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Lentivirus-mediated inhibition of tumour necrosis factor-α improves motor function associated with PRDX6 in spinal cord contusion rats.

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机构: [1]Center for Experimental Technology of Preclinical Medicine, Chengdu Medical College, Chengdu 610083, Sichuan, China [2]Institute of Neuronscience, Kunming Medical University, Kunming 650031, China [3]Institute of Neurological Diseases,Translational Neuroscience Center, West China Hospital, Sichuan University, Chengdu 610041, China.
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摘要:
The recovery of motor function in rats is inhibited following contusion spinal cord injury (cSCI). However, the mechanism of tumour necrosis factor α (TNF-α) in motor function after cSCI associated with peroxiredoxin 6 (PRDX6) remains unknown. We randomly divided rats into four groups: sham, cSCI, vector and lentivirus mediating TNF-α RNA interference (TNF-α-RNAi-LV) group. The Basso, Beattie, Bresnahan (BBB) scale was used to evaluate motor function. Real-time quantitative PCR (qRT-PCR) and western blotting were used to detect the expression of TNF-α and PRDX6, which were located in neurons using immunohistochemistry (IHC) and immunofluorescence. Subsequently, lentiviral-mediated TNF-α was used to determine the role of TNF-αand the relationship of PRDX6 and TNF-α in cSCI. After cSCI, the motor capability of hind limbs disappeared and was followed by recovery of function. IHC analysis indicated that TNF-α and PRDX6 were primarily located in spinal cord neurons. TNF-α interference significantly improved neural behaviour and increased expression of PRDX6. Our study suggests that inhibition of TNF-α can promote the recovery of motor function. The underlying mechanism of TNF-α-promoted motor function may be connected with the up-regulation of PRDX6. This provides a new strategy or target for the clinical treatment of SCI in future.

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出版当年[2015]版:
大类 | 2 区 综合性期刊
小类 | 2 区 综合性期刊
最新[2023]版:
大类 | 2 区 综合性期刊
小类 | 2 区 综合性期刊
第一作者:
第一作者机构: [1]Center for Experimental Technology of Preclinical Medicine, Chengdu Medical College, Chengdu 610083, Sichuan, China
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通讯作者:
通讯机构: [2]Institute of Neuronscience, Kunming Medical University, Kunming 650031, China [3]Institute of Neurological Diseases,Translational Neuroscience Center, West China Hospital, Sichuan University, Chengdu 610041, China.
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