Chitrakmool Plumbago Zeylanica safety, side effects, toxicity, review of plumbagin
In Ayurvedic medicine, chitrakmool has been mentioned as having pungent, astringent, diuretic, germicidal, and vesicant properties. Others mention chitrakmool to have benefit in terms of digestive, nervous and female reproductive system. Used in indigestion, gas, hemorrhoids, rheumatism, promotes sweating and small doses stimulate the central nervous system. See a list of Ayurvedic herbs. Chitrakmool is also a medicinal plant commonly used in Ethiopia for skin diseases.
As of April 2009 we could not find published human research with Chitrakmool herb.
Chitrakmool and prostate cancer
Human prostate cancer cell growth is inhibited by plumbagin, a constituent of the widely used medicinal herb chitrakmool.
Substances and chemicals found in
Aerial parts of chtrakmool have plumbagin, isoshinanolone, plumbagic acid, beta-sitosterol, 4-hydroxybenzaldehyde, trans-cinnamic acid, vanillic acid, 2, 5-dimethyl-7-hydroxychromone, and indole-3-carboxaldehyde.
Plumbagin, Isolated from Plumbago zeylanica, Induces Cell Death through Apoptosis in Human Pancreatic Cancer Cells.
Pancreatology. 2010; Department of Radiation Oncology, Far Eastern Memorial Hospital, Graduate Institute of Traditional Chinese Medicine, Chang Gung University, Taoyuan, Taiwan.
Pancreatic cancer is one of the most resistant malignancies. Several studies have indicated that plumbagin isolated from Plumbago zeylanica possesses anticancer activity. However, its antitumor effects against pancreatic cancer have not been explored. Methods: We investigated the effect of plumbagin on the growth of human pancreatic carcinoma cells and its possible underlying mechanisms. Results: Plumbagin inhibited the growth of Panc-1 and Bxpc-3 cells in a dose-dependent and time-dependent manner. Liu's staining and transmission electron microscopy demonstrated morphological changes resembling apoptosis in Panc-1 cells treated with plumbagin. The degree of apoptosis was assessed by measuring the proportions of sub-G(1), annexin V+/propidium iodide-, and terminal- deoxynucleotidyl-transferase-mediated-nick-end labeling (TUNEL)+ cells, and a significant increment in apoptotic cells was observed. Exposure to plumbagin caused the upregulation of Bax, a rapid decline in mitochondrial transmembrane potential, apoptosis-inducing factor overexpression in cytosol, and the cleavage of procaspase-9 and poly ADP-ribose polymerase. Activation of caspase-3, but not caspase-8, was evidenced by fluorometric substrate assay. Pretreatment with caspase inhibitors did not block plumbagin-induced apoptosis. Alternatively, it is possible that plumbagin downregulated phosphoinositide 3-kinase activity through a negative feedback mechanism. In an orthotopic pancreatic tumor model, plumbagin markedly inhibited the growth of Panc-1 xenografts without any significant effect on leukocyte counts or body weight. Plumbagin may induce apoptosis in human pancreatic cancer cells primarily through the mitochondria-related pathway followed by both caspase-dependent and caspase-independent cascades. It indicates that plumbagin can be potentially developed as a novel therapeutic agent against pancreatic cancer.
Chitrakmool safety, side effects,
Genotoxicity of plumbagin and its effects on catechol and NQNO-induced DNA damage in mouse lymphoma cells.
Toxicol In Vitro. 2009; Demma J, Hallberg K, Hellman B. Department of Pharmaceutical Biosciences, Uppsala University, Division of Toxicology Uppsala, Sweden.
Plumbagin, a naphtoquinone present in the roots of plumbago zeylanica has been reported to have many beneficial effects such as antibacterial, antifungal, anticancer, antimutagenic and antioxidant effects, but this compound has also been reported to have many side effects. Given the wide use of P. zeylanica in traditional medicine and the various potential therapeutic uses of plumbagin, the present study was carried out to further elucidate the potential genotoxicity and antigenotoxicity of plumbagin in mouse lymphoma L5178Y cells, using the comet assay. Without affecting the cell viability, plumbagin itself was found to induce significant DNA damage at low concentrations. When the cells were exposed to non-DNA damaging concentrations of plumbagin, together with NQNO (known to interact with DNA in many different ways) or catechol (known to induce oxidative DNA damage), plumbagin was found to significantly reduce the catechol-induced DNA damage, but to be without protective effect against the NQNO-induced damage. The fact that non-DNA damaging concentrations of plumbagin diminished the DNA damage induced by catechol, provides further support for the idea that plumbagin may act as an antioxidative agent at low concentrations.
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