动物造模 z-bio 2021-06-03 928

　　Objective To explore the therapeutic effect of tacrolimus on spinal cord injury in rats and its regulation of NF-kB/JNK signaling pathway.

　　Method Experimental rats were randomly divided into three groups (n=15): sham operation group, model group, and tacrolimus treatment group. Allen's method was used to establish animal models of spinal cord injury. After modeling, the rats were given tacrolimus (0.3 mg/kg) for 21 days. Basso-Beattie-Bresnahan (BBB) spinal cord injury behavioral scoring test was performed on days 0, 1, 7, 14, and 21, respectively. HE staining was used to observe the state of spinal cord injury in experimental rats and the activity of antioxidant enzymes in spinal cord tissue was measured. The expression of IL-4mRNA and TGF-β mRNA in spinal cord tissue was measured by RT-PCR, and NF-kB in spinal cord tissue was measured by Westernblot experiment. / JNK signaling pathway related protein expression.

　　Results Tacrolimus can significantly improve the BBB score of rats with spinal cord injury (P<0.05), increase SOD, CAT, GPX enzyme activities and reduce MDA content (P<0.05), and reduce the abnormal apoptosis of spinal cord neurons , Reduce the ratio of IL-4mRNA, TGF-β mRNA expression and NF-kB p-p65/NF-kB p-p65 and p-JNK/JNK protein expression in spinal cord tissue (P<0.05).

　　Conclusion Tacrolimus can significantly improve spinal cord injury, which may be through anti-oxidation, anti-inflammatory response, anti-apoptosis of spinal cord neurons, and inhibit the activation of NF-kB/JNK signaling pathway.