Ewelina Bratek is PhD student in Dept. of Neurochem at Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland. Ewelina Bratek has published more than 3 papers in reputed journals.
Hypoxic-ischemic encephalopathy is one of the leading causes of neonatal mortality and permanent neurological disability worldwide. It was shown recently that mGluR2/3 activation before or after ischemic insult results in neuroprotection, but the exact mechanism of this effect is not clear. The aim of present study was to investigate whether mGluR2/3 activation after hypoxia-ischemia reduces brain damage and inhibits apoptotic processes. We used an animal model of hipoxia-ischemia (H-I) on 7-day old rat pups. Animals underwent unilateral common carotid artery ligation combined with 75 min hypoxia at 7.4% oxygen. Control pups were sham-operated (anaesthetized and left c.c.a. dissected, but not ligated). Animals were injected intraperitoneally with mGluR2 (LY 379268) and mGluR3 (NAAG) agonists 1 h or 6 h after H-I (5 mg/kg of body weight). We examined the weight deficit of the ischemic brain hemisphere and the expression of caspase independent apoptosis factors (AIF, HTR/OMI, endonuclease G). The expression of trophic factors GDNF, BDNF, TGF-beta was also measured. Our results show that application of each agonist decreased brain tissue weight loss in ischemic hemisphere independently on the time of application (from 40% in H-I to 15 - 20% in treated). Both agonists of mGluR2/3 applied 1h or 6h after H-I decreased expression of AIF, HTR/OMI and endonuclease G proteins compared to untreated H-I. mGluR2/3 agonists application decreased expression of TGF-beta and increased BDNF and GDNF in the ischemic hemisphere compared to H-I. Conclusion. This study demonstrated the neuroprotective effect of mGluR 2/3 agonists on neonatal hypoxic-ischemic brain injury. Presented data suggest that this effect is connected with decreasing apoptosis.
Katerina Stambolieva is associate professor of physiology at the Institute of Neurobiology at the Bulgarian Academy of Sciences. Her scientific interests are in the field of neurophysiology, posture and equilibrium, prevention and treatment of diseases of the peripheral nervous system, motor and cognitive behavior, vestibular rehabilitation.
Background: Diabetic peripheral neuropathy (DPN) is one of the most common complications of diabetes mellitus which usually affects peripheral nerves and leads to the tingling, pain, loss of sensation in the legs and postural instability that worse the quality of life and often provokes anxiety and depression on some of patients with DPN. The aim of this study was to evaluate the prevalence rate of anxiety on the patients with DPN before and after combined therapy with Alpha- Llipoic Acid (ALA) and benfotiamin, pyridoxine and cyancobalamine together. Patients and Methods: Sixty-four patients with main duration of DPN 8.5 ± 4.7 years and aged between 50 and 65 years took part in this investigation. All patients were treated with combined therapy. The degree of anxiety in patients was evaluated by hospital anxiety and depression scale (HADS) and the postural stability –by using static posturography. The investigations were made on the first and 60th day after the therapy. Results: Before treatment all patients demonstrated high postural instability. Middle level of anxiety (HADS_A mean score 12.2±1.9) persisted in 47.8% of patients with DPN. The correlation between duration of diabetes and DPN and anxiety not observed. After treatment with combined therapy the symptoms of DPN such as tingling, and pain of legs decrease. An improvement of the postural instability and decrease of the level of anxiety (HADS_A mean score 8.6±1.3) were observed. Conclusion: Treatment with combined therapy decrease the naturopathic symptomatic and level of anxiety, caused to improvement the quality of life of patient with DPN.