(antiproliferative, pro-apoptosis, +P53, +P21, -CyclinD1,G2, immune/NK stimulation, anti-Her2, HDAC inhib, Wnt, C-myc, pro-oxidation, glycolysis, reversal of chemo resistance via PGP/ trapping in cell, leaf and seed component may be critical)
WARNING: May be harmful to pregnancies
Some supplement sources
Memorial Sloan Kettering summary
Cancer Res. 2010 Feb 23. [Epub ahead of print]
Bitter Melon (Momordica charantia) Extract Inhibits Breast Cancer Cell Proliferation by Modulating Cell Cycle Regulatory Genes and Promotes Apoptosis.
Ray RB,
Raychoudhuri A,
Steele R,
Nerurkar P.
Authors' Affiliations: Departments of Pathology and Internal Medicine, Saint Louis University, St. Louis, Missouri and Laboratory of Metabolic Disorders and Alternative Medicine, University of Hawaii, Honolulu, Hawaii.
Breast cancer is one of the most common cancers among women in the United States. Although there are effective drugs for treating advanced stages of breast cancers, women eventually develop resistance. One of the approaches to control breast cancer is prevention through diet, which inhibits one or more neoplastic events and reduces cancer risk. In this study, we have used human breast cancer cells, MCF-7 and MDA-MB-231, and primary human mammary epithelial cells as an in vitro model to assess the efficacy of bitter melon (Momordica charantia) extract (BME) as an anticancer agent.
BME treatment of breast cancer cells resulted in a significant decrease in cell proliferation and induced apoptotic cell death. Apoptosis of breast cancer cells was accompanied by increased poly(ADP-ribose) polymerase cleavage and caspase activation. Subsequent studies showed that BME treatment of breast cancer cells inhibited survivin and claspin expression. Fluorescence-activated cell sorting analysis suggested that MCF-7 cells treated with BME
accumulated during the G(2)-M phase of the cell cycle. Further studies revealed that BME treatment
enhanced p53, p21, and pChk1/2 and inhibited cyclin B1 and cyclin D1 expression, suggesting an additional mechanism involving cell cycle regulation. Together, these results show that
BME modulates signal transduction pathways for inhibition of breast cancer cell growth and can be used as a dietary supplement for prevention of breast cancer. Cancer Res; 70(5); 1925-31.
PMID: 20179194 [PubMed - as supplied by publisher]
Pharm Res. 2010 Mar 3. [Epub ahead of print]
Bitter Melon: Antagonist to Cancer.
Nerurkar P,
Ray RB.
Laboratory of Metabolic Disorders and Alternative Medicine, University of Hawaii, Honolulu, Hawaii, USA.
The incidence of cancer is increasing worldwide, in spite of substantial progress in the development of anti-cancer therapies. One approach to control cancer could be its prevention by diet, which inhibits one or more neoplastic events and reduces cancer risk. Dietary compounds offer great potential in the fight against cancer by inhibiting the carcinogenesis process through the regulation of cell homeostasis and cell-death machineries.
For centuries, Ayurveda (Indian traditional medicine) has recommended the use of bitter melon (Momordica charantia) as a functional food to prevent and treat diabetes and associated complications. It is noteworthy to mention that bitter melon extract has no-to-low side effects in animals as well as in humans. The anti-tumor activity of bitter melon has recently begun to emerge. This review focuses on recent advancements in cancer chemopreventive and anti-cancer efficacy of bitter melon and its active constituents. Several groups of investigators have reported that treatment of bitter-melon-related products in a number of cancer cell lines induces cell cycle arrest and apoptosis without affecting normal cell growth. Therefore, the effect of bitter melon should be beneficial for health, and use of the non-modified dietary product is cost effective.
PMID: 20198408 [PubMed - as supplied by publisher]
Cancer Prev Res (Phila Pa). 2009 Oct;2(10):879-86. Epub 2009 Sep 29.
Eleostearic Acid inhibits breast cancer proliferation by means of an oxidation-dependent mechanism.
Grossmann ME,
Mizuno NK,
Dammen ML,
Schuster T,
Ray A,
Cleary MP.
University of Minnesota, 801 16th Avenue NE, Austin, MN 55912, USA.
Eleostearic acid (alpha-ESA) is a conjugated linolenic acid that makes up approximately 60% of Momordica charantia (bitter melon) seed oil. Prior work found that water extract from bitter melon was able to inhibit breast cancer. Here, we investigated effects of alpha-ESA on both estrogen receptor (ER)-negative MDA-MB-231 (MDA-wt) and ER-positive MDA-ERalpha7 human breast cancer cells. We found that
alpha-ESA inhibited proliferation of both MDA-wt and MDA-ERalpha7 cells, whereas conjugated linoleic acid had comparatively weak antiproliferative activity at 20 to 80 micromol/L concentrations. We also found that alpha-ESA (40 micromol/L) treatment led to apoptosis in the range of 70% to 90% for both cell lines, whereas conjugated linoleic acid (40 micromol/L) resulted in only 5% to 10% apoptosis, similar to results for control untreated cells. Addition of alpha-ESA also caused loss of mitochondrial membrane potential and translocation of apoptosis-inducing factor as well as endonuclease G from the mitochondria to the nucleus. Additionally,
alpha-ESA caused a G(2)-M block in the cell cycle. We also investigated the potential for lipid peroxidation to play a role in the inhibitory action of alpha-ESA. We found that when the breast cancer cells were treated with alpha-ESA in the presence of the antioxidant alpha-tocotrienol (20 micromol/L), the growth inhibition and apoptosis effects of alpha-ESA were lost. An AMP-activated protein kinase inhibitor (Dorsomorphin) was also able to partially abrogate the effects of alpha-ESA, whereas a caspase inhibitor (BOC-D-FMK) did not. These results illustrate that
alpha-ESA can block breast cancer cell proliferation and induce apoptosis through a mechanism that may be oxidation dependent.
PMID: 19789297 [PubMed - indexed for MEDLINE]
Cancer Chemother Pharmacol. 2004 Dec;54(6):525-30. Epub 2004 Jul 10.
Inhibition of P-glycoprotein activity and reversal of cancer multidrug resistance by Momordica charantia extract.
PURCHASE TEXT
Limtrakul P,
Khantamat O,
Pintha K.
Department of Biochemistry, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.
plimtrak@mail.med.cmu.ac.th
PURPOSE: Multidrug resistance (MDR) is known as a problem limiting the success of therapy in patients treated long term with chemotherapeutic drugs. The drug resistance is mainly due to the overexpression of the 170 kDa P-glycoprotein (Pgp), which causes a reduction in drug accumulation in the cancer cells. In this study, novel chemical modulator(s) from bitter melon (Momordica charantia L.) extracts obtained from leaves, fruits and tendrils were tested for their abilities to modulate the function of Pgp and the MDR phenotype in the multidrug-resistant human cervical carcinoma KB-V1 cells (high Pgp expression) in comparison with wildtype drug-sensitive KB-3-1 cells (lacking Pgp). METHODS: The KB-V1 and KB-3-1 cells were exposed to bitter melon extracts in the presence of various concentrations of vinblastine, and cytotoxicity was assessed by means of the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) colorimetric assay. Relative resistance was calculated as the ratio of the IC50 value of the KB-V1 cells to the IC50 value of the KB-3-1 cells. Accumulation and efflux of vinblastine in KB-V1 and KB-3-1 cells were measured using a [3H]-vinblastine incorporation assay. RESULTS:
The leaf extracts increased the intracellular accumulation of [3H]-vinblastine in KB-V1 cells in a dose-dependent manner, but extracts from the fruits and tendrils had no effect. By modulating Pgp-mediated vinblastine efflux, the leaf extracts decreased the [3H]-vinblastine efflux in KB-V1 cells in a dose-dependent manner, but not in KB-3-1 cells. Treatment of drug-resistant KB-V1 cells with bitter melon leaf extracts increased their sensitivity to vinblastine, but similar treatment of KB-3-1 cells showed no modulating effect. The fruit and tendril extracts did not affect the MDR phenotype in either cell line. CONCLUSION:
The leaf extracts from bitter melon were able to reverse the MDR phenotype, which is consistent with an increase in intracellular accumulation of the drug. The exact nature of the active components of bitter melon leaf extracts remains to be identified.
PMID: 15248030 [PubMed - indexed for MEDLINE]
Anticancer Res. 2000 Mar-Apr;20(2A):653-9.
Inhibition of MDA-MB-231 human breast tumor xenografts and HER2 expression by anti-tumor agents GAP31 and MAP30.
Lee-Huang S,
Huang PL,
Sun Y,
Chen HC,
Kung HF,
Huang PL,
Murphy WJ.
Department of Biochemistry, New York University School of Medicine, NY 10016, USA.
GAP31 (Gelonium protein of 31 kDa) and MAP30 (Momordica protein of 30 kDa) are agents isolated from the medicinal plants Gelonium multiflorum and Momordica charantia, respectively. The current study was conducted to investigate the efficacy of GAP31 and MAP30 on estrogen-independent and highly metastatic human breast tumor MDA-MB-231 both in vitro and in vivo. The effect of these agents on the expression of breast tumor antigen HER2 (also known as neu or as c-erbB 2) was also examined. Treatment of MDA-MB-231 breast cancer cells with GAP31 and MAP30 resulted in
inhibition of cancer cell proliferation as well as inhibition of the expression of HER2 gene in vitro. When MDA-MB-231 human breast cancer cells were transferred into SCID mice, the mice developed extensive metastases and all mice succumbed to tumor by day 46.
Treatment of the human breast cancer bearing SCID mice with GAP31 or MAP30 at 10 micrograms/injection EOD for 10 injections resulted in significant increases in survival, with 20-25% of the mice remaining tumor free for 96 days. Thus, anti-tumor agents GAP31 and MAP30 are effective against human breast cancer MDA-MB-231 in vitro and in vivo. These agents may therefore be a potential therapeutic use against breast carcinomas.
PMID: 10810336 [PubMed - indexed for MEDLINE]
J Med Assoc Thai. 2003 Jan;86(1):61-8.
Effect of bitter melon (Momordica charantia Linn) on level and function of natural killer cells in cervical cancer patients with radiotherapy.
Pongnikorn S,
Fongmoon D,
Kasinrerk W,
Limtrakul PN.
Lampang Regional Cancer Center, Lampang 52000, Thailand.
Cervical cancer patients have a defective immune system. There is a decrease of total white blood cell count including lymphocytes and natural killer (NK) cells. NK cells, one type of lymphocytes, play a role to eliminate cancer cells by antibody dependent cell mediated cytotoxicity (ADCC) mechanism. Previous studies have shown that P-glycoprotein (170 kDa, transmembrane protein) may be a transporter for cytokine releasing in ADCC mechanism. This study proposed to explore the role of bitter melon intake in cervical cancer patients undergoing normal treatment (radiotherapy). Subjects were divided into three groups: 1) normal control (women 35-55 years, n = 35), 2) patient control (n = 30) and 3) patient treatment (n = 30) groups. Patient control and patient treatment groups were cervical cancer patients (stage II or III) treated with radiotherapy (without or with bitter melon ingestion). Blood samples of patient control and patient treatment groups were analyzed for NK cells percentage and P-glycoprotein level. Bitter melon is a Thai herb. Previous studies have shown that bitter melon can stimulate lymphocyte activity in vitro and in vivo (mouse). The authors hope that bitter melon could stimulate the increase of NK cells percentage and P-glycoprotein level on the membrane in blood samples from cervical cancer patients who ingest bitter melon. The results showed an increased percentage of NK cells in patient control and patient treatment groups. The increase in each group is significant (p < 0.05) when compared with the percentage of NK cells from second and third blood sampling time (after radiation with of without bitter melon intake for 45 and 90 days) with first blood sampling time (before treatment). The results also show a
significant decrease of P-glycoprotein level (p < 0.05) in second and third blood sampling times when compared with first blood sampling time of the patient treatment group. There was no significant difference of P-glycoprotein (P-gp) level from first, second and third blood sampling times in patient control group.
Bitter melon ingestion did not affect NK cell level but it affected the decrease of P-gp level on NK cell membrane.
PMID: 12678140 [PubMed - indexed for MEDLINE]
Cell Immunol. 1990 Apr 1;126(2):278-89.
Induction of tumor cytotoxic immune cells using a protein from the bitter melon (Momordica charantia).
Cunnick JE,
Sakamoto K,
Chapes SK,
Fortner GW,
Takemoto DJ.
Division of Biology, Kansas State University, Manhattan 66506.
The fruit and seeds of the bitter melon (Momordica charantia) have been reported to have anti-leukemic and antiviral activities. This anti-leukemic and antiviral action was associated with an activation of murine lymphocytes. A partially purified protein factor from the bitter melon caused an infiltration and activation of peritoneal exudate cells in C57B1/6J, C3H/HeJ, and C3H/HeN mice. When the extract was injected twice a week at 8 micrograms of protein per ip injection for 0-4 weeks, the peritoneal exudate cells from the treated mice were cytotoxic in a long-term (18-hr) 51Cr-release assay against a range of labeled targets: L1210, P388, and MOLT-4 tumor cells. Cytotoxicity was also observed against YAC-1 targets in a short-term (4-hr) assay. Fractionation of the cytotoxic immune cells implicated a nonadherent cell population which was capable of killing an NK-sensitive cell line in a 4-hr 51Cr-release assay. Unit gravity sedimentation studies indicated that the cytotoxicity was due to either a neutrophil or a large lymphocyte. Antibody depletion experiments using antibody to asialo GM1, an NK cell-specific antibody, depleted cytotoxicity observed in nonadherent, Ficoll/Hypaque-separated PEC. This suggests that
at least part of the anti-leukemic activity of the bitter melon extract is due to the activation of NK cells in the host mouse.
PMID: 2311123 [PubMed - indexed for MEDLINE]
Am J Chin Med. 2002;30(2-3):195-205.
Effects of bitter melon (Momordica charantia l.) or ginger rhizome (Zingiber offifinale rosc) on spontaneous mammary tumorigenesis in SHN mice.
Nagasawa H,
Watanabe K,
Inatomi H.
Experimental Animal Research Laboratory, Meiji University, Kawasaki, Japan.
The effects of chronic
treatment with hot water extract of Bitter Melon (Momordica charantia L.) or Ginger Rhizome (Zingiber offifinale Rosc) on spontaneous mammary tumorigenesis were examined in SHN virgin mice.
In mice given free access to extract of Bitter Melon (0.5%) or Ginger (0.125%) in drinking water, the development of mammary tumors was significantly inhibited. Furthermore, the former inhibited uterine adenomyosis with a common pathological background to mammary tumors and the latter inhibited mammary tumor growth. While the mechanism of the effects of these natural products remains to be clarified, there were no adverse effects of chronic treatment with these agents as estimated from body weight, food and water intake and various plasma component levels as well as external appearance. Thus, these natural products, popular in Japan as foodstuffs, also appear to have a health benefit.
PMID: 12230008 [PubMed - indexed for MEDLINE]
Int J Cancer. 2009 Aug 15;125(4):774-82.
Ribosome-inactivating proteins isolated from dietary bitter melon induce apoptosis and inhibit histone deacetylase-1 selectively in premalignant and malignant prostate cancer cells.
Xiong SD,
Yu K,
Liu XH,
Yin LH,
Kirschenbaum A,
Yao S,
Narla G,
DiFeo A,
Wu JB,
Yuan Y,
Ho SM,
Lam YW,
Levine AC.
Institute of Hematology and Tumor Biology Research, First Affiliated Hospital of Wenzhou Medical College, Wenzhou, China.
Erratum in:
- Int J Cancer. 2009 Oct 15;125(8):1995.
Epidemiologic evidence suggests that a diet rich in fruits and vegetables is associated with a reduced risk of prostate cancer (PCa) development. Although several dietary compounds have been tested in preclinical PCa prevention models, no agents have been identified that either prevent the progression of premalignant lesions or treat advanced disease. Momordica charantia, known as bitter melon in English, is a plant that grows in tropical areas worldwide and is both eaten as a vegetable and used for medicinal purposes.
We have isolated a protein, designated as MCP30, from bitter melon seeds. The purified fraction was verified by SDS-PAGE and mass spectrometry to contain only 2 highly related single chain Type I ribosome-inactivating proteins (RIPs), alpha-momorcharin and beta-momorcharin.
MCP30 induces apoptosis in PIN and PCa cell lines in vitro and suppresses PC-3 growth in vivo with no effect on normal prostate cells. Mechanistically, MCP30 inhibits histone deacetylase-1 (HDAC-1) activity and promotes histone-3 and -4 protein acetylation. Treatment with MCP30 induces PTEN expression in a prostatic intraepithelial neoplasia (PIN) and PCa cell lines resulting in inhibition of Akt phosphorylation. In addition, MCP30 inhibits Wnt signaling activity through reduction of nuclear accumulation of beta-catenin and decreased levels of c-Myc and Cyclin-D1. Our data indicate that MCP30 selectively induces PIN and PCa apoptosis and inhibits HDAC-1 activity. These results suggest that Type I RIPs derived from plants are HDAC inhibitors that can be utilized in the prevention and treatment of prostate cancer.
PMID: 19384952 [PubMed - indexed for MEDLINE]
J Agric Food Chem. 2008 Nov 26;56(22):10515-20.
Alpha-eleostearic acid and its dihydroxy derivative are major apoptosis-inducing components of bitter gourd.
Kobori M,
Ohnishi-Kameyama M,
Akimoto Y,
Yukizaki C,
Yoshida M.
National Food Research Institute, National Agricultural and Food Research Organization, Tsukuba, Ibaraki, Japan.
Bitter gourd ( Momordica charantia L.) pericarp, placenta, and seed extracts were previously shown to induce apoptosis in HL60 human leukemia cells.
To determine the active component that induces apoptosis in cancer cells, bitter gourd ethanol extract was fractionated by liquid-liquid partition and silica gel column chromatography. Several fractions obtained by silica gel column chromatography inhibited growth and induced apoptosis in HL60 cells. Among them, fraction 7 had the strongest activity in inhibiting growth and inducing apoptosis in HL60 cells. A component that induced apoptosis in HL60 cells was then isolated from fraction 7 by another silica gel column chromatography and high-performance liquid chromatography (HPLC) using a C18 column and was identified as (9Z,11E,13E)-15,16-dihydroxy-9,11,13-octadecatrienoic acid (15,16-dihydroxy alpha-eleostearic acid). 15,16-Dihydroxy alpha-eleostearic acid induced apoptosis in HL60 cells within 5 h at a concentration of 160 microM (50 microg/mL). (9Z,11E,13E)-9,11,13-Octadecatrienoic acid (alpha-eleostearic acid) is known to be the major conjugated linolenic acid in bitter gourd seeds. Therefore, the effect of alpha-eleostearic acid on the growth of some cancer and normal cell lines was examined. alpha-Eleostearic acid strongly inhibited the growth of some cancer and fibroblast cell lines, including those of HL60 leukemia and HT29 colon carcinoma. alpha-Eleostearic acid induced apoptosis in HL60 cells after a 24 h incubation at a concentration of 5 microM. Thus, alpha-eleostearic acid and the dihydroxy derivative from bitter gourd were suggested to be the major inducers of apoptosis in HL60 cells.
PMID: 18959405 [PubMed - indexed for MEDLINE]
J Nat Prod. 2007 Aug;70(8):1233-9. Epub 2007 Aug 9.
Cucurbitane-type triterpenoids from the fruits of Momordica charantia and their cancer chemopreventive effects.
Akihisa T,
Higo N,
Tokuda H,
Ukiya M,
Akazawa H,
Tochigi Y,
Kimura Y,
Suzuki T,
Nishino H.
College of Science and Technology, Nihon University, 1-8 Kanda Surugadai, Tokyo 101-8308, Japan.
akihisa@chem.cst.nihon-u.ac.jp
Thirteen cucurbitane-type triterpene glycosides, including eight new compounds named charantosides I (6), II (7), III (10), IV (11), V (12), VI (13), VII (16), and VIII (17), and five known compounds, 8, 9, 14, 15, and 18, were isolated from a methanol extract of the fruits of Japanese Momordica charantia. The structures of the new compounds were determined on the basis of spectroscopic methods. On evaluation of these triterpene glycosides and five other cucurbitane-type triterpenes, 1-5, also isolated from the extract of M. charantia fruits, for their inhibitory effects on the induction of Epstein-Barr virus early antigen (EBV-EA) by 12-O-tetradecanoylphorbol-13-acetate (TPA) in Raji cells, these compounds showed inhibitory effects on EBV-EA induction with IC(50) values of 200-409 mol ratio/32 pmol TPA. In addition, upon evaluation of compounds 1-5 for inhibitory effects against activation of (+/-)-(E)-methyl-2[(E)-hydroxyimino]-5-nitro-6-methoxy-3-hexemide (NOR 1), a nitrogen oxide (NO) donor, compounds 1-3 showed moderate inhibitory effects. Compounds 1 and 2 exhibited marked inhibitory effects in both 7,12-dimethylbenz[a]anthracene (DMBA)- and peroxynitrite (ONOO-; PN)-induced mouse skin carcinogenesis tests.
PMID: 17685651 [PubMed - indexed for MEDLINE]
J Ethnopharmacol. 2009 Dec 10;126(3):533-7. Epub 2009 Sep 8.
Fruit extracts of Momordica charantia potentiate glucose uptake and up-regulate Glut-4, PPAR gamma and PI3K.
Kumar R,
Balaji S,
Uma TS,
Sehgal PK.
Bio-products Laboratory, Central Leather Research Institute, Council of Scientific and Industrial Research, Adyar, Chennai 600 020, Tamil Nadu, India.
ETHNOPHARMACOLOGICAL RELEVANCE: Momordica charantia fruit is a
widely used traditional medicinal herb as, anti-diabetic, anti-HIV, anti-ulcer, anti-inflammatory, anti-leukemic, anti-microbial, and anti-tumor. AIMS OF STUDY: The present study is undertaken to investigate the possible mode of action of fruit extracts derived from Momordica charantia (MC) and study its pharmacological effects for controlling diabetic mellitus. Effects of aqueous and chloroform extracts of Momordica charantia fruit on glucose uptake and up-regulation of glucose transporter (Glut-4), peroxisome proliferator activator receptor gamma (PPAR gamma) and phosphatidylinositol-3 kinase (PI3K), were investigated to show its efficacy as a hypoglycaemic agent. MATERIALS AND METHODS: Dose dependent glucose uptake assay was performed on L6 myotubes using 2-deoxy-D-[1-(3)H] glucose. Up-regulatory effects of the extracts on the mRNA expression level of Glut-4, PPAR gamma and PI3K have been studied. RESULTS: The association of Momordica charantia with the aqueous and chloroform
extracts of Momordica charantia fruit at 6 microg/ml has shown significant up-regulatory effect, respectively, by 3.6-, 2.8- and 3.8-fold on the battery of targets Glut-4, PPAR gamma and PI3K involved in glucose transport. The up-regulation of glucose uptake was comparable with insulin and rosiglitazone which was approximately 2-fold over the control. Moreover, the inhibitory effect of the cyclohexamide on Momordica charantia fruit extract mediated glucose uptake suggested the requirement of new protein synthesis for the enhanced glucose uptake. CONCLUSION: This study demonstrated the significance of Glut-4, PPAR gamma and PI3K up-regulation by Momordica charantia in augmenting the glucose uptake and homeostasis.
PMID: 19744549 [PubMed - indexed for MEDLINE]
Toxicon. 1990;28(10):1183-92.
Toxicities of trichosanthin and alpha-momorcharin, abortifacient proteins from Chinese medicinal plants, on cultured tumor cell lines.
Tsao SW,
Ng TB,
Yeung HW.
Department of Anatomy, Chinese University of Hong Kong, Shatin.
Trichosanthin and alpha-momorcharin are abortifacient proteins extracted from Chinese medicinal herbs. Study of their in vitro cytotoxicities showed that the two proteins selectively injured choriocarcinoma and melanoma cells. Hepatoma cells represented the most resistant cell line among the various cell lines investigated. Cytotoxicity profiles of trichosanthin and alpha-momorcharin differed from those of anti-cancer drugs which interfere with DNA metabolism such as cisplatin, methotrexate and 5-fluorouracil. Radioactive precursor incorporation studies suggested that the two abortifacient proteins inhibited cellular protein synthesis. The marked decrease in secretion of human chorionic gonadotrophin and progesterone by choriocarcinoma cells after treatment with the proteins could be attributed mainly to loss of cells.
PMID: 2175958 [PubMed - indexed for MEDLINE]
Cancer Res. 1983 Nov;43(11):5151-5.
In vivo antitumor activity of the bitter melon (Momordica charantia).
Jilka C,
Strifler B,
Fortner GW,
Hays EF,
Takemoto DJ.
The in vivo antitumor activity of a crude extract from the bitter melon (Momordica charantia) was determined. The extract inhibited tumor formation in CBA/H mice which had been given i.p. injections of 1.0 X 10(5) CBA/Dl tumor cells (77% of the untreated mice with tumors versus 33% of the treated mice with tumors after 6 weeks). The extract also inhibited tumor formation in DBA/2 mice which had been given i.p. injections of either 1 X 10(5) P388 tumor cells (0% of untreated mice survived after 30 days versus 40% survival of the treated mice) or 1 X 10(5) L1210 tumor cells (0% survival of untreated mice versus 100% of treated mice after 30 days). The in vivo antitumor effect required both the prior exposure of tumor cells to the extract (2 hr) in vitro and i.p., biweekly injections of the extract into the mice.
The optimum dose for tumor inhibition (8 micrograms protein, biweekly, i.p.) was not toxic to mice for at least 45 days of treatment. This same treatment caused a marked enhancement of C3H mouse thymic cell response to concanavalin A in vitro. When compared to the untreated control mice, the bitter melon-injected animals exhibited a 4-fold-higher incorporation of tritiated thymidine into trichloroacetic acid-precipitable material after 48 hr of exposure to 50 micrograms of concanavalin A. Nylon wool-purified spleen cells from these same bitter melon-treated mice exhibited an enhanced mixed lymphocyte reaction when exposed to irradiated P388 stimulator cells (186% of the untreated control mice). These data indicate that
in vivo enhancement of immune functions may contribute to the antitumor effects of the bitter melon extract.
PMID: 6616452 [PubMed - indexed for MEDLINE]
Yao Xue Xue Bao. 1998 Nov;33(11):839-42.
[Triterpenes and steroidal compounds from Momordica dioica]
[Article in Chinese]
Luo L,
Li Z,
Zhang Y,
Huang R.
Department of Chemistry, Yunnan Education College, Kunming 650031.
Three triterpenes and two steroidal compounds were isolated from the dry root of Momordica dioica. Their structures were elucidated by spectral analyses (MS, IR, 1HNMR, 13CNMR and DEPT) and chemical methods. These compounds are alpha-spinasterol octadecanonate(I), alpha-spinasterol-3-O-beta-D-glucopyranoside(II), 3-O-beta-D-glucuronopyranosyl gypsogenin(III), 3-O-beta-D-glucopyranosyl gypsogenin(IV) and 3-O-beta-D-glucopyranosyl hederagenin(V). Constituent III is a new compound. The CHCl3 extract of Momordica dioica roots and five isolated constituents showed anticancer activity in pharmacologic testing on cancer cell(L1210). The growth inhibitory index(%) of compound II was shown to be 50%, at the dose of 4 micrograms.ml-1.
PMID: 12016945 [PubMed - indexed for MEDLINE]
Med Hypotheses. 2004;63(2):340-3.
Does bitter melon contain an activator of AMP-activated kinase?
McCarty MF.
NutriGuard Research, 1051 Hermes Ave., Encinitas, CA 92024, USA.
mccarty@pantox.com
Extracts of the unripe fruit of Momordica charantia--bitter melon, which flourishes throughout the tropics--appear to have utility in the management of type 2 diabetes.
Rodent studies suggest that the thus-far-uncharacterized active components of such extracts enhance the efficiency of postprandial glucose storage in muscle and liver, and likely diminish excessive hepatic glucose output, while often down-regulating serum insulin--effects comparable to those reported for metformin. Other parallels between the actions of metformin and bitter melon in rodents appear to include: analogous effects on the hepatic activity of certain enzymes of glucose metabolism; increased expression of GLUT4 in the plasma membrane of skeletal muscle; a tendency to prevent weight gain; favorable effects on serum lipids; and an anti-promotional impact on cancer induction. Inasmuch as the clinical efficacy of metformin has recently been traced to its ability to activate AMP-activated kinase, it would be of interest to determine whether bitter melon extracts contain activators of this enzyme. The fact that bitter melon has the potential to down-regulate insulin suggests that, beyond its likely utility in the management of diabetes, it may have preventive value with respect to a wide range of disorders in which hyperinsulinemia plays a pathogenic role--and possibly could even favorably impact the aging process.
PMID: 15236800 [PubMed - indexed for MEDLINE]
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