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Taurine Promotes Axonal Sprouting Through Mitochondrial Improvement in Stroke


 BackgroundBrain plasticity including axonal sprouting has been recognized in restoring motor function in ischemic stroke. Mitochondrion plays a crucial role in determining axonal sprouting in ischemic injury. Taurine (TAU) could protect brain against experimental stroke as one of the richest amino acids. However, the role of TAU on axonal sprouting and the specific potential mechanism on mitochondria of stroke were unclear. MethodsFocal cerebral cortical ischemia in C57BL/6 mice was preceded. Motor function was assayed by the Rota-Rod test on D7, D14, and D28 after stroke. Axonal sprouting was detected using immunocytochemistry with biotinylated dextran amine (BDA). The expressions of mitochondrial DNA (mtDNA), Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PCG-1a) and Transcription factor A of mitochondria (TFAM) were measured by RT-qPCR. ResultsTAU treatment significantly recovered the motor function of focal cerebral cortical ischemic mice. And TAU promoted axonal sprouting. It was also observed that TAU enhanced mtDNA content, increased the levels of Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PCG-1a) and Transcription factor A of mitochondria (TFAM). ConclusionsCollectively, the data illustrated that TAU exerted a promoting influence on axonal sprouting, through mitochondrial improvement in cerebral ischemic stroke.