科研之友
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摘要
Objective To observe the anti-inflammation effect of the Mongolian medicine narru-3 (Naru-3) prescription in the treatment of spinal cord injury, and explore its related mechanism. Methods SD rats were randomly divided into sham group, model group, methylprednisolone (MP, 30 mg/kg) group and Naru-3 low, medium and high dose (10, 20, 30 mg/kg) group, with 12 rats in each group. The sham group was exposed to surgery only, but not attacked. The other groups were used Allen's attacking method to establish rat spinal cord injury model. Rats were ig administered in each group 30 min after operation, and rats in sham and model group was administered with normal saline once a day for 21 d. The relative expression levels of interleukin (IL)-1β, IL-6 and tumor necrosis factor-alpha (TNF-α) in spinal cord tissues were detected by real-time fluorescence quantitative PCR (qRT-PCR) and Western blotting. The levels of IL-1β, IL-6 and TNF-α in serum were detected by ELISA. The localization and expression of monocyte chemoattractant protein-1 (MCP-1) in spinal cord tissues were determined by immunohistochemistry. The proportion of M1 and M2 phenotypic macrophages in spinal cord tissue was analyzed. Results Compared with model group, Naru-3 and MP significantly reduced the levels of IL-1β, IL-6 and TNF-α protein in serum and the mRNA and protein levels of IL-1β, IL-6 and TNF-α in spinal cord tissue (P < 0.05, 0.001). The effect of Naru-3 was dose-dependent and time-dependent. Immunohistochemical results showed that Naru-3 and MP could significantly reduce the expression of MCP-1 in spinal cord compared with the model group. The results of flow cytometry showed that, compared with model group, Naru-3 and MP significantly induced M1 phenotype macrophages to differentiate into M2 phenotype (P < 0.001).Conclusion Naru-3 can effectively reduce the inflammatory response induced by spinal cord injury, and the mechanism is related to inducing M1 phenotype macrophages to differentiate into M2 phenotype.
