Every-other-day fasting attenuated inflammation in rats after spinal cord injury via the aryl hydrocarbon receptor/suppressor of cytokine signaling 2/nuclear transcription factor-κB signaling pathway / 中国康复理论与实践

ABSTRACT

ObjectiveTo explore the role of aryl hydrocarbon receptor/suppressor of cytokine signaling 2/nuclear transcription factor-κB (AHR/SOCS2/NF-κB) signaling in the reduction of spinal cord injury (SCI) inflammation with every-other-day fasting (EODF). MethodsA total of 36 healthy male Sprague-Dawley rats were randomly divided into sham group (n = 12), model group (n = 12) and EODF group (n = 12). The latter two groups were established C5 spinal cord hemi-clamp model. The EODF group received EODF, namely fasting and feeding per 24 hours (water free), for two weeks after operation. They were assessed with Grooming Test before operation, and one, seven and 14 days after operationt, respectively. Pathological injury of spinal cord was observed with HE staining 14 days after operation, while the expression of AHR, SOCS2 and NF-κB proteins were detected with Western blotting, and the mRNA of AHR, SOCS2, inhibitor α of NF-κB (IκBα), NF-κB and tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) were measured with reverse transcription real-time quantitative polymerase chain reaction. ResultsCompared with the sham group, the Grooming Test score decreased in the other two groups (P < 0.05), and cavity, edema and structural disorder appeared in the spinal cord. Compared with the model group, the pathology of EODF group improved, and the Grooming Test score increased (P < 0.05). The mRNA and protein expression of AHR and SOCS2 increased (P < 0.05), the mRNA and protein expression of NF-κB decreased (P < 0.05), the mRNA expression of IκBα increased (P < 0.05), and the mRNA expression of TNF-α and IL-6 decreased (P < 0.05). ConclusionEODF may promote the recovery of motor function of forelimb in rats with SCI, and relieve damage and inflammation, which may associate with the activation of AHR/SOCS2/NF-κB signaling pathway.