Inhibition of prostanoid synthesis protects against neuronal damage induced by focal ischemia in rat brain

Buccellati, Carola; Folco, Giancarlo; Sala, Angelo; Scelsi, R; Masoero, Elisabetta; Poggi, Paola; Govoni, Stefano; Favalli, L.; Rozza, A.

doi:10.1016/s0304-3940(98)00745-9

Cited by 30 publications

(15 citation statements)

References 12 publications

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“…On the other hand, MMP-9 is involved in the destruction of the basal membrane (Johnson et al, 1998) and degradation of proteins, such as plasminogen activator or ␤-amyloid, whose activity has been correlated with the progression of neurodegeneration (Deb and Gottschall, 1996;Gottshall, 1996). PGE 2 has since long been related with inflammation in different tissues; recently, cyclooxygenase metabolites have been involved in CNS inflammatory reactions as well as in brain ischemia processes (Buccellati et al, 1998), providing insight into the onset mechanisms and suggesting novel therapeutic interventions for brain inflammationrelated diseases (Kalaria, 1999).…”

Section: Discussionmentioning

confidence: 99%

Estrogen Prevents the Lipopolysaccharide-Induced Inflammatory Response in Microglia

Vegeto¹,

Bonincontro²,

Pollio³

et al. 2001

J. Neurosci.

433

297

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After neuronal injury and in several neurodegenerative diseases, activated microglia secrete proinflammatory molecules that can contribute to the progressive neural damage. The recent demonstration of a protective role of estrogen in neurodegenerative disorders in humans and experimental animal models led us to investigate whether this hormone regulates the inflammatory response in the CNS. We here show that estrogen exerts an anti-inflammatory activity on primary cultures of rat microglia, as suggested by the blockage of the phenotypic conversion associated with activation and by the prevention of lipopolysaccharide-induced production of inflammatory mediators: inducible form of NO synthase (iNOS), prostaglandin-E 2 (PGE 2 ), and metalloproteinase-9 (MMP-9). These effects are dose-dependent, maximal at 1 nM 17␤-estradiol, and can be blocked by the estrogen receptor (ER) antagonist ICI 182,780. The demonstration of ER␣ and ER␤ expression in microglia and macrophages and the observation of estrogen blockade of MMP-9 mRNA accumulation and MMP-9 promoter induction further support the hypothesis of a genomic activity of estrogen via intracellular receptors. This is the first report showing an anti-inflammatory activity of estrogen in microglia. Our study proposes a novel explanation for the protective effects of estrogen in neurodegenerative and inflammatory diseases and provides new molecular and cellular targets for the screening of ER ligands acting in the CNS.

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Section: Discussionmentioning

confidence: 99%

Estrogen Prevents the Lipopolysaccharide-Induced Inflammatory Response in Microglia

Vegeto¹,

Bonincontro²,

Pollio³

et al. 2001

J. Neurosci.

433

297

View full text Add to dashboard Cite

show abstract

“…[16,19] The neuroprotective effects may also be explained by mechanisms other than anti-inflammatory actions, for example mitochondrial depolarization, [20] inhibition of caspase activity along with the reversal of depletion in glutathione, [15] or antithrombotic effects. [21] Because of the absence of neuroinflammation in our study population, cognitive improvement after the administration of indomethacin cannot be addressed. However, it can be deduced that acute cognitive decline is not a predicted adverse effect in conjunction with the other aforementioned side effects in healthy individuals.…”

Section: Discussionmentioning

confidence: 97%

A Single Dose of Indomethacin Does Not Prolong Premotor Reaction Time in Young, Healthy Adults: A Randomized, Placebo-Controlled, Double-Blind, Cross-Over Study

et al. 2012

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Amaç: Bu çalışmada sağlıklı bireylerde tek doz indometazinin bilgi işlem hızını etkileyebileceği hipotezi araştırıldı. Objectives: In this study, we aimed to investigate the hypothesis that a single dose of indomethacin may affect information processing speed in healthy subjects. Hastalar ve yöntemler: Patients and methods:In this cross-sectional, randomized, placebo controlled, double-blind, cross-over study, 30 healthy adults (8 males, 22 females; mean age 32.4±5.3 years; range 24 to 42 years) received a single dose of 25 mg indomethacin (Endol, oral capsule, DEVA Pharmaceutics, Kartepe, Turkey) and placebo. Premotor reaction and response times were measured electromyographically before and after the administration of preparations by a blinded researcher in the Electrophysiology Laboratory at Gazi University, Faculty of Medicine, Department of Physical Medicine and Rehabilitation, Ankara.Results: Premotor reaction time measurements before and after a single dose of indomethacin were 169.1±36.3 and 160.2±29.5 msec, respectively (p=0.113). Premotor reaction time measurements before and after a single dose of placebo were 158.7±35.5 and 161.5±36.3 msec, respectively (p=0.516). There was also no statistically significant difference between premotor reaction time measurements of the indomethacin and placebo groups. Conclusion:A single dose of indomethacin did not change premotor reaction time and response time in healthy adults. This may suggest that indomethacin has no effect on the information processing speed in healthy adults.

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“…In the sa me way, in do met ha cin pre vents de la yed ne u ro nal de ath. 10,11 Buc ce lat ti et al 11 de mons tra ted that in do met ha cin tre at ment with 20 mg/kg/do se one ho ur pri or to isc he mi a dec re a sed in farct si ze in fo cal isc he mic rat bra in com pa red to the con trol gro up. Tu tak et al 9 re por ted that tre at ment with 0.2 mg/kg in do met ha cin (to tal thre e do ses every 12 ho urs) 30 mi nu tes af ter H-I dec re a sed in farct si ze in ex pe ri men tal hypo xic isc he mic rat bra in compa red to the con trol gro up.…”

Section: Discussionmentioning

confidence: 99%

Indomethacin Prevents Neuronal Apoptosis in Newborn Rats with Hypoxic-Ischemic Brain Injury

Taşkın¹,

Satar²,

Zorludemir³

et al. 2011

Turkiye Klinikleri J Med Sci

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A AB BS S T TR RA AC CT T O Ob b j je ec c t ti i v ve e: : Cyclo oxy ge na se path way and pros tag lan dins play an im por tant ro le in the pat ho ge ne sis and de la yed mec ha nisms of hypo xic-isc he mic bra in in jury. The aim of this study was to in ves ti ga te the ef fect of dif fe rent do ses of in do met ha cin, a non se lec ti ve cyclo oxy ge na se in hi bitor, on ne u ro nal apop to sis in rats with hypo xic-isc he mic bra in in jury. M Ma a t te e r ri i a al l a an nd d M Me et t h ho od ds s: : Seven-day-old rat pups with the Ri ce mo del of hypo xic-isc he mic ce reb ral in jury we re ran domly di vi ded in to fi ve gro ups. Gro up 1 (n= 15) pups we re gi ven physi o lo gic sa li ne, ne it her li ga ti on nor hypo xi a we re per for med. Gro up 2 (n= 15) pups we re tre a ted with physi o lo gic sa li ne af ter hypoxic-isc he mi a. Gro up 3 (n= 15) pups we re tre a ted with in do met ha cin at a do se of 2 mg/kg be fo re hypo xic isc he mi a. Gro up 4 (n= 15) pups we re tre a ted with thre e do ses of in do met ha cin at a dose of 2 mg/kg every 12 h af ter hypo xic-isc he mi a. Gro up 5 (n= 15) pups we re tre a ted with thre e do ses of in do met ha cin, at a do se of 4mg/kg every 12 h af ter hypo xic isc he mi a. Af ter 72 ho urs, the rats we re de ca pi ta ted and bra in he misp he res we re eva lu a ted by the TU NEL (Terminal deoxynucleotidyl transferase mediated dUTP nick end labeling) sta i ning met hod. R Re e s su ul lt ts s: : In do met ha cin tre at ment, eit her be fo re or af ter hypo xi a, re sul ted in a sig ni fi cant re duc ti on in the num bers of apopto tic cells in the rat bra in when com pa red to tho se who we re tre a ted with physi o lo gic sa li ne af ter hypo xic-isc he mi a (P< 0.001). C Co on nc c l lu u s si i o on n: : Our re sults de mons tra ted that in do met ha cin ad mi nistra ti on, eit her be fo re or af ter hypo xic-isc he mi a, re du ces ne u ro nal apop to sis; and we pro po se that in do met ha cin may be a po ten ti al cho i ce of tre at ment for hypo xic-isc he mic bra in in jury.K Ke ey y W Wo or rd ds s: : Hypo xi a-isc he mi a, bra in; apop to sis; in do met ha cin Ö ÖZ ZE ET T A Am ma aç ç: : Sik lo ok si je naz yo la ğı ve pros tag lan din ler, hi pok sik-is ke mik be yin ha sa rı nın pa to gene zin de ve geç dö nem ki sü re cin de önem li rol oy na mak ta dır. Bu ça lış ma nın ama cı, bir non-se lektif sik lo ok si je naz in hi bi tö rü olan in do me ta zi ni fark lı doz lar da uy gu la rak hi pok sik-is ke mik be yin ha sar lı rat lar da nö ro nal apo pi to zis üze ri ne et ki le ri ni araş tır mak tır. G Ge e r re eç ç v ve e Y Yö ön n t te em m l le er r: : Le vi neRi ce me to du na gö re hi pok sik is ke mi oluş tu ru lan ye di gün lük rat yav ru la rı rast ge le beş gru ba ay rıl -dı. Grup 1'de ki (n: 15) yav ru la ra ne li gas yon ne de hi pok si uy gu lan ma dan sa de ce se rum fiz yo lo jik ve ril di. Grup 2'de ki (n: 15) yav ru la ra hi pok sik-is ke mik ha le ge ti ril dik ten son ra se rum fiz yo lo jik veril di. Grup 3'te ki (n: 15) yav...

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Inhibition of prostanoid synthesis protects against neuronal damage induced by focal ischemia in rat brain

Cited by 30 publications

References 12 publications

Estrogen Prevents the Lipopolysaccharide-Induced Inflammatory Response in Microglia

Estrogen Prevents the Lipopolysaccharide-Induced Inflammatory Response in Microglia

A Single Dose of Indomethacin Does Not Prolong Premotor Reaction Time in Young, Healthy Adults: A Randomized, Placebo-Controlled, Double-Blind, Cross-Over Study

Indomethacin Prevents Neuronal Apoptosis in Newborn Rats with Hypoxic-Ischemic Brain Injury

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