Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Inhibitory effect of a bitter melon extract on the P-glycoprotein activity in intestinal Caco-2 cells.

ABSTRACT: Extracts of bitter melon, soybean, dokudami and welsh onion by 40% methanol increased the accumulation of rhodamine-123 by Caco-2 cells, suggesting that these extracts inhibited P-glycoprotein (P-gp). The extract of bitter melon was separated in a tC18 cartridge column and the eluate from 80% acetonitrile most markedly increased the [(3)H]-daunomycin accumulation by Caco-2 cells. The inhibitory compounds in the bitter melon fraction were isolated by HPLC with Pegasil C4 and Pegasil ODS columns. The HPLC fraction having the highest activity was analyzed by (1)H-NMR and FAB-MS, and the active compound was identified as 1-monopalmitin. The inhibitory activities of 1-monopalmitin and its related compounds suggested that the inhibition of P-gp activity was not dependent on the degree of unsaturation of fatty acid in the monoglyceride, but on the chain length. It was also suggested that the monoglyceride structure played an important role in the inhibition of P-gp activity. Monoglycerides could therefore alter the pharmacokinetics of drugs by inhibiting the P-gp-mediated efflux.

SUBMITTER: Konishi T

PROVIDER: S-EPMC1575343 | biostudies-other | 2004 Oct

REPOSITORIES: biostudies-other

ACCESS DATA

Json Xml

Similar Datasets

Anticancer Activity of Bitter Melon-Derived Vesicles Extract against Breast Cancer.

Project description:Due to their low immunogenicity, high biocompatibility and ready availability in large quantities, plant-derived vesicles extracts have attracted considerable interest as a novel nanomaterial in tumor therapy. Bitter melon, a medicinal and edible plant, has been reported to exhibit excellent antitumor effects. It is well-documented that breast cancer gravely endangers women's health, and more effective therapeutic agents must be urgently explored. Therefore, we investigated whether bitter melon-derived vesicles extract (BMVE) has antitumor activity against breast cancer. Ultracentrifugation was used to isolate BMVE with a typical "cup-shaped" structure and an average size of approximately 147 nm from bitter melon juice. The experimental outcomes indicate that 4T1 breast cancer cells could efficiently internalize BMVE, which shows apparent anti-proliferative and migration-inhibiting effects. In addition, BMVE also possesses apoptosis-inducing effects on breast cancer cells, which were achieved by stimulating the production of reactive oxygen species (ROS) and disrupting mitochondrial function. Furthermore, BMVE could dramatically inhibit tumor growth in vivo with negligible adverse effects. In conclusion, BMVE exhibits a pronounced antitumor effect on 4T1 breast cancer cells, which has great potential for use in tumor therapy.

| S-EPMC10047160 | biostudies-literature

Bitter Melon Seed Extract does not Alter Photoperiodic Effects on Reproduction of Male Golden Hamsters.

Project description:Bitter melon (Momordica charantia, MC) has been used in traditional Korean medicine in treating diabetes. In addition, some reports were emerged, showing the antifertility activities of MC in mammals. We investigated the effects of ethanolic MC extract on the reproductive activity of golden hamsters whose spermatogenetic capacity is controlled by their photoperiods. The animals were divided into 4 groups: long photoperiod (LP) control, short photoperiod (SP) control, and LP animals treated with MC. The animals were orally ingested with low (0.03 g/kg) or high (0.15 g/kg) concentrations of the ethanolic extracts for 8 weeks on the daily basis. The control animals received the vehicle. The animals were then mated with age-matched females, experienced pregnancy. As results, the LP control animals showed active large testes but SP control animals displayed remarkably reduced testes. The animals treated with both concentrations of MC extracts demonstrated large testes, indicating fertile activity as animals in LP. LP control animals had litters as expected, but SP controls had no litters at all. MC extract showed the same results as LP animals in generating offsprings. These results suggest that the MC extract does not change the photoperiodic influence on reproductive activity of male golden hamsters.

| S-EPMC5532313 | biostudies-other

Immunomodulatory role of bitter melon extract in inhibition of head and neck squamous cell carcinoma growth.

Project description:Head and neck squamous cell carcinoma (HNSCC) is the sixth most common cancer and leading cause of cancer related mortality worldwide. Despite the advancement in treatment procedures the overall survival rate of patients has not considerably enhanced in the past few decades. Therefore, new strategies to achieve a favorable response for the improvement in the prognosis of HNSCC are urgently needed. In this study, we examined the role of bitter melon extract (BME) in HNSCC tumor microenvironment. Mouse head and neck cancer (SCCVII) cells were subcutaneously injected into the flanks of syngeneic mice. We observed that oral gavage of BME significantly inhibits the tumor growth in mice as compared to control group. Further study suggested that BME inhibits cell proliferation as evident from low expression of proliferating cell nuclear antigen (PCNA) and c-Myc in the tumors of BME fed mice as compared to that of control group. We next investigated the role of BME as an immunomodulator in HNSCC model. Forkhead box protein P3+ (FoxP3+) T cells suppress tumor immunity. Our data suggested that BME treatment decreases the infiltrating regulatory T (Treg) cells by inhibiting FoxP3+ populations in the tumors and in spleens. Additionally, BME treatment reduces Th17 cell population in the tumor. However, BME treatment did not alter Th1 and Th2 cell populations. Together, our findings offer a new insight into how bitter melon extract inhibits head and neck tumor growth by modulating cell proliferation and Treg populations, with implications for how to control tumor-infiltrating lymphocytes and tumor progression.

| S-EPMC5078086 | biostudies-other

Evaluation of acute and sub-chronic toxicity of bitter melon seed extract in Wistar rats.

Project description:Pharmacological studies have revealed the potential antidiabetic effects of bitter melon seeds (Momordica charantia) in animals and humans. However, the sub-chronic safety of bitter melon seeds remains elusive. This exploratory study aimed to assess the acute and sub-chronic toxicity of a bitter melon seed extract from supercritical carbon dioxide (scCO2) extraction in Wistar rats based on the Organization for Economic Co-operation and Development (OECD) guidelines No. 423 and 408. No mortality and toxicity were observed in rats treated with a single dose of the extract during the 14-day observation period. The median lethal dose (LD50) of the extract was considered greater than 2000 mg/kg body weight (BW). For the sub-chronic toxicity study, male and female rats were orally administered daily doses of 0, 250, 500, and 1000 mg/kg BW for 90 days. No mortality, morbidity, and abnormal pathological and biochemical alterations were observed. The no-observed-adverse-effect-level (NOAEL) of the bitter melon seed extract was greater than 1000 mg/kg BW. Accordingly, bitter melon seed extract from scCO2 extraction may be considered a non-toxic dietary ingredient.

| S-EPMC9742884 | biostudies-literature

Bitter Melon (Momordica charantia) Extract Inhibits Tumorigenicity and Overcomes Cisplatin-Resistance in Ovarian Cancer Cells Through Targeting AMPK Signaling Cascade.

Project description:UnlabelledObjective Acquired chemoresistance is a major obstacle in the clinical management of ovarian cancer. Therefore, searching for alternative therapeutic modalities is urgently needed. Bitter melon (Momordica charantia) is a traditional dietary fruit, but its extract also shows potential medicinal values in human diabetes and cancers. Here, we sought to investigate the extract of bitter melon (BME) in antitumorigenic and cisplatin-induced cytotoxicity in ovarian cancer cells.MethodsThree varieties of bitter melon were used to prepare the BME. Ovarian cancer cell lines, human immortalized epithelial ovarian cells (HOSEs), and nude mice were used to evaluate the cell cytotoxicity, cisplatin resistance, and tumor inhibitory effect of BME. The molecular mechanism of BME was examined by Western blotting.ResultsCotreatment with BME and cisplatin markedly attenuated tumor growth in vitro and in vivo in a mouse xenograft model, whereas there was no observable toxicity in HOSEs or in nude mice in vivo Interestingly, the antitumorigenic effects of BME varied with different varieties of bitter melon, suggesting that the amount of antitumorigenic substances may vary. Studies of the molecular mechanism demonstrated that BME activates AMP-activated protein kinase (AMPK) in an AMP-independent but CaMKK (Ca(2+)/calmodulin-dependent protein kinase)-dependent manner, exerting anticancer effects through activation of AMPK and suppression of the mTOR/p70S6K and/or the AKT/ERK/FOXM1 (Forkhead Box M1) signaling cascade.ConclusionBME functions as a natural AMPK activator in the inhibition of ovarian cancer cell growth and might be useful as a supplement to improve the efficacy of cisplatin-based chemotherapy in ovarian cancer.

| S-EPMC5689379 | biostudies-literature

Extra Virgin Olive Oil Phenolic Extract on Human Hepatic HepG2 and Intestinal Caco-2 Cells: Assessment of the Antioxidant Activity and Intestinal Trans-Epithelial Transport.

Project description:In the framework of research aimed at promoting the nutraceutical properties of the phenolic extract (BUO) obtained from an extra virgin olive oil of the Frantoio cultivar cultivated in Tuscany (Italy), with a high total phenols content, this study provides a comprehensive characterization of its antioxidant properties, both in vitro by Trolox equivalent antioxidant capacity, oxygen radical absorbance capacity, ferric reducing antioxidant power, and 2,2-diphenyl-1-picrylhydrazyl assays, and at the cellular level in human hepatic HepG2 and human intestinal Caco-2 cells. Notably, in both cell systems, after H2O2 induced oxidative stress, the BUO extract reduced reactive oxygen species, lipid peroxidation, and NO overproduction via modulation of inducible nitric oxide synthase protein levels. In parallel, the intestinal transport of the different phenolic components of the BUO phytocomplex was assayed on differentiated Caco-2 cells, a well-established model of mature enterocytes. The novelty of our study lies in having investigated the antioxidant effects of a complex pool of phenolic compounds in an extra virgin olive oil (EVOO) extract, using either in vitro assays or liver and intestinal cell models, rather than the effects of single phenols, such as hydroxytyrosol or oleuropein. Finally, the selective trans-epithelial transport of some oleuropein derivatives was observed for the first time in differentiated Caco-2 cells.

| S-EPMC7829860 | biostudies-literature

Bitter melon extract attenuating hepatic steatosis may be mediated by FGF21 and AMPK/Sirt1 signaling in mice.

Project description:We sought to evaluate the effects of Momordica charantia (bitter melon, BM) extract on insulin sensitivity, NAFLD, hepatic FGF21 and AMPK signaling in mice fed a high-fat diet. Male C57/B6 mice were randomly divided into HFD and HFD supplementation with BM for 12 week. Body weight, plasma glucose, FGF21 and insulin levels, hepatic FGF21 and AMPK signaling proteins were measured. The results showed that plasma FGF21 and insulin concentrations were significantly decreased and hepatic FGF21 content was significantly down-regulated, while FGF receptors 1, 3 and 4 (FGFR1, FGFR3 and FGFR4) were greatly up-regulated in BM group compared to the HFD group (P < 0.05 and P < 0.01). BM also significantly increased hepatic AMPK p, AMPK α1 AMPK α2 and Sirt1 content compared to the HFD mice. We, for the first time, demonstrated that BM extract attenuated hepatic steatosis in mice by enhancing hepatic FGF21 and AMPK/Sirt1 signaling.

| S-EPMC3912441 | biostudies-literature

Sangiovese cv Pomace Seeds Extract-Fortified Kefir Exerts Anti-Inflammatory Activity in an In Vitro Model of Intestinal Epithelium Using Caco-2 Cells.

Project description:Inflammatory bowel disease and food allergies are a growing topic in the field of nutrition science. Polyphenols, which are the most important secondary metabolites of plants, demonstrated to modulate the expression and/or production of numerous proteins, but also to regulate the intestinal ecosystem. In this context, our aim was the investigation of protective effects against the gastrointestinal mucosa of fortified milk kefir obtained by adding seeds extract from Sangiovese cv. Pomace. Methods: An ultrasound-assisted method was used to obtain the extracts. All the extracts were assayed for the antioxidant activity. The best extract was used as an additive of fermented milk kefir to obtain a fortified final product. Kefir samples were analyzed by NMR spectroscopy. The efficiency of the barrier functions was evaluated by measuring trans-epithelial electric resistance (TEER) using a voltmeter. Results: the enriched kefir (Ksgn) possesses higher antioxidant performances compared to the unfortified sample (Kwht). Kwht and Ksgn did not alter Caco-2 TEER in basal condition.

| S-EPMC7022605 | biostudies-literature

Wild Bitter Melon Leaf Extract Inhibits Porphyromonas gingivalis-Induced Inflammation: Identification of Active Compounds through Bioassay-Guided Isolation.

Project description:Porphyromonas gingivalis has been identified as one of the major periodontal pathogens. Activity-directed fractionation and purification processes were employed to identify the anti-inflammatory active compounds using heat-killed P. gingivalis-stimulated human monocytic THP-1 cells in vitro. Five major fractions were collected from the ethanol/ethyl acetate extract of wild bitter melon (Momordica charantia Linn. var. abbreviata Ser.) leaves and evaluated for their anti-inflammatory activity against P. gingivalis. Among the test fractions, Fraction 5 effectively decreased heat-killed P. gingivalis-induced interleukin (IL)-8 and was subjected to separation and purification by using chromatographic techniques. Two cucurbitane triterpenoids were isolated from the active fraction and identified as 5?,19-epoxycucurbita-6,23-diene-3?,19,25-triol (1) and 3?,7?,25-trihydroxycucurbita-5,23-dien-19-al (2) by comparing spectral data. Treatments of both compounds in vitro potently suppressed P. gingivalis-induced IL-8, IL-6, and IL-1? levels and the activation of mitogen-activated protein kinase (MAPK) in THP-1 cells. Both compounds effectively inhibited the mRNA levels of IL-6, tumor necrosis factor (TNF)-?, and cyclooxygenase (COX)-2 in P. gingivalis-stimulated gingival tissue of mice. These findings imply that 5?,19-epoxycucurbita-6,23-diene-3?,19,25-triol and 3?,7?,25-trihydroxycucurbita-5,23-dien-19-al could be used for the development of novel therapeutic approaches against P. gingivalis infections.

| S-EPMC6273076 | biostudies-literature

Bitter melon extract ameliorates palmitate-induced apoptosis via inhibition of endoplasmic reticulum stress in HepG2 cells and high-fat/high-fructose-diet-induced fatty liver.

Project description:Bitter melon (BM) improves glucose level, lipid homeostasis, and insulin resistance in vivo. However, the preventive mechanism of BM in nonalcoholic fatty liver disease (NAFLD) has not been elucidated yet.To determine the protective mechanism of bitter melon extract (BME), we performed experiments in vitro and in vivo. BME were treated palmitate (PA)-administrated HepG2 cells. C57BL/6J mice were divided into two groups: high-fat/high-fructose (HF/HFr) without or with BME supplementation (100 mg/kg body weight). Endoplasmic reticulum (ER) stress, apoptosis, and biochemical markers were then examined by western blot and real-time PCR analyses.BME significantly decreased expression levels of ER-stress markers (including phospho-eIF2?, CHOP, and phospho-JNK [Jun N-terminal kinases]) in PA-treated HepG2 cells. BME also significantly decreased the activity of cleaved caspase-3 (a well known apoptotic-induced molecule) and DNA fragmentation. The effect of BME on ER stress-mediated apoptosis in vitro was similarly observed in HF/HFr-fed mice in vivo. BME significantly reduced HF/HFr-induced hepatic triglyceride (TG) and serum alanine aminotransferase (ALT) as markers of hepatic damage in mice. In addition, BME ameliorated HF/HFr-induced serum TG and serum-free fatty acids.These data indicate that BME has protective effects against ER stress mediated apoptosis in HepG2 cells as well as in HF/HFr-induced fatty liver of mouse. Therefore, BME might be useful for preventing and treating NAFLD.

| S-EPMC5883859 | biostudies-other

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data