(magnolia extract alone, w/chemo & rads: G1, PI3K/AKT/mTOR, antiang, better in Her2- or w/Lapatinib)
Some honokiol(magnolia) sources on Google
HERE
"Inflamaway" Combo supplement with Honokiol
HERE (enter into search bar)
liposomal versions of supplements are preferable when available.
Eur J Pharmacol. 2008 Sep 4;591(1-3):43-51. Epub 2008 Jun 12.
Anti-tumor effect of honokiol alone and in combination with other anti-cancer agents in breast cancer.
Liu H,
Zang C,
Emde A,
Planas-Silva MD,
Rosche M,
Kühnl A,
Schulz CO,
Elstner E,
Possinger K,
Eucker J.
Department of Oncology and Hematology, University Hospital Charité, Humboldt University of Berlin, Berlin, Germany.
Honokiol, an active component isolated and purified from Chinese traditional herb magnolia, was demonstrated to inhibit growth and induce apoptosis of different cancer cell lines such as human leukaemia, colon, and lung cancer cell lines; to attenuate the angiogenic activities of human endothelial cells in vitro; and to efficiently suppress the growth of angiosarcoma in nude mice. In this study, we have demonstrated that treatment of different human breast cancer cell lines with honokiol resulted in a
time- and concentration-dependent growth inhibition in both estrogen receptor-positive and -negative breast cancer cell lines, as well as in drug-resistant breast cancer cell lines such as adriamycin-resistant and tamoxifen-resistant cell lines. The inhibition of growth was associated with a G1-phase cell cycle arrest and induction of caspase-dependent apoptosis. The effects of honokiol might be reversely related to the expression level of human epidermal growth receptor 2, (HER-2, also known as erbB2, c-erbB2) since knockdown of her-2 expression by siRNA significantly enhanced the sensitivity of the her-2 over-expressed BT-474 cells to the honokiol-induced apoptosis. Furthermore,
inhibition of HER-2 signalling by specific human epidermal growth receptor 1/HER-2 (EGFR/HER-2) kinase inhibitor lapatinib synergistically enhanced the anti-cancer effects of honokiol in her-2 over-expressed breast cancer cells. Finally, we showed that
honokiol was able to attenuate the PI3K/Akt/mTOR (Phosphoinositide 3-kinases/Akt/mammalian target of rapamycin) signalling by down-regulation of Akt phosphorylation and upregulation of PTEN (Phosphatase and Tensin homolog deleted on chromosome Ten) expression. Combination of honokiol with the mTOR inhibitor rapamycin presented synergistic effects on induction of apoptosis of breast cancer cells. In conclusion, honokiol, either alone or in combination with other therapeutics, could serve as a new, promising approach for breast cancer treatment.
PMID: 18588872 [PubMed - indexed for MEDLINE]
Phytother Res. 2008 Aug;22(8):1125-32.
Synergistic antitumor effects of liposomal honokiol combined with adriamycin in breast cancer models.
Hou W,
Chen L,
Yang G,
Zhou H,
Jiang Q,
Zhong Z,
Hu J,
Chen X,
Wang X,
Yuan Y,
Tang M,
Wen J,
Wei Y.
State Key Laboratory of Biotherapy, West China Hospital, School of Life Science, Sichuan University, Chengdu, China.
Honokiol, a novel antitumor agent, could induce apoptosis and inhibit the growth of vascular endothelium in several tumor cell lines and xenograft models. It has been suggested that the antitumor effect of chemotherapy could be increased by combining it with an antiangiogenesis agent in anticancer strategy. The present study explored the potential to increase the antitumor effect of adriamycin by combining it with honokiol in mouse 4T1 breast cancer models, and the underlining mechanism was investigated. Honokiol was encapsulated in liposomes to improve the water insolubility. In vitro, liposomal honokiol inhibited the proliferation of 4T1 cells via apoptosis and significantly enhanced the apoptosis of 4T1 cells induced by adriamycin. In vivo, the systemic administration of liposomal honokiol and adriamycin significantly decreased tumor growth through increased tumor cell apoptosis compared with either treatment alone. Collectively, these findings suggest that liposomal honokiol may augment the induction of apoptosis in 4T1 cells in vitro and in vivo, and this combined treatment has shown synergistic suppression in tumor progression according to the analysis of isobologram. The present study may be important in future exploration of the potential application of the combined approach in the treatment of breast cancer.
PMID: 18570244 [PubMed - indexed for MEDLINE]
1:
J Immunother. 2009 May 28. [Epub ahead of print]
Honokiol-mediated Inhibition of PI3K/mTOR Pathway: A Potential Strategy to Overcome Immunoresistance in Glioma, Breast, and Prostate Carcinoma Without Impacting T Cell Function.
Crane C, Panner A, Pieper RO, Arbiser J, Parsa AT.
*Department of Neurological Surgery, University of California, San Francisco, CA daggerDepartment of Dermatology, Emory University School of Medicine, Atlanta, GA.
Inhibition of the phosphoinositide 3-kinase (PI3K)/mammalian target of rapamycin (mTOR) pathway is an appealing method for decreasing the immunoresistance and augmenting T cell-mediated immunotherapy. A major impediment to this strategy is the impact of conventional PI3K/mTOR pathway inhibitors on T cell function. In particular, rapamycin, is a well-known immunosuppressant that can decrease the activity of the PI3K/mTOR pathway in tumor cells, but also has a profound inhibitory effect on T cells. Here we show that Honokiol, a natural dietary product isolated from an extract of seed cones from Magnolia grandiflora, can decrease PI3K/mTOR pathway-mediated immunoresistance of glioma, breast and prostate cancer cell lines, without affecting critical proinflammatory T cell functions. Specifically, we show that at doses sufficient to down-regulate levels of phospho-S6 and the negative immune regulator B7-H1 in tumor cells, Honokiol does not significantly impair T cell proliferation or proinflammatory cytokine production. In contrast to classic inhibitors, including LY294002, wortmannin, AKT inhibitor III and rapamycin, Honokiol specifically decreases the PI3K/mTOR pathway activity in tumor cells, but not in freshly stimulated T cells. Collectively, our data define a unique application for Honokiol and provide the impetus to more fully elucidate the mechanism by which T cells are resistant to the effects of this particular inhibitor. Honokiol is clinically available for human testing and may serve to augment T cell-mediated cancer immunotherapy.
PMID: 19483651 [PubMed - as supplied by publisher
http://herbalmedicine.suite101.com/article.cfm/honokiol
Honokiol appears to be non toxic, easily absorbed, and systematically available. This is important since many promising materials like Epigallocatechin Gallate (EGCG) are not absorbed well in the digestive tract. Honokiol also avoids immediate clearing by the liver (first pass effect) and crosses blood barriers that often exclude other compounds.
Recent studies have explored honokiol and found validation for it as a treatment option for anxiety, cancer, peridontal disease, stroke, inflammation, and even weight loss.
Cancer Management
Honokiol has been effective in vitro and in vivo against several types of cancers. It appears to turn off the division of some cancer cells while inducing others to kill themselves (apoptosis). It has antiangiogenesis properties (eliminating the blood supply to tumors) and some studies are recommending it as adjunct treatment with other types of chemotherapy.
Clincancerres.aacrjournals.org/cgi/content/abstract/14/4/1248; Apoptosis
www.jbc.org/cgi/content/abstract/278/37/35501;Antiangiogenesis
Antioxid Redox Signal. 2009 May;11(5):1139-48.
Honokiol, a multifunctional antiangiogenic and antitumor agent.
Fried LE,
Arbiser JL.
Department of Dermatology, Emory University School of Medicine, Winship Cancer Institute, Atlanta VA Medical Center, Atlanta, Georgia 30322, USA.
Honokiol is a small-molecule polyphenol isolated from the genus Magnolia. It is accompanied by other related polyphenols, including magnolol, with which it shares certain biologic properties. Recently, honokiol has been found to have antiangiogenic, antiinflammatory, and antitumor properties in preclinical models, without appreciable toxicity. These findings have increased interest in bringing honokiol to the clinic as a novel chemotherapeutic agent. In addition, mechanistic studies have tried to find the mechanism(s) of action of honokiol, for two major reasons. First, knowledge of the mechanisms of action may assist development of novel synthetic analogues. Second, mechanistic actions of honokiol may lead to rational combinations with conventional chemotherapy or radiation for enhanced response to systemic cancers. In this review, we describe the findings that honokiol has two major mechanisms of action. First, it blocks signaling in tumors with defective p53 function and activated ras by directly blocking the activation of phospholipase D by activated ras. Second, honokiol induces cyclophilin D, thus potentiating the mitochondrial permeability transition pore, and causing death in cells with wild-type p53. Knowledge of the dual activities of honokiol can assist with the development of honokiol derivatives and the design of clinical trials that will maximize the potential benefit of honokiol in the patient setting.
PMID: 19203212 [PubMed - in process]
Exp Mol Med. 2008 Dec 31;40(6):617-28.
Liposomal honokiol, a potent anti-angiogenesis agent, in combination with radiotherapy produces a synergistic antitumor efficacy without increasing toxicity.
FREE TEXT
Hu J,
Chen LJ,
Liu L,
Chen X,
Chen PL,
Yang G,
Hou WL,
Tang MH,
Zhang F,
Wang XH,
Zhao X,
Wei YQ.
State Key Laboratory of Biotherapy, West China Hospital, West China Medical School, Sichuan University, Chengdu 610041, China.
lijuan17@hotmail.com
Honokiol is an active compound purified from magnolia that has been shown to induce cell differentiation, apoptosis, and anti-angiogenesis effects, as well as an enhancement in tumor growth delay in combination with chemotherapeutic agents in several mouse xenograft models. Our goal was to investigate the radiosensitization effect of honokiol on lung carcinoma. The radiosensitization effect of liposomal honokiol in Lewis lung carcinoma cells (LL/2) was analyzed using an in vitro clonogenic survival assay. For an in vivo study, Lewis lung carcinoma-bearing C57BL/6 mice were treated with either liposomal honokiol at 25 mg/kg or 5 Gy of single tumor radiation, or a combination of both over 12 days of treatment. The tumor growth delay and the survival time were evaluated. In addition, histological analysis of tumor sections was performed to examine changes by detecting the microvessel density and apoptosis in tumor tissues. In the clonogenic survival assay, LL/2 cells treated with IC(50) Lipo-HNK for 24 h showed a radiation enhancement ratio of 1.9. After 12 days of combination treatment, the tumor volume decreased 78% and produced an anti-tumor activity 1.3-fold greater than a predicted additive effect of honokiol and radiation alone. This combination treatment also caused an 8.7 day delay in tumor growth. The cell cycle distribution and histological analysis demonstrated that
liposomal honokiol has an anti-tumor effect via inducing apoptosis and inhibiting angiogenesis. Liposomal honokiol can enhance tumor cell radiosensitivity in vitro and in vivo, indicating that radiotherapy combined with liposomal honokiol can lead to greater anti-tumor efficacy.
PMID: 19116447 [PubMed - indexed for MEDLINE]
Mol Cancer Res. 2006 Sep;4(9):621-33.
Honokiol potentiates apoptosis, suppresses osteoclastogenesis, and inhibits invasion through modulation of nuclear factor-kappaB activation pathway.
FREE TEXT
Ahn KS,
Sethi G,
Shishodia S,
Sung B,
Arbiser JL,
Aggarwal BB.
Cytokine Research Laboratory, Department of Experimental Therapeutics, The University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA.
Recent reports have indicated that honokiol can induce apoptosis, suppress tumor growth, and inhibit angiogenesis. In this report, we found that honokiol potentiated the apoptosis induced by tumor necrosis factor (TNF) and chemotherapeutic agents, suppressed TNF-induced tumor cell invasion, and inhibited RANKL-induced osteoclastogenesis, all of which are known to require nuclear factor-kappaB (NF-kappaB) activation. Honokiol suppressed NF-kappaB activation induced by a variety of inflammatory stimuli, and this suppression was not cell type specific. Further studies showed that honokiol blocked TNF-induced phosphorylation, ubiquitination, and degradation of IkappaBalpha through the inhibition of activation of IkappaBalpha kinase and of Akt. This led to suppression of the phosphorylation and nuclear translocation of p65 and NF-kappaB-dependent reporter gene expression. Magnolol, a honokiol isomer, was equally active. The expression of NF-kappaB-regulated gene products involved in antiapoptosis (IAP1, IAP2, Bcl-x(L), Bcl-2, cFLIP, TRAF1, and survivin), proliferation (cyclin D1, cyclooxygenase-2, and c-myc), invasion (matrix metalloproteinase-9 and intercellular adhesion molecule-1), and angiogenesis (vascular endothelial growth factor) were also down-regulated by honokiol. Honokiol also down-regulated NF-kappaB activation in in vivo mouse dorsal skin model. Thus, overall, our results indicate that NF-kappaB and NF-kappaB-regulated gene expression inhibited by honokiol enhances apoptosis and suppresses osteoclastogenesis and invasion.
PMID: 16966432 [PubMed - indexed for MEDLINE]
Honokiol/Magnolia Extract Magnolol and honokiol are the constituents of the bark of Magnolia officinalis. Both are phenolic compounds in which honokiol is an isomer of magnolol. Magnolia extract is known to be beneficial for brain and heart health. More recent studies have shown that magnolia extract also helps prevent Alzheimer’s, relieves anxiety, kills bacteria and fungus and inhibits cancer.
Honokiol is the compound responsible for most of the cancer-inhibiting properties of magnolia extract. It fights cancer by inducing caspase-dependent apoptosis through a p53 independent pathway and by inhibiting angiogenesis
Honokiol is water insolubile, which hampers its administration for therapy of cancer. A couple of the studies using honokiol on cancer implemented a liposome delivery system to enhance its delivery. I have not found a liposome supplement, so it would be best to take magnolia extract with fat or oil.
We examined whether honokiol can overcome apoptotic resistance in primary tumor cells derived from B-CLL patients. Honokiol induced caspase-dependent cell death in all of the B-CLL cells examined and was more toxic toward B-CLL cells than to normal mononuclear cells, suggesting greater susceptibility of the malignant cells. Honokiol-induced apoptosis was characterized by the activation of caspases 3, 8, and 9 and cleavage of PARP. Exposure of B-CLL cells to honokiol resulted in up-regulation of bax and down-regulation of the expression of the key survival protein Mcl-1, which is associated with response to treatment in B-CLL patients. In addition, B-CLL cells pre-treated with IL-4, a cytokine known to support B-CLL survival, underwent apoptosis when subsequently incubated with honokiol, indicating that honokiol could also overcome the pro-survival effects of IL-4. Furthermore, honokiol enhanced cytotoxicity induced by fludarabine, cladribine, or chlorambucil. These data indicate that honokiol is a potent inducer of apoptosis in B-CLL cells and should be examined for further clinical application either as a single agent or in combination with other anticancer agents.
The natural product honokiol induces caspase-dependent apoptosis in B-cell chronic lymphocytic leukemia (B-CLL) cells, Blood. 2005 Jul 15;106(2):690-7. Epub 2005 Mar 31;
Our results showed that honokiol induced apoptosis of RKO cells in a time- and dose-dependent manner. At 5-10 microg/mL for 48 h, honokiol induced apoptosis through activating Caspase cascades. Pharmacokinetics study demonstrated that, honokiol could be absorbed quickly by intraperitoneal injection, and maintained in plasma for more than 10 h. In nude mice bearing RKO-incubated tumor, honokiol displayed anticancer activity by inhibiting tumor growth and prolonging the lifespan of tumor bearing mice. With little toxicity to normal cells and potent anticancer activity in vitro and in vivo, honokiol might be a potential chemotherapy candidate in treating human colorectal carcinoma.
Honokiol: a potent chemotherapy candidate for human colorectal carcinoma World J Gastroenterol. 2004 Dec 1;10(23):3459-63
Honokiol induced RKO cell apoptosis in a dose-dependent manner. The mRNA expression level and protein level of Bid were up-regulated while that of Bcl-xl was down-regulated, but no changes in Bax and Bcl-2 were observed. Western blotting showed p53 expression had no remarkable changes in honokiol-induced RKO cell apoptosis. LS180 cells treated with honokiol exhibited apparent growth inhibition like RKO cells and Sw480 cells. Honokiol can induce RKO cells apoptosis through activating caspase cascade by p53-indepenent pathway.
Honokiol induces apoptosis through p53-independent pathway in human colorectal cell line RKO, World J Gastroenterol. 2004 Aug 1;10(15):2205-8.
The exposure of human lymphoid leukemia Molt 4B cells to honokiol led to both growth inhibition and the induction of apoptosis. Morphological change showing apoptotic bodies was observed in the cells treated with honokiol. The fragmentation by honokiol of DNA to oligonucleosomal-sized fragments that are characteristics of apoptosis was observed to be concentration- and time-dependent. These findings suggest that growth inhibition by honokiol of Molt 4B cells results from the induction of apoptosis in the cells.
Honokiol induces apoptosis in human lymphoid leukemia Molt 4B cells. Int J Mol Med. 1998 Dec;2(6):671-3.
Honokiol exhibited potent anti-proliferative activity against SVR cells in vitro. In addition, honokiol demonstrated preferential inhibition of primary human endothelial cells compared with fibroblasts and this inhibition was antagonized by antibodies against TNF alpha-related apoptosis-inducing ligand. In vivo, honokiol was highly effective against angiosarcoma in nude mice. Our preclinical data suggests that honokiol is a systemically available and non-toxic inhibitor of angiogenesis and should be further evaluated as a potential chemotherapeutic agent.
Honokiol, a small molecular weight natural product, inhibits angiogenesis in vitro and tumor growth in vivo. J Biol Chem. 2003 Sep 12;278(37):35501-7. Epub 2003 Jun 19
In the current study, we encapsulated honokiol with liposome and tested it on cisplatin-sensitive (A2780s) and -resistant (A2780cp) human ovarian cancer models... Administration of Lipo-HNK resulted in significant inhibition (84-88% maximum inhibition relative to controls) in the growth of A2780s and A2780cp tumor xenografts and prolonged the survival of the treated mice. These anti-tumor responses were associated with marked increases in tumor apoptosis, and reductions in intratumoral microvessel density. Lipo-HNK may provide an effective approach to inhibit tumor growth in both cisplatin sensitive and -resistant human ovarian cancer with minimal side effects.
J Cancer Res Clin Oncol. 2008 Sep;134(9)
37-45. Epub 2008 Mar 19
In a human ovarian carcinoma mouse model, combination treatment with H-PEGL (0.4 mg/day for 30 days; intraperitoneal) and DDP (5 mg/kg on days 7, 11, 15, 19; intraperitoneal) acted synergistically to inhibit tumor growth by 91.48% without notable toxicity, but H-PEGL and DDP alone only inhibit tumor growth by 66.83% and 52.5% as compared to the NaCl solution control, respectively. Assessment of microvessel density and apoptosis index by CD31 and terminal deoxynucleotidyl transferase-mediated nick end labeling immunohistochemistry respectively suggested that the antitumor activity of H-PEGL is mediated by angiogenesis inhibition and introduction of apoptosis. Our results showed us a splendid prospect of the clinical application of combination treatment on patients suffering from ovarian cancer with H-PEGL and DDP.
Int J Gynecol Cancer. 2008 Jul-Aug;18(4):652-9. Epub 2007 Sep 24
One of the effects of Ras is to drive pumps that remove chemotherapy drugs from cancer cells. In breast cancer cell lines with activations in Ras family genes, honokiol appears to prevent Ras from turning on an enzyme called phospholipase D, Arbiser and his colleagues found. It also has similar effects in lung and bladder cancer cells in the laboratory. Phospholipase D provides what have come to be known as “survival signals” in cancer cells, allowing them to stay alive when ordinary cells would die.
Previous reports have shown that honokiol induces apoptosis in numerous cancer cell lines and showed preclinical efficacies against apoptosis-resistant B-cell chronic lymphocytic leukemia and multiple myeloma cells from relapse-refractory patients. Here, we show that honokiol can induce a cell death distinct from apoptosis in HL60, MCF-7, and HEK293 cell lines. The death was characterized by a rapid loss of integrity of plasma membrane without externalization of phosphatidyl serine. The broad caspase inhibitor z-VAD-fmk failed to prevent this cell death. Consistently, caspase activation and DNA laddering were not observed. The death was paralleled by a rapid loss of mitochondrial membrane potential, which was mechanistically associated with the mitochondrial permeability transition pore regulated by cyclophilin D (CypD) based on the following evidence: (a) cyclosporin A, an inhibitor of CypD (an essential component of the mitochondrial permeability transition pore), effectively prevented honokiol-induced cell death and loss of mitochondrial membrane potential; (b) inhibition of CypD by RNA interference blocked honokiol-induced cell death; (c) CypD up-regulated by honokiol was correlated with the death rates in HL60, but not in K562 cells, which underwent apoptosis after being exposed to honokiol. We further showed that honokiol induced a CypD-regulated death in primary human acute myelogenous leukemia cells, overcame Bcl-2 and Bcl-XL–mediated apoptotic resistance, and was effective against HL60 cells in a pilot in vivo study. To the best of our knowledge, this is the first report to document an induction of mitochondrial permeability transition pore–associated cell death by honokiol.
Cancer Res 2007;67(10):4894–903
The mice treated with 15 and 10 mg/kg liposomal honokiol showed different inhibiting response to tumor compared with control group, including free liposome group and PBS controls. When the dose of liposomal honokiol was elevated to 25 mg/kg, there are significantly inhibitions of tumor growth, whereas there was no further enhancement of the antitumor activity at the dose of 50 mg/kg. Hence, we selected the dose of 25 mg/kg as optimum dose.
BMC Cancer. 2008; 8: 242
Oral gavage of 2 mg honokiol/mouse (thrice a week) significantly retarded growth of PC-3 xenografts without causing weight loss. Tumors from honokiol-treated mice exhibited markedly higher count of apoptotic bodies and reduced proliferation index and neovascularization compared with control tumors.
Clinical Cancer Research 14, 1248, February 15, 2008
Inhibition of the phosphoinositide 3-kinase (PI3K)/mammalian target of rapamycin (mTOR) pathway is an appealing method for decreasing the immunoresistance and augmenting T cell-mediated immunotherapy. A major impediment to this strategy is the impact of conventional PI3K/mTOR pathway inhibitors on T cell function. In particular, rapamycin, is a well-known immunosuppressant that can decrease the activity of the PI3K/mTOR pathway in tumor cells, but also has a profound inhibitory effect on T cells. Here we show that Honokiol, a natural dietary product isolated from an extract of seed cones from Magnolia grandiflora, can decrease PI3K/mTOR pathway-mediated immunoresistance of glioma, breast and prostate cancer cell lines, without affecting critical proinflammatory T cell functions. Specifically, we show that at doses sufficient to down-regulate levels of phospho-S6 and the negative immune regulator B7-H1 in tumor cells, Honokiol does not significantly impair T cell proliferation or proinflammatory cytokine production. In contrast to classic inhibitors, including LY294002, wortmannin, AKT inhibitor III and rapamycin, Honokiol specifically decreases the PI3K/mTOR pathway activity in tumor cells, but not in freshly stimulated T cells.
Honokiol-mediated inhibition of PI3K/mTOR pathway: a potential strategy to overcome immunoresistance in glioma, breast, and prostate carcinoma without impacting T cell function, J Immunother. 2009 Jul-Aug;32(6):585-92
Magnolia Extract Fights Difficult-to-Treat Cancers
By
Linda Fugate PhD
Created
06/22/2011 - 05:21
Oral
squamous cell carcinoma, B-cell
chronic lymphocytic leukemia, and
lung cancer are all difficult to treat with conventional chemotherapy. Researchers have found that extracts from the Magnolia grandiflora plant are effective in fighting these three cancers in laboratory models. The reported mechanism was induction of apoptosis in each case. Honokiol, magnolol, and parthenolide are the compounds believed to be the active ingredients.
Dr. Xi-rui Chen of the University of Toronto, Ontario, Canada, and colleagues tested honokiol on
squamous cell carcinoma. This type of
cancer has a response rate of only 30 to 40 percent to most commonly used cytotoxic chemotherapy agents in large studies. Earlier research indicates that these
cancer cells become resistant to chemotherapy drugs by a mechanism of circumventing apoptosis. The toxicity to peripheral blood mononuclear cells and primary cultured human cells has been reported to be low. Since normal cells have a different physiology from
cancer cells, Chen suggested that honokiol's ability to induce apoptosis could make it a novel treatment agent, selectively killing the
cancer. Honokiol was effective in killing oral
squamous cell carcinoma cells in lab studies by induction of apoptosis in Chen's work.
Dr. Gustavo H. Marin and colleagues at the National University of La Plata, Buenos Aires, Argentina, reported similar results for B-cell
chronic lymphocytic leukemia (B-CLL). This type of
cancer can be managed, but not cured, as the name suggests. The prognosis has not improved despite years of research. Marin used a water extract of Magnolia seeds to induce apoptosis in B-CLL cells, including cells that were resistant to chlorambucil. From the successful results, he concluded that the herbal extract is a promising therapy strategy.
For
lung cancer, Dr. Qi-qi Jiang and colleagues at the West China Medical School reported that honokiol kills
lung cancer cells in a lab xenograph model, both alone and in combination with the standard chemotherapy agent cisplatin. The mechanism was apoptosis, as in the other studies.
For safety issues, Dr. Melissa E. Munroe and colleagues at the University of Iowa reported that honokiol had no adverse effects in treating an animal model of
rheumatoid arthritis. Honokiol “has long been used in traditional Asian medicine without toxic side effects,” she added.
I found clinical trials of magnolia extracts for other conditions at
http://clinicaltrials.gov. For
cancer, the promising lab results have not yet been verified in humans.
References:
1. Chen XR et al, “Honokiol: A promising small molecular weight natural for the growth inhibition of oral
squamous cell carcinoma cells”, International Journal of Oral Science 2011; 3:34-42.
http://www.ncbi.nlm.nih.gov/pubmed/21449214
2. Marin GH et al, “Apoptosis induced by Magnolia Grandiflora extract in chlorambucil-resistant B-chronic lymphocytic leukemia cells”, Journal of
Cancer Research and Therapeutics 2010 October-December; 6(4): 463-5.
http://www.ncbi.nlm.nih.gov/pubmed/21358081
3. Jiang QQ et al, “Improved therapeutic effectiveness by combining liposomal honokiol with cisplatin in
lung cancer model” BMC
Cancer 2008; 8: 242.
http://www.ncbi.nlm.nih.gov/pubmed/18706101
4. Munroe ME et al, “Honokiol, a natural plant product, inhibits inflammatory signals and alleviates inflammatory arthritis”, Journal of Immunology 2007 Jul 15; 179(9): 753-63.
http://www.ncbi.nlm.nih.gov/pubmed/17617564
Reviewed June 22, 2011
Edited by Alison Stanton
Linda Fugate is a scientist and writer in Austin, Texas. She has a Ph.D. in Physics and an M.S. in Macromolecular Science and Engineering. Her background includes academic and industrial research in materials science. She currently writes song lyrics and health articles.
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