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The chemical constituents of Rhubarb root are not yet completely known. Recent investigations indicate that the most important constituents are a number of substances which may be divided into two groups, viz. tannoid constituents and purgative constituents, several of which have been isolated in a free state: the former are astringent and the latter laxative.
Three crystalline tannoids have been extracted. The purgative constituents apparently exist in the form of an unstable crystalline substance: Rheopurgarin. This splits up into four glucosides: two of these yield Chrysophanic acid (so named from its forming yellow crystals) and Rheochrysidin respectively. The other two glucosides have not yet been isolated, but they appear to yield Emodin and Rhein.
There are also several resinous matters, one of which, Phaoretin, is purgative, and mineral compounds are also present, especially Oxalate of Calcium. The astringency of Rhubarb is due to a peculiar tannic acid (Rheo-tannic), which is soluble in water and alcohol. (http://www.botanical.com/botanical/mgmh/mgmh.html)
Toxicology – Oxalates are contained in all parts of Rhubarb plants, and there is some evidence that the anthraquinones are partly responsible. The toxicology is described as more akin to heavy metal poisoning than organic poisoning.
The quantities of leaf required for serious poisoning is quite large. There will be weakness, burning in the mouth and throat, abdominal pain, nausea, vomiting, respiratory and cardiac collapse, convulsions, coma and death.
Pharmacology – The anthraquinones were found to inhibit in vitro growth of Bacillus subtilis, and Staphylococcus aureus. This activity is the result of mitochondrial respiratory chain inhibition. A water extract has been found to have an action against Herpes and Influenza viruses.
A significant haemostatic effect occurs clinically in gastro-intestinal bleeding. It shortens coagulation time, reduced capillary permeability, promoted platelet formation in bone marrow, and induced proliferation of capillaries.
Emodin was found to be a strong inhibitor of respiration in Ehrlich ascites carcinoma cells. In vivo, rhein, emodin and aloe emodin inhibited P388 leukaemia in mice. It is thought the antineoplastic action is mainly due to the inhibition of oxidation and dehydrogenation of cancer cells.
The purgative action appears to be due to rhein and the sennoside components
Rhubarb has a suppressive action on the effect of methamphetamine in rats. Irritability and aggressiveness induced in rats is markedly suppressed by rhubarb.
Biochem Pharmacol. 2005 Jul 15;70(2):229-41.
Emodin induces apoptosis in human lung adenocarcinoma cells through a reactive oxygen species-dependent mitochondrial signaling pathway.
Su YT, Chang HL, Shyue SK, Hsu SL.
Institute of Medical Science, China Medical University, Taichung, Taiwan, ROC.
Emodin, a natural anthraquinone derivative isolated from Rheum palmatum L., has been reported to exhibit anti-cancer effect on several human cancers such as liver cancers and lung cancers. However, the molecular mechanisms of emodin-mediated tumor regression have not been fully defined. In this study, we show that treatment with 50 microM emodin resulted in a pronounced release of cytochrome c, activation of caspase-2, -3, and -9, and apoptosis in human lung adenocarcinoma A549 cells. These events were accompanied by the inactivation of ERK and AKT, generation of reactive oxygen species (ROS), disruption of mitochondrial membrane potential ((Delta)psi(m)), decrease of mitochondrial Bcl-2, and increase of mitochondrial Bax content. Ectopic expression of Bcl-2, or treatment with aurintricarboxylic acid, furosemide or caspase inhibitors markedly blocked emodin-induced apoptosis. Conversely, pharmacologic ERK and AKT inhibition promoted emodin-induced apoptosis. Furthermore, the free radical scavenger ascorbic acid and N-acetylcysteine attenuated emodin-mediated ROS production, ERK and AKT inactivation, mitochondrial dysfunction, Bcl-2/Bax modulation, and apoptosis. Take together, these findings suggest that in A549 cells, emodin-mediated oxidative injury acts as an early and upstream change in the cell death cascade to antagonize cytoprotective ERK and AKT signaling, triggers mitochondrial dysfunction, Bcl-2 and Bax modulation, mitochondrial cytochrome c release, caspase activation, and consequent leading to apoptosis.
Int J Cancer. 2005 Dec 30;
Emodin inhibits vascular endothelial growth factor-A-induced angiogenesis by blocking receptor-2 (KDR/Flk-1) phosphorylation.
Kwak HJ, Park MJ, Park CM, Moon SI, Yoo DH, Lee HC, Lee SH, Kim MS, Lee HW, Shin WS, Park IC, Rhee CH, Hong SI.
Laboratory of Functional Genomics, Korea Institute of Radiological and Medical Sciences, Seoul, Korea.
Emodin (1,3,8-trihydroxy-6-methylanthraquinone), an active component in the root and rhizome of Rheum palmatum, is a tyrosine kinase inhibitor with a number of biological activities, including antitumor effects. Here, we examine the effects of emodin on vascular endothelial growth factor (VEGF)-A-induced angiogenesis, both in vitro and in vivo. In vitro, emodin dose-dependently inhibits proliferation, migration into the denuded area, invasion through a layer of Matrigel and tube formation of human umbilical vein endothelial cells (HUVECs) stimulated with VEGF-A. Emodin also inhibits basic fibroblast growth factor-induced proliferation and migration of HUVECs and VEGF-A-induced tube formation of human dermal microvascular endothelial cells. Specifically, emodin induces the cell cycle arrest of HUVECs in the G(0)/G(1) phase by suppressing cyclin D1 and E expression and retinoblastoma protein phosphorylation, and suppresses Matrigel invasion by inhibiting the basal secretion of matrix metalloproteinase-2 and VEGF-A-stimulated urokinase plasminogen activator receptor expression. Additionally, emodin effectively inhibits phosphorylation of VEGF-A receptor-2 (KDR/Flk-1) and downstream effector molecules, including focal adhesion kinase, extracellular signal-regulated kinase 1/2, p38 mitogen-activated protein kinase, Akt and endothelial nitric oxide synthase. In vivo, emodin strongly suppresses neovessel formation in the chorioallantoic membrane of chick and VEGF-A-induced angiogenesis of the Matrigel plug in mice. Our data collectively demonstrate that emodin effectively inhibits VEGF-A-induced angiogenesis in vitro and in vivo. Moreover, inhibition of phosphorylation of KDR/Flk-1 and downstream effector molecules is a possible underlying mechanism of the anti-angiogenic activity of emodin. Based on these data, we propose that an interaction of emodin with KDR/Flk-1 may be involved in the inhibitory function of emodin toward VEGF-A-induced angiogenesis in vitro and responsible for its potent anti-angiogenic in vivo.
Eur J Pharmacol. 2005 Mar 7;510(1-2):113-20.
A new tactic to treat postprandial hyperlipidemia in diabetic rats with gastroparesis by improving gastrointestinal transit.
Xie W, Xing D, Zhao Y, Su H, Meng Z, Chen Y, Du L.
Institute of Medicinal Plant, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100094, China.
Improvement of gastrointestinal transit was thought to be a new tactic to treat postprandial hypertriglyceridemia in diabetic individuals with gastroparesis. Diabetic gastroparesis, lipid load testing, and the effect of domperidone or aqueous extract of rhizomes of Rheum palmatum L. on postprandial hypertriglyceridemia were evaluated in alloxan-induced diabetic rats. Alloxan diabetic animals had a slow gastrointestinal transit, together with delayed and exaggerated postprandial hypertriglyceridemia, after oral administration of olive oil, which was significantly improved after oral administration of domperidone or R. palmatum L. However, atropine could prevent the effects of R. palmatum L. The reduced postprandial hypertriglyceridemia was highly correlated with the improvement in gastrointestinal transit. These results suggest that promotion of gastrointestinal transit may be useful for the treatment of postprandial hypertriglyceridemia in diabetic patients with gastroparesis. R. palmatum L. may become a new choice for these patients since it has more potential benefits than domperidone.
Ann Acad Med Singapore. 2005 Jan;34(1):44-51.
Herbal treatment for renal diseases.
Peng A, Gu Y, Lin SY.
Department of Nephrology, Nephrology Research Institute, Huashan Hospital, Fudan University, China.
Renal fibrosis is a common consequence of chronic kidney diseases (CKD). Standard therapy to prevent progression of CKD in western medicine includes dietary protein restriction, blood pressure control, angiotensin-converting enzyme inhibition and angiotensin receptor blockade. However, little is known about the renoprotective effects of Chinese herbal medicine. Cumulative evidence suggests that some Chinese herbal medicines, including Astragalus and a mixture of Astragalus plus Angelica, Ligusticum, Triptolide and Rhubarb, have a beneficial role in slowing the progression of CKD. This effect is multi-functional and multi-targeted, and is often associated with a reduction in proteinuria and the amelioration of dyslipidaemia, but not with changes in systemic blood pressure. These mechanisms include anti-inflammation and inhibition of TGF-b overproduction. On the other hand, some Chinese herbal medicines may be hazardous to patients with renal diseases. In this review, we discuss recent advances in the research of some Chinese herbs for pharmacological intervention of progressive renal diseases and kidney-related injuries.
Toxicol Appl Pharmacol. 2004 Oct 1;200(1):1-6.
Inhibitory effect of Daesungki-Tang on the invasiveness potential of hepatocellular carcinoma through inhibition of matrix metalloproteinase-2 and -9 activities.
Ha KT, Kim JK, Lee YC, Kim CH.
National Research Laboratory for Glycobiology, Korean Ministry of Science and Technology, Dongguk University, Kyungju, Kyungbuk 780-714, South Korea.
Daesungki-Tang (DST), a drug preparation consisting of four herbs, that is, Rhei radix et rhizoma (RR; the roots of Rheum coreanum Nakai, Daehwang in Korean), Aurantiii frutus immaturus (AFI; immature fruits of Poncirus trifolita Rafin., Jisil in Korean), Magnoliae cortex (MC; the stem bark of Magnolia officinalis Rehd. Et Wils., Hubak in Korean), and Mirabilite (MS; Matrii sulfas, Mangcho in Korean), is a traditional Korean herbal medicine that is widely used in the treatment of cancer metastasis, gastrointestinal complaints, vascular disorders, and atherosclerosis-related disorders. In this study, water extracts of DST and each of the four ingredient herbs were prepared. The extracts were tested for cytotoxic activity on human hepatocellular carcinoma cells, Hep3B cells using the XTT assay method. The inhibitory effect of the extracts on the invasion of Hep3B cells was also tested using matrigel precoated transwell chambers. DST effectively inhibited the invasion of Hep3B cells, compared with the control groups in a dose-dependent manner. In addition, a gelatin zymography assay showed that DST decreased the gelatinolytic activity of matrix metalloproteinases-2 (MMP-2; IC50 = 87 microg/ml) and -9 (MMP-9; IC50 = 75 microg/ml) that are secreted from Hep3B cells, respectively. Among the four herbal ingredients of DST, only MC has been shown to significantly inhibit the invasion of Hep3B cells and MMP-2 and -9 activities. From these results, it can be concluded that DST has some potential for use as an antitumor agent.