جستجوی مقالات مرتبط با کلیدواژه "کلشی سین" در نشریات گروه "پزشکی"

Alkaloids are important compounds that have a high potential in the treatment of diseases, including types of tumors. Different alkaloids have antiproliferative and antimetastatic effects on different types of cancer in vitro and in vivo. Compounds such as camptothecin, vinblastine, and colchicine have already been successfully developed into anticancer drugs. Colchicine binds to tubulin and interferes with tubulin polymerization, thereby disrupting microtubule formation. This issue leads to inhibiting the migration of leukocytes and other inflammatory cells and inhibiting the mitosis of dividing cells. Colchicine can also increase free cellular tubulin to limit mitochondrial metabolism in cancer cells through the inhibition of mitochondrial membrane voltage-gated anion channels. In addition, extensive research has shown that colchicine has anti-proliferative and anti-cancer properties in a wide variety of cell lines and animals. In addition, recent studies have shown that colchicine, as an anticancer agent, can effectively induce apoptosis. This is shown by its inhibitory effects on the growth of several tumor cell lines in vitro and in vivo, including gastric cell, hepatocellular carcinoma, hepatocellular carcinoma, and cholangiocarcinoma. To Colchicine is highly toxic at high doses, which limits its use in human cell therapy. Apoptosis is a regulated and programmed cell death process that involves the activation of various molecules to initiate cell death. Specific activation of apoptosis in tumor cells is a promising approach for cancer treatment. Considering the role of colchicine in inducing apoptosis, it can be considered a suitable candidate for investigating anticancer effects in the form of in vitro studies on breast cancer cell models and in vivo studies on mouse models with mammary tumors. However, the specific mechanisms of colchicine-induced cytotoxicity are controversial due to the variability of signaling pathways in different cell types. In addition, colchicine is highly toxic at high doses and the exact mechanism of its apoptotic effects in breast cancer cells is still unclear. Colchicine is an alkaloid widely used to treat gout. It also has a therapeutic effect on cancer through the induction of apoptosis, but the pathways involved in this process remain unclear. The present study was conducted to investigate the effect of this drug on mouse Breast cancer cell line in vitro and in vivo.

This research is of a fundamental type that was carried out experimentally. First, mouse mammary cancer cells (4T1) purchased from Pasteur Institute of Iran were cultured. Then, the effect of colchicine on apoptosis and related signaling pathways was determined using various tests including cell viability assay, real-time PCR, annexin V and propidium iodide staining, and western blot analysis. In vivo studies were also performed after tumor induction in mice and then their treatment.Effect of colchicineand related signaling pathways were determined using different tests including cell viability assay, real-time PCR, annexin V and propidium iodide staining and western blot analysis. In vivo studies were investigated through tumor induction with 4T1 cells in mice and then their treatment. After tumor formation, the antitumor activity of colchicine was compared in cancer mice. Tumor tissues after isolation, fixation and staining with hematoxylin and eosin were examined with a microscope for the presence of cancer symptoms.

The results showed that colchicine at a concentration of about 300 μg/ml killed 50% of 4T1 cancer cells. Colchicine significantly increased Bax and P53 mRNA expression and decreased Bcl-2 gene expression. In the in vivo study, it was shown that in the tumor tissue of mice treated with colchicine, the evidence of apoptosis and the area of ​​destruction and necrosis was much wider than that of the untreated group. The in vivo study showed that in the group treated with colchicine, the tumor tissue showed more evidence of apoptosis than the control group, and in the treated group, the area of destruction and necrosis was much wider than in the untreated group. In the tumor tissues of mice in the control group (without treatment), the signs of malignancy were more severe than in the group that had been treated, and abnormal mitotic forms were abundantly seen. Also, no metastases to the liver and spleen were observed in the treated group as well as in the control group. Finally, it can be concluded that the oral intake of pure colchicine reduces the size of induced tumors in mice, prevents further proliferation and metastasis, and induces Apoptotic. Studies have shown that tumors that grow faster, such as tumors from 4T1 cancer cells, are more invasive and metastasize to the surrounding tissues, but the cells of these tumors (with a high proportion of dividing cells) are the most sensitive to toxic compounds of the cell cycle, such as colchicine. They have sin. Continuous use of these compounds causes a high percentage of exposed cells to be destroyed. Reduction in the size of tumors and metastasis of cells to other places in mice treated with colchicine was observed in the present study.

Studies have shown that tumors that grow faster, such as tumors from 4T1 cancer cells, are more invasive and metastasize to the surrounding tissues, but the cells of these tumors (with a high proportion of dividing cells) are the most sensitive to They have cell cycle toxic compounds such as colchicine. Continuous use of these compounds causes a high percentage of exposed cells to be destroyed. Reduction in the size of tumors and metastasis of cells to other places in mice treated with colchicine was clearly observed in the present study. Colchicine had an effective role in inhibiting the proliferation of breast cancer cells, and its oral use reduced the size of induced tumors in mice, prevented further proliferation and metastasis, and induced apoptosis. The mechanism of toxicity of colchicine for cancer treatment is still not clear enough. In the present research, the results of all the tests showed that colchicine has an effective role in inhibiting the proliferation of mouse breast cancer cells and apoptosis through increasing the expression of pro-apoptotic genes and proteins Bax and p53, decreasing the expression of anti-apoptotic Bcl2 genes and proteins, and ultimately induces the activation of caspases.

Hypoxia can lead to body function impairment. It is linked to the pathology of acute mountain sickness, cardiovascular disease, and stroke. Colchicine, an anti-inflammatory drug, is used chiefly in treatment of gout, but it is also valuable in other inflammatory conditions. Preliminary data shows that colchicine has beneficial effects on COVID-19. Nothing is known about the protective effect of this drug against hypoxia-induced lethality in mice.

Protective effects of colchicine against hypoxia-induced lethality in mice at 0.5, 1, and 1.5 mg/kg, P.O. were evaluated in three experimental models of hypoxia.

Colchicine showed good activity in some models. In the circulatory model, at 0.5 mg/kg, it significantly prolonged mice survival time for 4.5 min (P<0.05). At this dose, it showed similar activity to propranolol 30 mg/kg which was used as the positive control. At 1.5 mg/kg, it was more effective than propranolol (P<0.0001). In the haemic antihypoxic model, colchicine at 1 mg/kg, significantly increased survival time and showed the same activity as propranolol (P>0.05). In the asphyctic model, colchicine did not show any activity.

Colchicine showed good protective effects against hypoxia in circulatory and haemic models where the drug at 1.5 mg/kg, was more effective than the positive control, propranolol at 30 mg/kg.

Colchicum kurdicum (Bornm.) Stef. is a monocotyledon plant which is endemic to Iran. The corm and seeds of this plant have some bioactive compounds, especially tropolone alkaloids that are used in treatment of inflammations, rheumatoid arthritis, gout, joint pains, and cancers. This study aimed at optimization of colchicine extraction from the corms of C. kurdicum and evaluating anti-inflammatory and anti-oxidant activities of the extracts.

The extraction of colchicine from C. kurdicum was optimized by the ultrasonic-assisted extraction method in methanol/deionized water (70:30) solvent system. The response-surface method was also used for analysis and optimization of the extraction. The effects of extraction time, solvent/plant ratio, and temperature were analyzed. Moreover, the extracted colchicine was assayed by HPLC. Finally, anti-inflammatory and anti-oxidant activities of the extracts were evaluated.

Colchicine/g corm (0.98±0.04 mg) was achieved in optimum condition; extraction time of 180 min, solvent/plant ratio of 20 ml/g, and temperature of 60 oC. Also, increase in temperature decreased the extraction time and solvent/plant ratio. The highest anti-inflammatory and anti-oxidant activities were found in extracts 7 and 12.

In this study, ultrasonic-assisted extraction was found as an effective method for extraction of colchicine from C. kurdicum.

Biocompatibility of dressing materials is one of the most important properties to be studied. Calcium hydroxide is one of the most widely used dressing materials. The aim of this study was to compare the cytotoxic effects of colchicine with those of calcium hydroxide.

In this experimental in vitro study, different concentrations (10, 5, 2.5 mg/mL) of calcium hydroxide and colchicine were prepared and added to C165 human gingival fibroblast cells after they were incubated in the culture medium. After 24 and 72 hours and 7 days of incubation, tetrazolium salt was added to the cells, and the amount of formazan was determined by spectrophotometry using an ELISA reader. To assess the cytotoxicity of these two materials and after drug treatment, 0.4% trypan blue dye was used to stain the cells; viable cells were counted under a light microscope. Data were analyzed using Kruskal-Wallis and Mann-Whitney tests and t-test.

The control group, without adding any material, had the highest optical density. Optical density of different concentrations (10, 5, 2.5 mg/mL) of calcium hydroxide at all the time intervals was higher than that of colchicine (p value < 0.05). In addition, trypan blue dye showed that the mean of fibroblast cells destroyed by colchicines was significantly higher than that by calcium hydroxide (p value < 0.001).

Based on the results of this study, the cytotoxic effects of both calcium hydroxide and colchicine were higher than the control group and cytotoxicity of colchicine was higher than that of calcium hydroxide. Therefore, it seems that calcium hydroxide is still the best choice for canal dressing between treatment sessions.

Generally، the root canal walls become contaminated with MTA during MTA plug placement. On the other hand، the dentinal tubules need to be open for penetration of sealer. The aim of this study was to compare dentinal tubule contamination during MTA apexification between one-visit and two-visit appointments.

In this in vitro experimental study، 38 single-canal human teeth، consisting of two groups of 17 and one control group of 4، were placed in 5. 25% NaOCl for 30 minutes. The tooth crowns were removed at CEJ; then 2 mm of root ends were cut to create open-apex roots. Canal preparation and shaping were performed up to file #100 and Gates Gliden drill #4 using the step-back technique. The smear layer was removed using NaOCl and EDTA. Finally، the canals were dried. In groups one and two، MTA plug was condensed at root end at a thickness of 3 mm. In group one (one-visit)، the samples were prepared for SEM immediately after cleaning the canal walls. In group two (two-visit)، the samples were kept under 100% humidity at 37ºC in an incubator for 24 hours. Then، the canals were irrigated with ultrasonic and 2. 5% NaOCl and prepared for SEM. In the control group، only the smear layer was removed and the samples were prepared for SEM without MTA plug. Mann-Whitney and Kruskal-Wallis statistical tests were used for statistical analysis (α=0. 05).

There was a significant difference between the groups in relation to contamination of the dentinal tubules with significantly more MTA on the canal walls in group one compared to group two (p value < 0. 001). The dentinal tubules were completely open in the control group.

The results of this study showed that in apexification with MTA in open apex teeth، two-visit treatment sessions are superior to one-visit sessions.

According to previous studies, colchicine causes neuronal destruction and learning depression. In this project, effects of colchicine injection into the CA1 and interaction between colchicine and nitric oxide (NO) in this area on the expression of drug-seeking behavior were investigated.

Wistar rats (250-300 g) were bilaterally cannulated at the CA1 area. Colchicine (2-8 μg/rat) was bilaterally administered after the placement of the cannulas and the treated animals were then allowed to recover for about 1 week before behavioral measurements began. Place conditioning was induced by morphine (2.5-5 mg/kg/day, s.c.) and conducted using a five-day schedule of an unbiased task including familiarization, conditioning and testing. NO agents were injected into the CA1 on the day of the testing and the data were analyzed by ANOVA after reviewing the data recorded by Ethovision.

Colchicine significantly reduced the drug-seeking behaviors but morphine caused an increase in these behaviors of colchicine treated rats. NO agents did not show any significant effect except for the compartment entering.

Colchicine may decrease the CA1 neural cell population but morphine increases the signs through a mechanism, which is probably dopamine dependent. The NO agents may produce the effects by dopamine due to induction of morphine.

Among late complications of sulfur mustard gas, respiratory problems, especially chronic bronchitis and pulmonary fibrosis, are the greatest causes of long-term disability. Colchicine has anti-inflammatory effects and also indication of its usage in pulmonary fibrosis. According to these and note to the effect of oxidative stress in pathogenesis of chronic bronchitis and pulmonary fibrosis, the therapeutic effects of Cochicine and the role of oxidative stress in its mechanism was studied.

One group of mice that had inhaled sulfur mustard one month ego was treated by colchicine. After sacrificing and sampling, biochemical indeces of chronic inflammation and pulmonary fibrosis of experimental group was compared with positive and negative control groups.

A significant decrease was seen in alveolar space percentage, serum vitamin C, and catalase and an increase was seen in hydroxylproline concentration, lymphocyte infiltration, and serum H2O2 in positive control group in comparison with negative control. Vitamin C and catalase increase and hydroxylproline concentration, lymphocyte infiltration and serum H2O2 decrease in experimental group in comparison with positive control group were obtained.

Colchicine has therapeutic effects on delayed lung complications of sulfur mustard gas injury and diminishing the oxidative stress can be one of mechanisms of this drugs.