Int Immunopharmacol. 2003 May;3(5):713-21.
Combined treatment with colchicine and Herba Taraxaci (Tarazacum mongolicum Hand.-Mazz.) attenuates Behcet's disease-like symptoms in mice and influences the expressions of cytokines.

Sohn S, Bang D, Lee SI, Kim YA, Lee ES, Ha JY, Kim JH, Choi SY, Lee S.

Laboratory of Cell Biology, Institute for Medical Sciences, Ajou University, Suwon 442-749, South Korea. sohnsadang.ajou.ac.kr

Herbal medicine, Herba Taraxaci (Tarazacum mongolicum Hand.-Mazz.), was administered to mice with Behcet's disease (BD)-like symptoms induced by herpes simplex virus (HSV). BD is a chronic recurrent inflammatory disease. Herba Taraxaci (6 mg) was administered alone or in combination with 2 microg of colchicine to BD-like mice. Colchicine is a drug that is widely used as a medication for BD patients. The water extracts of Herba Taraxaci were administered orally once per day for 20 days. Eighty percent (8 of 10) of mice treated with Herba Taraxaci combined with colchicine showed improvement in mucocutaneous symptoms compared to 0% (0 of 10) of the nontreated group and 30% (3 of 10) treated with colchicine alone. Cytokine expression in spleen tissue collected from treated mice was analyzed by RT-PCR and FACS. Treatment with Herba Taraxaci induced IL-4 mRNA, and spleen from mice receiving the combined treatment (Herba Taraxaci and colchicines) showed an increased number of splenocytes staining with anti-IL-10 (46.8+/-6.80) compared to Herba Taraxaci (35.4+/-2.17) (p<0.05) or colchicine alone (26.2+/-4.47) (p<0.001). These results suggest that the Herba Taraxaci may be an effective complementary agent in the treatment of BD.


Online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12757740&dopt=Abstract colchicine [PubMed - in process]



Eur J Obstet Gynecol Reprod Biol. 2003 Jun 10;108(2):171-6.
Familial Mediterranean fever and its implications for fertility and pregnancy.

Mijatovic V, Hompes PG, Wouters MG.

Department of Obstetrics & Gynaecology, VU University Medical Center, De Boelelaan 1117, 1081 HV, Amsterdam, The Netherlands. mijatovis4all.nl

Familial Mediterranean fever (FMF) is a recessively inherited disease of episodic fever in combination with severe abdominal pain, pleurisy, arthritis or erysipelas-like skin rashes. The disease is mainly prevalent in Sephardic Jews, Armenians, Turks and Arabs. The gene responsible for FMF was cloned in 1997. The gene expresses a protein called pyrin which is believed to play a role in the downregulation of mediators of inflammation. Several mutations have been identified of which the homozygous form of the M694V mutation is associated with a more severe expression of FMF. Prophylactic administration of colchicine is effective in relieving most patients from their attacks and preventing the development of amyloidosis, which usually leads to end-stage renal disease. Unfortunately, there is little awareness of the disease in gynaecological practice although a FMF full blown episode may mimic an acute abdominal calamity suggesting several possible gynaecological diagnoses. FMF is also associated with subfertility. In females, infertility was mainly related to oligomenorrhea although the causes remain unclear. In male FMF patients, progression of the disease may induce testicular impairment, consequently affecting spermatogenesis. Some controversy exists as to the adverse effects of colchicine on sperm production and function although the impression is that the occurrence of sperm pathology in FMF patients, using the recommended dosage of colchicine, is very low. In pregnant FMF patients, an increased occurrence of miscarriage has been found. However, the mechanisms involved remain unclear. Although colchicine is a mitotic inhibitor and transplacental crossing of colchicine has been demonstrated, no increased risk of foetal abnormalities in colchicine-treated pregnant FMF patients has been found. Therefore, amniocentesis should not be done for reassurance alone.


Online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12781406&dopt=Abstract colchicine [PubMed - in process]



Brain Res Bull. 2003 Jun 30;61(1):63-72.
Fos induction in the rat deep cerebellar and vestibular nuclei following central administration of colchicine: a qualitative and quantitative time-course study.

Pirnik Z, Mikkelsen JD, Kiss A.

Institute of Experimental Endocrinology, Slovak Academy of Sciences, Vlarska 3, 833 06, Bratislava, Slovak Republic.

The present study was conducted to demonstrate Fos expression at four levels (anterior, prefastigial, postfastigial, posterior) of the cerebellar-vestibular nuclear complex in rats exposed to 1, 6, 24, and 48h of colchicine treatment using a light microscopic avidin biotin peroxidase (ABC) immunohistochemistry. Intracerebroventricular administration of colchicine (60microg per 10microl saline) elicited a continuous increase in the number of Fos-positive cells in the main cerebellar (fastigial, interpositus, dentatus) and vestibular (superior, medial, lateral, spinal, Y) nuclei. One and six hours after colchicine treatment, intensive Fos labeling was observed only in the pyriform cortex and the hypothalamic paraventricular nucleus, respectively, and there was no Fos immunolabeling in any of the cerebellar or vestibular structures investigated. On the other hand, moderate number of Fos-positive cells was visible in each of the cerebellar and vestibular nuclei 24h after colchicine treatment. Exposure of the animals to 48h of colchicine treatment induced an additional, more than 50%, rise in the accumulation of Fos-positive profiles in almost all the cerebellar and vestibular nuclei. In addition, at this time-point, a characteristic pattern of Fos distribution appeared almost in all of the cerebellar and vestibular nuclei, however, the numerical incidence of Fos-positive profiles in paired structures along the neuroaxis was bilaterally symmetric. The present data demonstrate for the first time that the central administration of colchicine causes a persistent and, in comparison with other brain areas, time-delayed activation of certain population of neurons in both cerebellar and vestibular nuclei. We assume that the delayed Fos activation in these structures indicate that the cerebellar and vestibular nuclei are not the primary targets of the central effect of colchicine and their activation seems to be rather a result of a postponed functional consequences of the central action of colchicine probably related to the coordination of motor performance.


Online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12788208&dopt=Abstract colchicine



Mol Pharmacol. 2003 Jul;64(1):160-9.
Colchicine down-regulates cytochrome P450 2B6, 2C8, 2C9, and 3A4 in human hepatocytes by affecting their glucocorticoid receptor-mediated regulation.

Dvorak Z, Modriansky M, Pichard-Garcia L, Balaguer P, Vilarem MJ, Ulrichova J, Maurel P, Pascussi JM.

Institute of Medical Chemistry and Biochemistry, Medical Faculty, Palacky University Olomouc, Olomouc, Czech Republic.

The xenobiotic-mediated induction of three major human liver cytochrome P450 genes, CYP2B6, CYP2C9, and CYP3A4, is known to be regulated by the constitutive androstane receptor (CAR) and the pregnane X receptor (PXR). CAR and PXR are regulated, at least in part, by the glucocorticoid receptor (GR) and the hypothesis of a signal transduction cascade GR-[CAR/PXR]-P450 has been proposed. This study was aimed at testing this hypothesis in primary human hepatocytes by using the tubulin network disrupting agent colchicine. Colchicine (COL) decreased both basal and rifampicin- and phenobarbital-inducible expression of CYP2B6, CYP2C8/9, and CYP3A4. A parallel down-regulation of mRNA expression of CAR, PXR, and tyrosine aminotransferase, a prototypic gene directly regulated by GR, was observed. COL affected neither the level of GR mRNA nor ligand binding to GR. To evaluate the effect of colchicine on GR-mediated gene transactivation, HeLa cells stably or transiently transfected with a GR-responsive element-dependent luciferase reporter gene were used. COL decreased the dexamethasone-induced luciferase expression in stably transfected cell line by 50%, whereas GR transactivation in transiently transfected cells was not affected by COL. In contrast, ligand-dependent GR translocation in the human embryonic kidney 293 cell line transiently transfected with GFP-GR was inhibited by COL. We conclude that alteration of the signal transduction mediated through the GR-[CAR/PXR]-P450 cascade by colchicine is responsible for the down-regulation of CYP2C9 and CYP3A4, implicating cytoskeleton as necessary for correct functioning of this cascade under physiological conditions.


Online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12815172&dopt=Abstract colchicine