Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0085437 (
bacterial meningitis
)
4,038
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The aim of the present study was to evaluate the anti-inflammatory and neuroprotective effects of a
poly (ADP-ribose) synthetase
inhibitor 3-aminobenzamide during the early phase of experimental
bacterial meningitis
in the newborn piglet. Meningitis was induced by intracisternal injection of 10(8) colony forming units of Escherichia coli in 100 microl of saline. 3-Aminobenzamide, given 30 mg kg(-1) as a bolus i.v. injection 30 min before induction of meningitis, significantly attenuated the meningitis-induced acute inflammatory responses such as increased cerebrospinal fluid (CSF) lactate concentration, CSF leukocytosis and increased CSF tumor necrosis factor-alpha level. However, meningitis-induced increase in intracranial pressure and decrease in CSF glucose level were not significantly improved. Increased cerebral cortical cell membrane lipid peroxidation products (conjugated dienes) and decreased brain ATP/phosphocreatine levels observed in the meningitis group were also significantly improved with 3-aminobenzamide treatment. However, the improvement of reduced Na+, K+-ATPase activity did not reach a statistical significance (p = 0.06). In summary, 3-aminobenzamide significantly attenuated the acute inflammatory responses and the ensuing brain injury during the early phase of neonatal
bacterial meningitis
. These findings suggest that
poly (ADP-ribose) synthetase
inhibitors such as 3-aminobenzamide might be a promising novel anti-inflammatory and neuroprotective adjuvant therapy in neonatal
bacterial meningitis
.
...
PMID:3-Aminobenzamide, a poly (ADP-ribose) synthetase inhibitor, attenuates the acute inflammatory responses and brain injury in experimental Escherichia coli meningitis in the newborn piglet. 1142 23
Death and co-morbidity derived from acute
bacterial meningitis
remain unacceptably high and are mainly related to immune-mediated cerebral dysfunction. Cerebral edema, hydrocephalus and ischaemic cerebrovascular events are severe complications that eventually occur following the activation of a complex network of cytokines, chemokines, proteases and oxidants released after cerebrospinal fluid infection. The caspase pathway appears to play a central role in the induction and amplification of the host inflammatory response. Such overactive immune reactions induce brain cell damage but, importantly, they may potentially be blocked. Several agents have been developed aiming to counteract the deleterious effects of such immune imbalance. These drugs are candidates to become adjuvant therapy against acute
bacterial meningitis
in the future, in addition to dexamethasone. We review the current state-of-art of
bacterial meningitis
adjuvant therapy, including caspase inhibitors, antioxidants,
poly (ADP-ribose) polymerase
inhibitors, inhibitors of lipid peroxidation and metalloproteinase inhibitors.
...
PMID:Advances in adjuvant therapy against acute bacterial meningitis. 1557 71