PubMed · 9117170
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R W Smith, M I Cawley. 1997. Chrysiasis.. https://doi.org/10.1093/rheumatology%2F36.1.3
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Apoptosis of brain cells is observed in many inflammatory disorders of the central nervous system. Nitric oxide (NO) has been shown to induce apoptosis in several brain cell types, but not previously in astrocytes. In the present study, the hypothesis was examined that interleukin (IL)-1beta would induce production of NO by astrocytes which, in turn, would signal apoptotic death in these glial cells. TUNEL staining demonstrated apoptosis in astrocytes treated with IL-1beta. Using an ELISA method, IL-1 receptor antagonist protein completely abrogated this astrocyte apoptosis, while N(G)monomethyl-L-arginine partially prevented apoptosis but almost entirely blocked NO production. Thus, IL-1beta appears to signal apoptosis of astrocytes by a mechanism involving, in part, the induction of NO.
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The efficacy of weekly low-dose methotrexate treatment of rheumatoid arthritis is well documented. Efficacy and adverse events are both dose dependent, and side effects rather than lack of response are the main reason for discontinuing therapy. Several adverse effects appear to be related to folate deficiencies, and are largely due to the antifolate properties of methotrexate. In order to diminish side effects without compromising drug efficacy, clinical trials have been performed using folic acid or folinic acid concomitantly with methotrexate. Important to this achievement are both the timing of folate supplementation and the weekly folate-to-methotrexate ratio. Considering these and other factors, an individually adjusted supply of folic acid is proposed. For several patients a properly balanced diet is sufficient; they do not need additional folate supplements when using methotrexate.