Chebulinic acid is a potent natural inhibitor of M. tuberculosis DNA gyrase, also can inhibit SMAD-3 phosphorylation, inhibit H+ K+-ATPase activity; it also is a natural inhibitor of vascular endothelial growth factor-A mediated angiogenesis. Chebulinic acid has hypotensive, antioxidant, anti-HIV, and anti-ulcer activities. Chebulinic acid has inhibitory effect on erythroid differentiation likely through changing transcriptional activation of differentiation relative genes, it or other tannins might influence the efficiency of some anti-tumor drugs-induced differentiation or the hematopoiesis processes.
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Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C)
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
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The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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Toxicol In Vitro. 2009 Jun;23(4):667-73.
Chebulinic acid and tellimagrandin I inhibit DNA strand breaks by hydroquinone/Cu(II) and H(2)O(2)/Cu(II), but potentiate DNA strand breaks by H(2)O(2)/Fe(II).[Pubmed: 19328845
METHODS AND RESULTS:
The effects of two polyphenols, Chebulinic acid and tellimagrandin I, on DNA strand breaks mediated by H(2)O(2)/Cu(II), hydroquinone (HQ)/Cu(II) and H(2)O(2)/Fe(II) in pBR322 plasmid DNA and genomic DNA of cultured MRC-5 human embryo lung fibroblasts were examined. The results demonstrated that Chebulinic acid and tellimagrandin I obviously inhibited HQ/Cu(II)- and H(2)O(2)/Cu(II)-mediated pBR322 DNA strand breaks. When MRC-5 cells were treated with HQ/Cu(II), the presence of Chebulinic acid or tellimagrandin I inhibited HQ/Cu(II)-mediated double strand breaks of genomic DNA. The presence of Chebulinic acid or tellimagrandin I did not affect the H(2)O(2)- and HQ-mediated reduction of Cu(II) to Cu(I). Both polyphenols could slightly inhibit H(2)O(2)/Fe(II)-mediated plasmid DNA strand break at the lower concentration (1-10 microM), but potentiate the DNA strand break at the higher concentration (over 50 microM).
These results demonstrated that Chebulinic acid and tellimagrandin I possessed antioxidant action in certain conditions and exerted prooxidant action on DNA strand breaks in other conditions.
Clin Exp Pharmacol Physiol. 1996 Aug;23(8):747-50.
In vitro inhibitory effects of chebulinic acid on the contractile responses of cardiovascular muscles.[Pubmed: 8886502
1. The effects of Chebulinic acid, which has been shown to elicit blood pressure lowering effect in rats, on aortic vascular contraction as well as cardiac contraction were studied in rats.
METHODS AND RESULTS:
2. Chebulinic acid had no effect on KCl-induced aortic contraction, but irreversibly inhibited the contractile responses to phenylephrine in an apparently non-competitive manner. Chebulinic acid also inhibited contractile responses of rat aorta to 5-hydroxytryptamine and angiotensin II. 3. Chebulinic acid inhibited the binding of [3H]-prazosin to dog aortic microsomal membranes in a concentration-dependent manner with an IC50 value of 0.34 mmol/L. Results of saturation binding experiments suggest a mixed mode of inhibition by Chebulinic acid (i.e. a decrease in both the maximal number of binding sites and the affinity for prazosin). 4. Chebulinic acid concentration-dependently and reversibly inhibited the maximal left ventricular pressure of rat heart in a Langendorff preparation with 50% inhibition occurring at a concentration of 0.3 nmol/L. 5. We conclude that Chebulinic acid exerts non-specific inhibitory actions in vascular preparations. Its inhibitory effect on cardiac contraction was reversible and three orders of magnitude more potent than that on vascular contraction.
We suggest that the hypotensive effect of Chebulinic acid is probably mediated via the decrease in cardiac output resulting from reduced left ventricular contraction.
Phytomedicine. 2013 Apr 15;20(6):506-11.
Anti-secretory and cyto-protective effects of chebulinic acid isolated from the fruits of Terminalia chebula on gastric ulcers.[Pubmed: 23462212
In continuation of our drug discovery program on Indian medicinal plants, the gastro protective mechanism of Chebulinic acid isolated from Terminalia chebula fruit was investigated.
METHODS AND RESULTS:
Chebulinic acid was evaluated against cold restraint (CRU), aspirin (AS), alcohol (AL) and pyloric ligation (PL) induced gastric ulcer models in rats. Potential anti-ulcer activity of Chebulinic acid was observed against CRU (62.9%), AS (55.3%), AL (80.67%) and PL (66.63%) induced ulcer models. The reference drug omeprazole (10 mg/kg, p.o.) showed 77.73% protection against CRU, 58.30% against AS and 70.80% against PL model. Sucralfate, another reference drug (500 mg/kg, p.o.) showed 65.67% protection in AL induced ulcer model. Chebulinic acid significantly reduced free acidity (48.82%), total acidity (38.29%) and upregulated mucin secretion by 59.75% respectively.
Further, Chebulinic acid significantly inhibited H(+) K(+)-ATPase activity in vitro with IC50 of 65.01 μg/ml as compared to the IC50 value of omeprazole (30.24 μg/ml) confirming its anti-secretory activity.
Toxicol In Vitro. 2009 Apr;23(3):425-31.
Prooxidant action of chebulinic acid and tellimagrandin I: causing copper-dependent DNA strand breaks.[Pubmed: 19344683
METHODS AND RESULTS:
The prooxidant activity of two hydrolysable tannins, Chebulinic acid and tellimagrandin I, on plasmid DNA and genomic DNA of cultured MRC-5 human embryo lung fibroblasts was assessed. The results revealed that both hydrolysable tannins in combination with Cu(II) induced DNA strand breaks in pBR322 plasmid DNA in a concentration-dependent manner. Chebulinic acid and tellimagrandin I also induced genomic DNA strand breaks of MRC-5 human embryo lung fibroblasts in the presence of Cu(II). After treatment with Chebulinic acid or tellimagrandin I alone, the pBR322 plasmid DNA and genomic DNA in MRC-5 cells kept intact. In addition, addition of Cu(I) reagent bathocuproinedisulfonic acid or catalase markedly inhibited the copper-dependent DNA strand breaks by both tannins. However, three typical hydroxyl radical scavengers, DMSO, ethanol and mannitol, did not inhibit the DNA strand breaks. Both tannins were able to reduce Cu(II) to Cu(I).
These results indicated that Chebulinic acid and tellimagrandin I induced the copper-dependent strand breaks of pBR322 plasmid DNA and MRC-5 genomic DNA with prooxidant action, in which Cu(II)/Cu(I) redox cycle and H(2)O(2) were involved and hydroxyl radical formation is important in the hypothetical mechanism by which DNA strand breaks are formed.
Acta Pharmacol Sin. 2004 Feb;25(2):231-8.
Effects of chebulinic acid on differentiation of human leukemia K562 cells.[Pubmed: 14769215
To study effects of Chebulinic acid on erythroid and megakaryocytic differentiation in K562 cells.
METHODS AND RESULTS:
The benzidine staining method was used to evaluate hemoglobin synthesis; the expression of erythroid specific glycophorin A (GPA) protein and megakaryocytic surface marker CD61 was determined by flow cytometry using fluorescence labeled antibodies; erythroid and megakaryocytic mRNA expression was analyzed by RT-PCR. During erythroid differentiation induced by butyric acid (BA) or hemin, Chebulinic acid not only inhibited the hemoglobin synthesis of BA- and hemin-treated K562 cells in concentration-dependent manner with IC50 of 4 micromol/L and 40 micromol/L respectively, but also inhibited another erythroid differentiation marker acetylcholinesterase at the concentration of 50 micromol/L in the cells either treated or untreated with each erythroid differentiation inducers, whereas Chebulinic acid 50 micromol/L did not change GPA protein expression in these cells significantly. When K562 cells were treated with TPA 50 microg/L for 72 h to induce megakaryocytic differentiation, the presence of Chebulinic acid 50 micromol/L slightly provoked the decrease of GPA protein expression induced by TPA. Chebulinic acid did not change the TPA-induced CD61 expression at the same concentration. Chebulinic acid also reduced the mRNA levels of erythroid relative genes including gamma-globin, PBGD, NF-E2, and GATA-1 genes in K562 cells either treated or untreated with BA, whereas Chebulinic acid upregulated the mRNA levels of GATA-2 transcription factor in these cells.
Chebulinic acid had inhibitory effect on erythroid differentiation likely through changing transcriptional activation of differentiation relative genes, which suggests that Chebulinic acid or other tannins might influence the efficiency of some anti-tumor drugs-induced differentiation or the hematopoiesis processes.