Elsevier

Neuroscience Letters

Volume 270, Issue 3, 6 August 1999, Pages 188-190
Neuroscience Letters

Acute and transient increase of lipocalin-type prostaglandin D synthase (β-trace) level in cerebrospinal fluid of patients with aneurysmal subarachnoid hemorrhage

https://doi.org/10.1016/S0304-3940(99)00494-2Get rights and content

Abstract

We measured the concentration of lipocalin-type prostaglandin D synthase (PGDS) in cerebrospinal fluid (CSF) and serum in patients 1, 3, 5, 7, 9, 11, 14 and 17 days after subarachnoid hemorrhage (SAH) due to ruptured cerebral aneurysms. The PGDS level in lumbar CSF increased about two-fold at day 3 (20.85±2.71 μg/ml, mean±SE) and at day 5 (25.24±3.76), as compared with the level at day 1 (11.25±1.07). The CSF level gradually decreased and returned to the day 1 level at day 17. The serum PGDS level was much lower than the CSF level (0.39±0.06 at day 1) and almost unchanged until day 17. The neuron-specific enolase level in CSF, as an index of brain damage, was maximum at day 1 (29.83±7.32 ng/ml) and decreased at day 3 and at day 5 (18.28±2.65 and 11.95±1.82, respectively). These results suggest that the transient and delayed increase in the PGDS level in CSF is due to its induction of PGDS in the arachnoid membrane after SAH.

References (15)

There are more references available in the full text version of this article.

Cited by (32)

  • Neurobiological Basis of Hypersomnia

    2017, Sleep Medicine Clinics
    Citation Excerpt :

    These results suggest that the effect of LPS on sleep is partially dependent on PGs and is likely mediated mainly by other proinflammatory substances. On the other hand, the induction of L-PGDS or H-PGDS is observed in the brain of patients with various neurodegenerative diseases and their animal models, such as subarachnoid hemorrhage,80,81 demyelination,82–84 lysosomal storage disease,85 chronic multiple sclerosis,86 hypoxic ischemic injury,87,88 Alzheimer disease,89 and spinal cord contusion injury,90 the induction of which probably increases the PGD2 level in the brain91 and increases the production of various cytokines in the brain in a DP1 or DP2 receptor–dependent manner.82 Several natural compounds that induce NREM sleep after oral or IP administration to mice and rats have recently been identified, including hastatoside and verbenalin, which are iridoid compounds in the herbal tea Verbena92,93; ornithine94; crocin and crocetine from Crocus sativus L (saffron)95; glycine96; l-stepholidine,97 honokiol,98 and magnorol99 from Chinese herb and medicine; polyphenols from Korean seaweed100; methylthioadenosine from Japanese sake yeast101,102; Zn-containing yeast103,104; and triethylene glycol from the Indian medicine Ashwagandha (Fig. 8).105

  • Peroxisome-proliferator-activated receptor-gamma (PPARγ) activation protects neurons from NMDA excitotoxicity

    2006, Brain Research
    Citation Excerpt :

    We are currently investigating this possibility. 15d-PGJ2 is a downstream product of prostaglandin D2, a prostaglandin uniquely enriched in brain along with its synthesizing enzyme (prostaglandin-D synthase), suggesting a high likelihood for involvement of 15d-PGJ2 in endogenous brain processes (Hayaishi, 2000; Mase et al., 1999). More recently, analysis of 552 patients with an acute stroke admitted within 24 h after symptom onset demonstrated that increased blood plasma 15d-PGJ2 concentration is associated with good early and late neurological outcome and smaller infarct volume (Blanco et al., 2005), suggesting an important role for 15d-PGJ2 in stroke pathogenesis.

  • Protein kinase C activates human lipocalin-type prostaglandin D synthase gene expression through de-repression of notch-HES signaling and enhancement of AP-2β function in brain-derived TE671 cells

    2005, Journal of Biological Chemistry
    Citation Excerpt :

    Clinical studies showed the importance of many lipocalin gene family proteins including the L-PGDS (12). Actually, the L-PGDS level is enhanced in serum or cerebrospinal fluid of the patients with hypertension (57), arteriosclerosis (16), or subarachnoid hemorrhage (58). Thus, L-PGDS is thought to be useful as the diagnostic marker for those diseases (3, 4).

View all citing articles on Scopus
View full text