients who had received antibiotic therapy for at least three days prior to the study were excluded. The identification and characterization of the isolated species were achieved using the growth characteristics on MacConkey and blood agar, spot tests and API 20E or API 20NE biochemical testing systems. Screening for carbapenem resistance was performed using the disk diffusion method with carbapenem 10 μg and cephalosporin 30 μg disks and minimum inhibitory concentrations (MIC) determined using the Sensititre Gram-negative Xtra plate format (GNX2F). All strains demonstrating resistance or reduced susceptibility to one of the four carbapenems were subjected to carbapenememase activity detection using the RAPIDEC CARBA NP test, Modified Hodge test and carbapenem inactivation methods. Results: A total of one hundred and forty isolates representing fourteen bacterial species were isolated from 140 non-duplicated specimens. Clinical specimens included urine samples (96/140, 68.57%), sputum (15/140, 10.71%), surgical wound swabs (18/140, 12.85%), foot swabs from diabetes mellitus (DM) patients (6/140, 4.29%), ear swabs (3/140, 2.14%) and wound swabs (2/140, 1.43%). Thirty-four (24.29%) isolates demonstrated resistance to at least one of the four carbapenems with Klebsiella pneumoniae representing 73.53% (25 isolates) of all carbapenem resistant species, followed by 8.82% for Pseudomonas aeruginosa (3 isolates), 5.88% for both Proteus mirabilis (2 isolates) and Escherichia coli (2 isolates) and 2.94% for both Citrobacter koseri (1 isolate) and Rahnella aquatilis (1 isolate). The other isolates were either susceptible or cephalosporinase producers. Conclusion: This study has revealed the high rate of carbapenem resistance amongst Libyan patients and emphasizes the crucial need for accurate screening, identification and susceptibility testing to prevent further spread of nosocomial and community acquired resistance. This may be achieved through the establishment of antibiotic stewardship programmes along with firm infection control practices.National Research Foundation of South Africa; Libyan GovernmentWeb of Scienc

An in silico approach in predicting the possible mechanism involving restoration of wild-type p53 functions by small molecular weight compounds in tumor cells expressing R273H mutant p53

R273H mutant p53 is a DNA-contact mutant that renders p53 dysfunctional due to a single substitution of Arg273 for His273. Rescuing R273 mutant p53 implies that a competent molecule would have to bind to the site of DNA-contact hot spots to complement the loss of contact with the DNA-binding domain. Here, curcumin, flavokawain B, and alpinetin were docked against the crystal structure of R273H mutant p53 in silico. Consequently, all the compounds bind to the cavity of R273H mutant p53 with a dissociation constant estimated to have 36.57, 70.77, and 75.11 μM for curcumin, flavokawain B, and alpinetin, respectively. Subsequently, each molecule was able to bind to the R273H mutant p53 by interacting with the DNA-contact hot spot Arg248 and mutant R273H, thereby compensating for the loss of direct contact with the DNA-binding domain. Furthermore, all the molecules were able to induce a direct contact with the consensus site of the DNA binding domain, thus maintaining DNA-contact residues with the DNA. The present findings offer reliminary indirect supporting evidence that small molecular weight compounds may certainly rescue DNA-contact mutant p53, which may lay a foundation for designing a competent and effective molecule capable of rescuing mutant p53 in tumor cells expressing R273H mutant p53

Clausenidin induces caspase-dependent apoptosis in colon cancer

Background: Clausena excavata burm.f. Is a shrub traditionally used to treat cancer patients in asia. The main bioactive chemical components of the plant are alkaloids and coumarins. In this study, we isolated clausenidin from the roots of c. Excavata to determine its apoptotic effect on the colon cancer (ht-29) cell line. Method: We examined the effect of clausenidin on cell viability, ros generation, dna fragmentation, mitochondrial membrane potential in ht-29 cells. Ultrastructural analysis was conducted for morphological evidence of apoptosis in the treated ht-29 cells. In addition, we also evaluated the effect of clausenidin treatment on the expression of caspase 3 and 9 genes and proteins in ht-29 cells. Result: Clausenidin induced a g0/g1 cell cycle arrest in ht-29 cells with significant (p < 0.05) dose-dependent increase in apoptotic cell population. The dna fragmentation assay also showed apoptotic features in the clausenidin-treated ht-29 cells. Clausenidin treatment had caused significant (p < 0.05) increases in the expression of caspase 9 protein and gene in ht-29 cells and mitochondrial ros and mitochondrial membrane depolarization. The results suggest the involvement of the mitochondria in the caspase-dependent apoptosis in clausenidin-treated colon cancer cells. Conclusion: Clausenidin induces a caspase-dependent apoptosis in colon cancers through the stimulation of the mitochondria. The study demonstrates the potential of clausenidin for use in the treatment of colon cancers