Geniposide Protects Against Spinal Cord Injury In Rats Through Attenuating The Regulation Of Inflammatory Response And The Bcl2/Bax Pathway

INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL MEDICINE(2018)

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摘要
Spinal cord injury (SCI) causes loss of neurological function, depending upon the severity of injury, which may lead to paralysis. However, there is still no effective pharmacotherapy for SCI treatment so far. Geniposide (GEN), a traditional Chinese medicine, which is reported to possess a wide range of health benefits. A previous study shows that GEN displays various anti-inflammatory and anti-apoptosis properties in oxygen and glucose deprivation-induced brain microvascular injury. However, it is unclear whether GEN could protect against traumatic spinal cord injury, and the underlying molecular mechanisms associated with this process still remain unknown. In the present study, the Basso, Beattie, Bresnahan scores, and the water content of the spinal cord were used to analyze the therapeutic effects of GEN on neurological function in the SCI rats. The serum levels of nuclear factor-kappa B p65 unit, interleukin (IL)-4, IL-6 and IL-10 were detected using commercial kits. The expression levels of Bcl-2, Bax, Caspase-3, Caspase-6 and Caspase-7 were measured via western blot analysis. The results demonstrated that the neurological function and the water content of the spinal cord in these SCI rats began to ameliorate after GEN treatment. Meanwhile, GEN was found to have inhibitory effects on inflammatory response, compared with the SCI group. In addition, GEN significantly reduced the protein expression of Bax, Caspase-3, Caspase-6 and Caspase-7 and promoted the protein expression of Bcl-2 in the SCI rat model, which indicated that the protective effect of GEN might be associated to anti-apoptosis activation. In summary, GEN protected against spinal cord injury in rats through attenuating inflammatory response and the regulation of Bcl-2 and Bax pathway.
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关键词
Geniposide,spinal cord injury,inflammatory response,neuronal apoptosis,Bcl2/Bax
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