Retinoic acid protects from experimental cerebral infarction by upregulating GAP-43 expression

The aim of this study was to investigate whether exogenous retinoic acid (RA) can upregulate the mRNA and protein expression of growth-associated protein 43 (GAP-43), thereby promoting brain functional recovery in a rat distal middle cerebral artery occlusion (MCAO) model of ischemia. A total of 216 male Sprague Dawley rats weighing 300–320 g were divided into 3 groups: sham-operated group, MCAO+vehicle group and MCAO+RA group. Focal cortical infarction was induced with a distal MCAO model. The expression of GAP-43 mRNA and protein in the ipsilateral perifocal region was assessed using qPCR and immunocytochemistry at 1, 3, 7, 14, 21, and 28 days after distal MCAO. In addition, an intraperitoneal injection of RA was given 12 h before MCAO and continued every day until the animal was sacrificed. Following ischemia, the expression of GAP-43 first increased considerably and then decreased. Administration of RA reduced infarction volume, promoted neurological functional recovery and upregulated expression of GAP-43. Administration of RA can ameliorate neuronal damage and promote nerve regeneration by upregulating the expression of GAP-43 in the perifocal region after distal MCAO.

La enfermedad periodontal, ¿un factor de riesgo más para el infarto cerebral isquémico aterotrombótico? / Periodontal disease, is it one more risk factor for atherothrombotic ischemic stroke?

De forma compactada se explica la relación biológicamente plausible que existe entre la aparición de accidentes cerebrovasculares, particularmente de infarto cerebral isquémico aterotrombótico y la precedencia de enfermedad periodontal inmuno-inflamatoria crónica. Se sugiere la necesidad de estudios que vinculen ambas entidades para conciliar los resultados de las investigaciones internacionales con las realizadas en nuestro medio. Se propone el análisis del estado periodontal en los pacientes pertenecientes a grupos de riesgo o víctimas de enfermedades cerebrovasculares. La consideración de la enfermedad periodontal inmuno-inflamatoria crónica como un factor de riesgo más para el infarto cerebral isquémico aterotrombótico, debe pasar de una interrogante a una estrategia(AU)

The biologically plausible relation existing between the occurrence of cerebrovascular accidents, particularly of atherothrombotic ischemic stroke, and the presence of chronic immunoinflammatory periodontal disease is explained in a compacted way. The need for studies linking both entities is suggested for conciliating the results of the international researches with those carried out in our environment. The analysis of the periodontal state in patients from risk groups of victims on cerebrovascular disease is proposed. Considering the chronic immunoinflammatory periodontal disease as a risk factor for atherothrombotic ischemic stroke should pass from a question to a strategy(AU)

A forced running wheel system with a microcontroller that provides high-intensity exercise training in an animal ischemic stroke model

We developed a forced non-electric-shock running wheel (FNESRW) system that provides rats with high-intensity exercise training using automatic exercise training patterns that are controlled by a microcontroller. The proposed system successfully makes a breakthrough in the traditional motorized running wheel to allow rats to perform high-intensity training and to enable comparisons with the treadmill at the same exercise intensity without any electric shock. A polyvinyl chloride runway with a rough rubber surface was coated on the periphery of the wheel so as to permit automatic acceleration training, and which allowed the rats to run consistently at high speeds (30 m/min for 1 h). An animal ischemic stroke model was used to validate the proposed system. FNESRW, treadmill, control, and sham groups were studied. The FNESRW and treadmill groups underwent 3 weeks of endurance running training. After 3 weeks, the experiments of middle cerebral artery occlusion, the modified neurological severity score (mNSS), an inclined plane test, and triphenyltetrazolium chloride were performed to evaluate the effectiveness of the proposed platform. The proposed platform showed that enhancement of motor function, mNSS, and infarct volumes was significantly stronger in the FNESRW group than the control group (P<0.05) and similar to the treadmill group. The experimental data demonstrated that the proposed platform can be applied to test the benefit of exercise-preconditioning-induced neuroprotection using the animal stroke model. Additional advantages of the FNESRW system include stand-alone capability, independence of subjective human adjustment, and ease of use.

[ threshold assessment of ischemic tolerance induced by normobaric hyperoxia in rat stroke model]

Recent studies suggest that normobaric hyperoxia [HO] results in ischemic tolerance to reduce ischemia brain injury. In this research, attempts were made to assess threshold of ischemic tolerance induced by normobaric hyperoxia in rat stroke model. Rats were divided into two groups and each group into four experimental groups, each containing 21 animals. The first four groups were exposed to 95% inspired Ho for 4h, 8h, 16h, and 24 hr. The second four groups acted as controls, and were exposed to 21% oxygen in the same chamber [room air, RA] continuously for 4h, 8h, 16h, and 24h. All animals were subjected to 60 min right middle cerebral arterial occlusion [MCAO] 24h after pretreatment. After 24h reperfusion, each main group was subdivided to three subgroups [n=7] for assessment of neurologic deficit score [NDS], infarct volume, Evans blue [EB] extravasations, and brain water contents. Preconditioning with 16HO and 24HO decreased NDS and infarct volume significantly. Ischemic tolerance induced by 24 HO decreased EB extravasations significantly. Preconditioning with 4HO, 8HO, 16HO and 24 HO could not decrease brain water content significantly. Although further studies are necessary to clarify the mechanisms of ischemic tolerance, the lowest Ho duration for ischemic tolerance induction is 16h, but appropriate Ho duration for ischemic tolerance induction is 24 HO