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PubMed1989

The inhibitory effects of N-ethylmaleimide, colchicine and cytochalasins on human T-cell functions.

The thiol-alkylating agent, N-ethylmaleimide (NEM), was found to inhibit the response of human peripheral blood mononuclear cells to the T-cell mitogen, concanavalin A (Con A). NEM (10 microM) blocked Con A-induced agglutination, production of interleukin-2 (IL-2) and expression of the IL-2 receptors (Tac) without toxicity. In order to determine whether the effects of NEM on lymphokine production were related to inhibition of agglutination, we compared the immunosuppressive effects of NEM with those of cytochalasin A, cytochalasin B and colchicine. NEM did not inhibit E-rosette (ER) formation, suggesting that it does not interfere with actin filaments. Low concentrations of NEM (4 microM) inhibited IL-2 production and Tac expression without inhibiting agglutination, while 6-10 microM NEM blocked agglutination and DNA synthesis as well. In contrast, 5-10 microM cytochalasin B (CB) inhibited ER formation, agglutination, Tac expression and DNA synthesis, but augmented IL-2 production by three- to ten-fold. Colchicine (0.1-10 microM) had no effect on ER formation or agglutination and augmented IL-2 production by as much as 18-fold. However, colchicine blocked Tac expression by greater than 40% and DNA synthesis by greater than 80%. Cytochalasin A (CA), which has the thiol-reactive properties of NEM, the actin filament-disrupting properties of CB, and the microtubule-disrupting properties of colchicine, exhibited the immunosuppressive effects of all three compounds. These studies suggest that the inhibitory effects of NEM on IL-2 production do not appear to be due to reactivity with the cytoskeleton, but are probably due to effects on signal transduction pathways leading to IL-2 production and expression of IL-2 receptors.

Agglutination↗
PubMed1993

Chromatographic analysis of the enkephalin immunoreactivity in the nucleus locus coeruleus of the cat after local colchicine administration.

Cell bodies immunoreactive for methionine- and leucine-enkephalin are found in the area of the locus coeruleus (dorsolateral pons) of the cat after injection of colchicine in the ascending projections of the nucleus. Using radioimmunoassay procedures, it is shown that colchicine induces a significant increase in methionine- and leucine-enkephalin-immunoreactive material in this area of the brain. High pressure liquid chromatography analysis demonstrated that the immunoreactive materials were authentic methionine- and leucine-enkephalin. The methionine- and leucine-enkephalin patterns were identical in the colchicine injected and non-injected sides of the dorsolateral pons. It is suggested that, in this area of the brain, colchicine (i) does not significantly modify the processing of proenkephalin to form the pentapeptides methionine- and leucine-enkephalin, and (ii) does not induce the appearance of new substances reactive to the enkephalin antisera employed.

Animals↗
PubMed1981

Colchicine affects the distribution of isotope-labeled H2O and extracellular markers in rat liver and hepatomas.

Treatment of hepatoma-bearing rats with colchicine (175 or 250 micrograms/100 g body wt) greatly diminished the radioactivity in tumors when measured 10 min after subcutaneous injection of 3H2O. There were relatively small effects of colchicine treatment on the level of radioactivity in blood and little change in the ratio of radioactivity in blood and liver. Inhibitory effects of colchicine were also observed for the distribution in hepatomas of the extracellular markers [3H] methoxy-inulin and [14C] sucrose. An effect of colchicine on circulation in hepatomas may be a factor in the previously reported inhibitory action on metabolite uptake.

Animals↗
PubMed1984

Visualisation of catecholamine-fluorescent nerve cell bodies in the rat brain after colchicine treatment.

Central administration of colchicine causes accumulation of catecholamines in nerve cell bodies and enhances their visualisation in the rat brain by the formaldehyde-glutaraldehyde (FAGLU) histofluorescence method. The detection of catecholamine-containing nerve cells by the FAGLU method was considerably improved in rats pretreated with colchicine, and adrenaline-synthesising nerve cells, which are not normally detected by the FAGLU method, could be readily localized after colchicine. The identity of the FAGLU-fluorescent nerve cells was confirmed by simultaneous immunofluorescent detection of catecholamine-synthesising enzymes in sections of the medulla oblongata. The FAGLU method applied to colchicine-treated animals could provide a simple means of detecting central adrenaline nerve cells in other species.

Animals↗
PubMed1988

Intradentate colchicine impairs acquisition of a two-way active avoidance response in a Y-maze.

Male, Fischer-344 rats received bilateral injections of colchicine (2.0 micrograms/site) into the dorsal and ventral hippocampus to destroy dentate gyrus granule cells. Colchicine impaired the ability of rats to learn a brightness discrimination, active avoidance task in a Y-maze. Acquisition was measured in 120-trial sessions given once weekly for 3 or 4 weeks. In a second experiment, colchicine-treated rats were tested in a modified procedure in which only the tone warning stimulus and a light directional cue were presented; shock was not presented. Colchicine-treated rats showed an enhanced response bias under these conditions, selecting to go to the unlighted arm with a greater frequency than the control rats whenever the tone and light were activated. These data are consistent with other reports indicating that rats with hippocampal lesions are impaired in the acquisition of a simultaneous discrimination if a response bias exists to one of the choices.

Animals↗
PubMed1994

Neuroprotective effects of colchicine in the gerbil model of cerebral ischaemia.

The tropolonic alkaloid colchicine significantly reduces the behavioural, electroencephalographic and histological damage seen after a 6-min occlusion of the two common carotid arteries of the Mongolian gerbil if the compound is administered at 2 or 4 mg/kg i.p. immediately upon reperfusion. A 45% increase in high-frequency ECoG activity and significant reduction of 80% in the hypermotility of the gerbils, with 63% less faults in a passive avoidance paradigm, were observed in conjunction with considerable protection of the hippocampus, after a single dose of 4 mg/kg colchicine. No adverse effects of colchicine treatment on animal movement and body weight were observable. Colchicine's possible mode of action, via inhibition of cellular transport systems, is discussed.

Animals↗
PubMed1991

Colchicine inhibition of duodenal absorption of calcium.

1. The effect of colchicine on calcium absorption across rat duodenum has been investigated using the single-pass continuous perfusion technique and the two-compartment system model. 2. Perfusing the rat duodenum with 0.1 and 0.5 mM colchicine produced a dose-dependent inhibiting pattern of calcium transport with no effect noted for water transport. 3. Colchicine at 0.5 mM caused a significant decrease in the rate of calcium uptake and in the accumulation capacity of the duodenal cells. 4. Accumulation of calcium in the duodenal strips displayed saturation kinetics with increasing concentration of calcium in the incubation medium. Colchicine at 0.5 mM showed a lower saturation level and decreased the average maximal flux around 46%.

Animals↗
PubMed1992

The neurobiological effects of colchicine: modulation by nerve growth factor.

To study the effects of exogenously applied nerve growth factor (NGF) on colchicine-induced neurodegeneration in the dentate gyrus of the rat hippocampal formation, colchicine (COLCH) or artificial cerebrospinal fluid (ACSF) was infused into the dorsal hippocampus (HPC) followed by unilateral infusion of either purified beta-NGF (in ACSF) or cytochrome C. One week later, animals were tested in activity chambers when NGF treatment was found to reduce the COLCH-induced hyperactivity. Animals were sacrificed 3 or 12 weeks postlesion for neurochemical or morphological analysis. Carbachol-stimulated phosphatidyl inositol (PI) turnover performed in hippocampal slices was not affected by any treatment at 3 weeks. However, 12 weeks after the lesion, CARB stimulation of PI hydrolysis was increased in the COLCH/ACSF group. NGF treatment significantly reduced the hyperstimulation in COLCH-treated rats. Morphological analysis showed that COLCH treatment increased AChE staining in the hippocampus, whereas NGF treatment had no effect on AChE staining. There was no difference in the number of septal ChAT immunoreactive cell bodies of controls or colchicine-treated rats at either time point examined. However, NGF treatment resulted in a significant increase in the number of ChAT immunoreactive cell bodies 3 weeks postlesion. Results from this study indicate that NGF can modify colchicine-induced compensatory changes in hippocampal signal transduction and has transitory influences on cholinergic cells in the medial septum.

Acetylcholinesterase↗
PubMed1993

Decreased seizure threshold after intrahippocampal colchicine injection in rats.

Wet dog shaking elicited by perforant path stimulation is little affected by bilateral injection of colchicine into the dorsal hippocampal formation but virtually eliminated by bilateral injection into the ventral hippocampal formation. Injection of colchicine into either dorsal or ventral hippocampal formation lowers the threshold for eliciting forelimb clonus with rearing. This effect is more pronounced 8 weeks postinjection than 2 weeks postinjection when colchicine is injected in the ventral hippocampal formation. This suggests that inappropriate reactive synaptogenesis and/or neuronal degeneration continues for an extended period after intrahippocampal injection of colchicine, especially in the ventral hippocampal formation.

Animals↗
PubMedDate not supplied

Colchicine poisoning.

Colchicine poisoning is an unusual but serious form of drug intoxication. Although relatively uncommon, colchicine poisoning may produce life-threatening systemic effects that must be recognized and treated by the emergency physician. This alkaloid found in Colchicum autumnale is used primarily in the treatment of gout. In toxic doses it produces nausea and vomiting, and bone marrow suppression often leading to sepsis, hypocalcemia, adult respiratory distress syndrome, and direct cardiotoxic effects. Treatment requires early recognition and supportive care including fluid and electrolyte replacement and occasionally blood component replacement therapy. Recent experiments using colchicine-specific antibodies have demonstrated beneficial effects on colchicine intoxication.

Colchicine↗
PubMedDate not supplied

Effect of colchicine on micturition reflex in rats.

Intracerebral or intraspinal cord, but not intraperitoneal, injection of low doses of colchicine in rats induces specific toxic symptoms. This paper deals in particular with the effect of colchicine on micturition. After the injection of 5-25 micrograms/rat in cerebral ventricle or 2.5-20 micrograms/rat intraspinal cord, bladder content was markedly increased, due to a dramatic urine retention. Time of latency of vesical retention was related to the dose and to the route of colchicine administration. Cystometrographic analyses were performed in control and treated rats at various intervals of time after the injection: bladder tone, as expressed by the delta P/delta V ratio, monitored from 12 to 120 hr after colchicine injection, decreased more and more during time, suggesting that the observed vesical hypotonicity is an irreversible phenomenon.

Animals↗
PubMed1993

The effects of colchicine or vinblastine on the blood calcium level in rats.

In order to clarify how microtubule inhibitors induce hypocalcemia, rats were injected with intravenous colchicine (1 mg/kg) or vinblastine (2 mg/kg). The blood calcium levels decreased rapidly, and the minimum values, reached 4 h after the injection, were 7.55 +/- 0.70 mg/100 ml (mean +/- S.D., P < 0.001) for colchicine and 7.61 +/- 0.17 mg/100 ml (P < 0.001) for vinblastine. At 24 h, these values returned to the normal range (10.13 +/- 0.42 mg/100 ml). The blood calcium values in rats fed a low calcium diet and in thyroparathyroidectomized rats were also reduced by colchicine. The incorporation of blood 45Ca into bone was reduced by the injection of colchicine. Histologically, the bone cells of rats injected with either drug were severely damaged 8 h after the injection. These results indicate that hypocalcemia may be mediated by interference with the regulatory mechanisms of bone cell calcium homeostasis, and that the destruction of microtubules may be closely related to the development of the hypocalcemia.

Animals↗
PubMed2006

Colchicine vs. omega-3 fatty acids for prevention of chronic cyclosporine nephrotoxicity in Sprague Dawley rats: an experimental animal model.

BACKGROUND: In view of the high cost of the new immunosuppressive drugs, which represents a challenge for both patients and governmental resources especially in developing countries, trials to prevent side effects of the first calcineurin inhibitor discovered (cyclosporine, Cs) are of particular interest. METHODS: In this prospective randomized experimental study, 60 male Sprague Dawley rats were enrolled. Group 1 served as negative control group and received olive oil. Group 2 received Cs orally 100 mg/kg for 80 days and served as positive control group. Group 3 was given daily colchicine (30 microg/kg/day) in addition to Cs. Group 4 was given omega-3 fatty acids (100 mg/kg/day) in addition to Cs. Animals were subjected every other week to laboratory assessment for serum creatinine, sodium, potassium, and Cs whole-blood through levels. At the end point, the animals were sacrificed, and kidney tissue was examined for histopathological changes. RESULTS: There were no significant differences in serum creatinine, creatinine clearance, and serum sodium and potassium in all groups. Histopathological examination of kidney tissues showed focal tubular atrophy and interstitial fibrosis in inner medulla and inner strip of the outer medulla in all Cs-treated animals. Morphological changes were significantly less in colchicine-treated rats compared to omega-3 fatty acid-treated rats and absent in the negative control group. Furthermore, immunostaining showed positive reactions for vimentin in Cs-treated animals only. CONCLUSIONS: Colchicine and omega-3 fatty acids are protective for the kidney against cyclosporine-induced nephropathy; however, colchicine is more protective than omega-3 fatty acid.

Animals↗
PubMed2006

Synthesis and biological evaluation of B-ring modified colchicine and isocolchicine analogs.

A series of modified colchicine and isocolchicine analogs (C-7 substituent) were synthesized and evaluated in vitro against a PC3 cancer cell line and for inhibition of microtubule polymerization. The colchicine analogs all displayed strong inhibition of tubulin polymerization, while compounds 6 and 20 also possessed an increased cytotoxic activity as compared to colchicine. More importantly, isocolchicine analogs 7, 15, and 17 showed inhibition of microtubule polymerization with IC(50) values ranging from 58 to 68muM. In addition, 7 displayed strong cytotoxic activity with an IC(50)=93nM which was more potent than colchicine analog 12.

Antineoplastic Agents↗
PubMed2005

Interaction of colchicine with human serum albumin investigated by spectroscopic methods.

We investigated the interaction between colchicine and human serum albumin (HSA) by fluorescence and UV-vis absorption spectroscopy. In the mechanism discussion, it was proved that the fluorescence quenching of HSA by colchicine is a result of the formation of colchicines-HSA complex; van der Waals interactions and hydrogen bonds play a major role in stabilizing the complex. The modified Stern-Volmer quenching constant K(a) and corresponding thermodynamic parameters deltaH, deltaG, deltaS at different temperatures were calculated. The distance r between donor (Trp214) and acceptor (colchicine) was obtained according to fluorescence resonance energy transfer (FRET).

Binding Sites↗
PubMed2005

Mitotic arrest and toxicity in Biomphalaria glabrata (Mollusca: Pulmonata) exposed to colchicine.

Continuous exposure of Biomphalaria glabrata snails to 0.1% colchicine resulted in a significant increase, relative to non-exposed snails, in the number of arrested mitotic figures in the amebocyte-producing organ (APO) as soon as 4 h, with peak numbers after 12 h of exposure. The number of circulating hemocytes was significantly elevated at 24 h. However, by 72 h both the number of mitotic figures in the APO and the concentration of circulating hemocytes in the hemolymph had returned to control levels. Hemocytes appeared to possess normal morphology throughout this exposure, including the formation of long filopodia with supporting rodlike structures that have been reported to contain microtubules. Snail survival decreased as a function of exposure time. Significantly fewer snails, relative to controls, survived a 48-h exposure, and only 1 out of 30 snails recovered from a 72-h exposure to 0.1% colchicine. Colchicine-exposed snails displayed intoxicated behavior, even upon removal from the colchicine solution, although no histopathology was evident in the CNS of snails exposed for 72 h.

Animals↗
PubMed2026

Colchicine attenuates cardiac hypertrophy by targeting the macrophage-driven Interleukin-6 suppression.

Hypertrophic cardiomyopathy (HCM), the most prevalent inherited cardiovascular disease, is strongly linked to progressive heart failure and sudden cardiac death (SCD). However, its underlying pathogenic mechanisms remain incompletely understood, and effective therapeutic strategies are still lacking. Here, we established two murine HCM models harboring high SCD risk-associated mutations. Single-cell RNA sequencing revealed immune activation and enhanced fibrotic remodeling in the myocardium of these models. Therefore, we hypothesized that colchicine, a widely used anti-inflammatory drug known to reduce cardiovascular events in multiple cardiac disorders, may also represent a promising therapeutic candidate for HCM. As we expected, colchicine treatment attenuated pathological remodeling in our study, as evidenced by reduced cardiomyocyte hypertrophy, decreased fibrosis, and downregulation of cardiac stress markers (Anp, Bnp) and fibrotic mediators (Ctgf, Col1a1, Col3a1). In addition, colchicine attenuated pro-inflammatory macrophage populations and suppressed IL-6 expression, thereby contributing to the preservation of cardiac function. These findings provide the first preclinical evidence that colchicine alleviates myocardial inflammation and fibrosis in HCM, underscoring its potential as a novel therapeutic strategy to reduce fibrosis, lower SCD risk, and improve patient outcomes.

Animals↗
PubMed2004

Comparison of rDNA sequences from colchicine treated and untreated sporocysts of Phyllodistomum folium and Bucephalus polymorphus (Digenea).

The most frequently used antimitotic agent in cytogenetic studies is colchicine. We investigated whether the initial treatment of trematodes for karyological analysis with colchicine would have mutagenic or degradational effect on rDNA sequences. Dreissena polymorpha is the intermediate host of Phyllodistomum folium and Bucephalus polymorphus, and the sporocyst stage of these trematode species develop, respectively, in the gills and gonads of this mussel. Sporocysts of P. folium and B. polymorphus were obtained from D. polymorpha collected from waterbodies in Belarus and in Lithuania. 5.8S and 28S rDNA genes, ITS1 and ITS2 of P folium and B. polymorphus were sequenced and compared, and no nucleotide sequence differences between colchicine treated and untreated trematodes were found. Based on these results, we conclude that colchicine treatment for 3-5 h has no mutagenic or degradational effect on rDNA sequences. During the course of this investigation, two genetically different P. folium samples were noted in Belarus.

Animals↗