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The ribosome-inactivating proteins gelonin, Momordica charantia inhibitor, pokeweed antiviral protein, and one from Saponaria officinalis were enclosed in human erythrocyte ghosts. The proteins once trapped in ghosts and fused with CHO cells inhibited colony formation at concentrations of approximately 1 ng/ml (3 X 10(-11) M), whereas the free proteins only had an effect at concentrations of greater than 1 microgram/ml.
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This study investigated the beneficial effects and mechanism of action of the juice of Momordica charantia in streptozotocin (STZ)-induced diabetes mellitus in rats. Diabetes mellitus was associated with significant (p < 0.01) time course reductions in body weight, plasma insulin and the number of insulin positive cells per islet and significant (p < 0.01) time course elevation in blood glucose and osmolarity and systolic blood pressure compared to age-matched healthy controls. Oral intake of M. charantia juice by STZ-induced diabetic rats partially reversed all the diabetes-induced effects measured. Daily oral administration of M. charantia juice to STZ-induced diabetic rates significantly (p < 0.01) reduced the Na+- and K+-dependent absorptions of glucose by the brush border membrane vesicles of the jejunum compared to the responses obtained in STZ-induced diabetic rat. Either insulin (100 MM) or the fruit juice lyophilised extract (5 microg x ml(-1)) can stimulate 14C-D-glucose uptake in L6 myotubes. These effects were completely blocked by wortmannin, an inhibitor of phosphatidylinositol 3-kinase. High concentrations (10-200 microg x ml(-1)) of M. charantia juice extract inhibited 14C-D-glucose uptake in L6 myotubes compared to the control response. The effect of M. charantia treatment was also investigated on myelinated fibre abnormalities in the tibial nerve of STZ-induced diabetic and control rats. The results show that diabetes was associated with significant (p < 0.05) reduction in the mean cross-sectional myelinated nerve fibres, axonal area, myelin area and maximal fibre area compared to end controls. Treatment of STZ-induced diabetic rats with M. charantia juice normalised the structural abnormalities of peripheral nerves. The results indicate that M. charantia can exert marked beneficial effects in diabetic rats, and moreover, it can regulate glucose uptake into jejunum membrane brush border vesicles and stimulate glucose uptake into skeletal muscle cells similar to the response obtained with insulin.
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Bitter melon ( Momordica charantia Linnaeus) fruit extract was tested against 3,4 benzo(a)pyrene [B(a)P] induced forestomach papillomagenesis in Swiss albino mice. Extract of M. charantia in two concentrations, 2.5 and 5% of standard mice feed was used for the short-term and long-term studies. A significant decrease in tumour burden was observed in short and long-term treatment. Also, total tumour incidence reduced to 83.33% with 2.5% dose and 90.90% with 5% dose in short term treatment, while in long-term treatment tumor incidence decreased to 76.92% with 2.5% dose and 69.23% with 5% dose of M. charantia. The possible mechanism involved in the cancer chemoprevention has also been discussed.
Seven plant isolates exhibited significant survivability in host. The drug TP22C thus formulated showed 86% survivability in host. The surviving shrimps were nested PCR negative at the end of the 15 d experimentation. The lowest concentration of TP22C required intramuscularly for virucidal property was 10 mg/mL. The oral dosage of 750 mg/kg body weight/day survived at the rate of 86%. Neither VP28 nor ie 1 was expressed in the test samples at 42nd hour and 84th hour post viral infection.
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All primary nasopharyngeal carcinoma (NPC) tumors contain hypoxic regions which are implicated in decreased local control and increased distant metastases, as well as resistance to chemotherapy in advanced NPC patients. One of the promising therapeutic approaches for NPC is to use drugs that can target hypoxic factors in tumors. In the present investigation, the type I ribosome inactivating protein α-momorcharin (α-MMC), isolated from seeds of the bitter gourd Momordica charantia, reduced cell viability and inhibited clonogenic formation of human NPC CNE2 and HONE1 cells under normoxia and cobalt chloride-induced hypoxia. By comparison, α-MMC exhibited only slight cytotoxicity on human nasopharyngeal epithelial NP69 cells under normoxia. Interestingly, α-MMC suppressed the expression levels of hypoxia-inducible factor 1-alpha (HIF1α) and vascular endothelial growth factor (VEGF) in hypoxic NPC, as well as the growth of human umbilical vein endothelial cells. Further study disclosed that α-MMC targeted endoplasmic reticulum and down-regulated unfolded protein response (UPR) in NPC cells. Moreover, α-MMC induced apoptosis in NPC cells in a dose- and time-dependent manner. It initiated mitochondrial- and death receptor-mediated apoptotic signaling in CNE2 cells, but there was hardly any effect on HONE1 cells. In addition, α-MMC brought about G0/G1 phase cell cycle arrest in CNE2 cells and S phase arrest in HONE1 cells. Collectively, α-MMC preferentially exhibited inhibitory effect on normoxic and hypoxic NPC cells partly by blocking survival signaling (e.g. HIF1α, VEGF and UPR), and triggering apoptotic pathways mediated by mitochondria or death receptor. These observations indicate the potential utility of α-MMC for prophylaxis and therapy of NPC.
Effective doses of the Momordica charantia fruit pulp (MCF) ethanolic extract on pancreatic β-cells modulation in neonatally streptozotocin-induced type 2 diabetic rats were studied. Diabetic rats (n=8) were treated with MCF extract (400 mg kg(-1) day(-1)) or glibenclamide (5 mg kg(-1)) for 28 days. Control rats (n=11) and untreated diabetic rats (n=8) received only water. Fasting glucose, serum insulin (by ELISA) and β-cell function (HOMA %B by homeostasis model assessment) were measured. β- and α-cells were identified by immunostaining, nuclei by DAPI, and β-cell size and number by morphometry. Significant improvement of fasting blood glucose, serum insulin and β-cell function was observed with the MCF extract for the diabetic rat model. The islet size, total β-cell area and number of β-cells were increased to almost double in the diabetic rats treated with MCF extract as compared to the untreated diabetic rats. The number of α-cells did not change significantly. Insulin granules in β-cells were notably reduced in diabetic islets as compared to control islets. However, extract-treated diabetic rat β-cells were abundant with insulin granules, which was comparable to non-diabetic control islets. The modulation of pancreatic β-cells may be involved in the experimental observation of anti-diabetic effects of M. charantia extract.
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The anti-ulcerogenic effect of the oily extract of Momordica charantia fruits was investigated in male Sprague-Dawley rats. Animals were separated into six groups. Distilled water (control group), famotidine (40 mg/kg), oily extracts (5 and 10 ml/kg), and vehicles (olive oil -5 and 10 ml/kg) were given orally (gavage). Thirty minutes later indomethacin (25 mg/kg) was administrated to all the groups. Six hours later, animals were killed with decapitation. For each stomach, ulcerated and total areas were measured (mm2). The ulcer indexes for each stomach and the ulcer inhibition rates for each group were calculated, after which the stomachs were evaluated pathologically (polymorphonuclear leukocytes infiltration).
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The polysaccharide extract of Momordica charantia has various biological activities; however, its effect on endothelial dysfunction in myocardial infarction remains unclear. To elucidate this, myocardial infarction was induced in rats using isoproterenol (ISP). Pretreatment with M. charantia polysaccharides (MCP; 150 or 300mg/kg) for 25days significantly inhibited increases in heart weight, the heart-weight-to-body-weight ratio, and infarction size, and ameliorated the increased serum levels of aspartate transaminase, creatine kinase, lactate dehydrogenase, total cholesterol, triglycerides, very-low-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol. In addition, MCP enhanced the activity of superoxide dismutase, catalase, and non-protein sulfhydryls, and decreased the level of lipid peroxidation. Moreover, MCP pretreatment downregulated the expression of proinflammatory cytokines (tumor necrosis factor alpha, interleukin (IL)-6, and IL-10), inflammatory markers (nitric oxide, myeloperoxidase, and inducible nitric oxide synthase), and apoptotic markers (caspase-3 and BAX), and upregulated Bcl-2 expression. Pretreatment with MCP reduced myonecrosis, edema, and inflammatory cell infiltration, and restored cardiomyocytes architecture. This myocardial protective effect could be related to the enhancement of the antioxidant defense system through the nuclear factor kappa B (NF-kB) pathways, and to anti-apoptosis through regulation of Bax, caspase-3, and Bcl-2.
According to the World Health Organization malaria is one of the major public health problems in Brazil and all over developing countries, where 80% of the population use traditional medicine to solve their primary medical problems. Both treatment and control of this parasitosis have become difficult, because of parasite strains that are resistant to conventional drugs, such as chloroquine. That makes the search for new antimalarial drugs not only important but urgent. We aimed therefore at evaluating the effects of Momordica charantia L. (Cucurbitaceae) in mice infected with Plasmodium berghei. We used aquose and ethanotic extracts in a dose of 1000 mg/kg of body weight, orally, for five consecutive days (i.e. from day 2 to day 6 postinfection). We then followed up the parasitaemia during the course of infection. Although the population use this plant as an antimalarial, in our experimental conditions, M. charantia extracts have not shown such activity.
The structures of nine independent crystals of bitter gourd seed lectin (BGSL), a non-toxic homologue of type II RIPs, and its sugar complexes have been determined. The four-chain, two-fold symmetric, protein is made up of two identical two-chain modules, each consisting of a catalytic chain and a lectin chain, connected by a disulphide bridge. The lectin chain is made up of two domains. Each domain carries a carbohydrate binding site in type II RIPs of known structure. BGSL has a sugar binding site only on one domain, thus impairing its interaction at the cell surface. The adenine binding site in the catalytic chain is defective. Thus, defects in sugar binding as well as adenine binding appear to contribute to the non-toxicity of the lectin. The plasticity of the molecule is mainly caused by the presence of two possible well defined conformations of a surface loop in the lectin chain. One of them is chosen in the sugar complexes, in a case of conformational selection, as the chosen conformation facilitates an additional interaction with the sugar, involving an arginyl residue in the loop. The N-glycosylation of the lectin involves a plant-specific glycan while that in toxic type II RIPs of known structure involves a glycan which is animal as well as plant specific.
Since antiquity bitter melon has been in use for treating diabetes but clinical trials show conflicting results about its usefulness. The present study aims to asses and compare the hypoglycemic and antiatherogenic effects as well as the safety of two different doses of bitter melon with glibenclamide.
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Our data show that the natural compound MCL manifests antitumor activities towards HCC and therefore suggest MCL as a promising chemotherapeutic agent.