A growing body of studies has demonstrated that expression of Nog

A growing body of studies has demonstrated that expression of Nogo A is not restricted to neurons and oligodendrocytes in the CNS but occurs throughout the adult brain and spinal cord. It is a potent inhibitor of neurite outgrowth, and it is known to negatively regulate regeneration in the adult CNS. Treatment with anti Nogo A antibodies or an NgR receptor antagonist sellectchem can significantly promote axonal regeneration, neuroanatomical plasticity, and func tional recovery. Furthermore, recent studies have also demonstrated that the expression of Nogo A and NgRs is stimulated by the activated microgliamacrophages. This converging evidence points to an important role for Nogo A in mediating the inflammatory responses caused by various neurological conditions including TBI.

As the hippocampus was found to exhibit rather se vere neuronal loss after TBI, in Inhibitors,Modulators,Libraries this study, we sought to investigate TBI associated hippocampal Nogo A expres sion, cytokine levels, and axonal and neuronal damage. Inhibitors,Modulators,Libraries In addition, we aimed to elucidate the correlation between Nogo A production and post TBI neuroinflammation using indomethacin. Methods Experimental animals Adult male Wistar rats weighing 350 to 400 g were used in the current study. The rats were purchased from BioLASCO, Taiwan, Co. Ltd. and housed individually in hanging wire cages in a temperature controlled animal colony at 24 C, with a normal 12 hour12 hour lightdark cycle. The animals had free access to food and water, and they were allowed to acclimate to the lightdark cycle at room temperature for at least one week before undergoing the experiments.

Inhibitors,Modulators,Libraries All animal experiment protocols Inhibitors,Modulators,Libraries were approved by the Animal Care and Use Committee of the National Chia Yi University. As a TBI model, a special weight drop device which contained a foam bed on the bottom similar to that described by Marmarou et al. was used to deliver a standard traumatic impact to the animals. Each rat was placed under pentobarbital anesthesia, a midline incision was made on the head with a scalpel, and the skin flaps around the cutting site were peeled off laterally. After this, a metal helmet was sewn onto the top of the skull to prevent fracture from the trauma inducing impact. Rats were then placed in a prone position on the bottom plate of the weight drop device, and a 450 g weight was allowed to fall freely and vertically from a height of 1.

8 m onto the metal helmet to induce TBI. In the experiments studying drug effects on Inhibitors,Modulators,Libraries the expression of Nogo A and traumatic brain injury associated inflamma tion and axonal damage, the rats were injected with Nogo A antisense oligonucleotide or indomethacin at the time of surgery Vismodegib manufacturer while anesthetized. Nogo A mRNA assay The relative level of hippocampal Nogo A transcription was determined by RT PCR. After dissection of the brain, total hippocampal RNA was extracted with Trizol reagent, and 1 ug of each isolated RNA was subjected to cDNA synthesis.

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