[Recommendation with serious adverse effects].
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Anti-Inflammatory Agents, Non-Steroidal↗
Biomedical subjects
Ole Vang
Publications and source records attributed to Ole Vang.
(alpha)B-crystallin in cerebrospinal fluid of patients with multiple sclerosis.
BACKGROUND: (alpha)B-crystallin is a chaperone protein and a potential myelin antigen to human T cells in Multiple Sclerosis (MS). In this study we investigate the existence of (alpha)B-crystallin in the cerebrospinal fluid (CSF) of patients with clinical symptoms of MS and control individuals without these symptoms, using a newly developed (alpha)B-crystallin specific chicken antibody. METHODS: A chicken anti-(alpha)B-crystallin was raised against recombinant (alpha)B-crystallin, characterized and used in a semi-quantitative Western blot analysis of CSF from 16 MS patients and 16 neurological patients without MS. RESULTS: Western blot analysis revealed the presence of high molecular weight (alpha)B-crystallin in CSF. Possibly posttranslationally modified aggregates of (alpha)B-crystallin were found in human astroglioma U373 cells. CSF (alpha)B-crystallin was seen in the CSF in 100% of MS patients and 88% of neurological controls without MS. CONCLUSION: (alpha)B-crystallin is present in the CSF in patients with MS and other neurological controls. Furthermore, (alpha)B-crystallin in CSF and human astroglioma cell line U373 is found in aggregates.
Adult↗
Characterization of the N-methoxyindole-3-carbinol (NI3C)--induced cell cycle arrest in human colon cancer cell lines.
Recent results have shown that indole-3-carbinol (I3C) inhibits the cellular growth of human cancer cell lines. In some cruciferous vegetables, another indole, N-methoxyindole-3-carbinol (NI3C), is found beside I3C. Knowledge about the biological effects of NI3C is limited. The aim of the present study was to show the effect of NI3C on cell growth of two human colon cancer cell lines, DLD-1 and HCT-116. For the first time it is shown that NI3C inhibits cellular growth of DLD-1 and HCT-116 and that NI3C is a more potent inhibitor of cell proliferation than I3C. In addition to the inhibition of cellular proliferation, NI3C caused an accumulation of HCT-116 cells in the G2/M phase, in contrast to I3C, which led to an accumulation of the colon cells in G0/G1 phase. Furthermore, NI3C delays the G1-S phase transition of synchronized HCT-116 cells. The indole-mediated cell-cycle arrest may be related to the increased levels of the CDK-inhibitors p21 and p27 (only induced by NI3C). Only an initial increase of cdc2 protein was observed, whereas prolonged treatment with NI3C or I3C downregulates the mRNA and proteins of cyclin-dependent kinases and cyclins. These results indicate that both NI3C and I3C inhibit the proliferation of human colon cells but via different mechanisms.
Antineoplastic Agents↗
Indolo[3,2-b]carbazole inhibits gap junctional intercellular communication in rat primary hepatocytes and acts as a potential tumor promoter.
Indole-3-carbinol (I3C) is a naturally occurring substance that shows anti-carcinogenic properties in animal models. Besides its clear anti-carcinogenic effects, some studies indicate that I3C may sometimes act as a tumor promoter. Indolo[3,2-b]carbazole (ICZ), which is formed in the acidic environment of the stomach after intake of I3C, has a similar structure to, and shares biological effects with, the well-known tumor promoter 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Therefore, we hypothesized that ICZ could be responsible for the potential tumor-promoting activity of I3C. The aim of the present study was to investigate the effect of ICZ on gap junctional intercellular communication (GJIC) in primary cultured rat hepatocytes co-cultured with the rat liver epithelial cell line WB-F344. Indolo[3,2-b]carbazole inhibited GJIC in the rat hepatocytes in a dose- and time-dependent manner. Significant inhibition was observed after 8 and 12 h of treatment with 1 and 0.1 micro M ICZ, respectively. Maximum GJIC inhibition (cell-cell communication only 5% of control values) was observed after 24-48 h of ICZ treatment. Continued exposure to 1 micro M ICZ suppressed GJIC until approximately 120 h. Both ICZ and TCDD treatment reduced the Cx32 mRNA level as well as the plasma membrane Cx32 staining. Indolo[3,2-b]carbazole increased the Cyp1a1, Cyp1a2 and Cyp1b1 mRNA levels concurrently with an increase in 7-ethoxyresorufin O-deethylase (EROD) activities. Maximum EROD activity and Cyp1a1 mRNA levels were observed after approximately 12 h, whereas Cyp1a2 and Cyp1b1 mRNA levels peaked after 48 h. This study shows that ICZ may possess tumor promoter activity down-regulating GJIC by mechanisms, which seem to include activation of the Ah receptor and/or Cyp1 activity. Further studies are needed in order to clarify the anticarcinogenic/carcinogenic effects of I3C and ICZ before high doses of I3C may be recommended as a dietary supplement.
Animals↗