Naslov
Effects of enoxaparin on brain-derived neurotrophic factor and heat shock protein-70 expressions in the hippocampus following traumatic brain injury in rats

Autori
Pilipović, Kristina ; Župan, Željko ; Župan, Gordana

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni

Izvornik
Periodicum biologorum, 6th Croatian Congress of Pharmacology with International Participation, Vol 112, Suppl 1 / Župan, Gordana - Zagreb, 2010, 98-98

Skup
6.hrvatski kongres farmakologije sa međunarodnim sudjelovanjem

Mjesto i datum
Opatija, Hrvatska, 15.09.2010. - 18.09.2010

Vrsta sudjelovanja
Poster

Vrsta recenzije
Domaća recenzija

Ključne riječi
Enoxaparin; BDNF; HSP-70; traumatic brain injury; rat

Sažetak
Introduction: Neuronal damage following traumatic brain injury (TBI) is a result of direct, mechanical disruption of brain tissue and secondary, delayed mechanisms. Many of these secondary pathological events, including inflammation and oxidative stress, contribute to the neuronal death and neurological dysfunction after TBI. In addition to its anticoagulant activity, enoxaparin, a low-molecular weight heparin, has other pharmacological properties that may contribute to neuroprotection observed in experimental models of some acute and chronic neurological disorders. In experimental TBI enoxaparin reduces cerebral edema, lesion size and improves neurological recovery. Molecular mechanisms of its effects are not fully known. Present study was designed in order to investigate whether enoxaparin affects the expression of precursor and mature form ofbrain-derived neurotrophic factor (BDNF), as well as the expression of heat shock protein 70 (HSP70) in the hippocampus 48 h after the induction ofTBI in the rat. Materials and methods: Experiments were performed on adult male Wistar rats. TBI of moderate severity was induced over the left parietal cortex using the lateral fluid percussion brain injury model. Enoxaparin or vehicle were administered i.p. I h after TBI, followed by additional 7 injections given in intervals of 6 h. Sham-operated, vehicle-treated animals were used as the control group. Rats were sacrificed 48 h after the TBI induction, and left hippocampi were dissected and used for the Western blotting analyses of precursor and mature BDNF and HSP70 expressions. Results: TBI caused a significant decrease in HSP70 protein expression, while it had no effect on immunoreactivity of both forms ofBDNF. Enoxaparin treatment significantly upregulated protein expression of precursor to BDNF, whereas it had no effect on lowered HSP70 protein content. Conclusion: Our preliminary results for the first time suggest that neuroprotective effects of enoxaparin treatment in experimental TBI could be the result of the induction of precursor to BDNF expression.

Izvorni jezik
Engleski

Znanstvena područja
Temeljne medicinske znanosti

POVEZANOST RADA