丹参酮ⅡA对长春新碱诱导神经病理痛大鼠痛觉过敏的影响及其机制

doi:10.3969/j.issn.1006-6233.2020.07.001

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Abstract Objective: To investigate the effect of intraperitoneal tanshinone IIA on hyperalgesia induced by vincristine in rats with neuropathic pain and its possible mechanism. Methods: A total of 40 healthy male SD rats were randomly divided into 4 groups (10 in each): control group, chemotherapy-induced neuropathic pain (CINP) group (modeled by intraperitoneal injection of vincristine every other day), CINP+NS group (Successful establishment of CINP model and intraperitoneal injection of normal saline), CINP +Tan group (Successful establishment of CINP model and intraperitoneal injection of tanshinone IIA). Mechanical allodynia and heat hyperalgesia was evaluated with thermal withdrawal latency (TWL) and mechanical withdrawal threshold (MWT). Western blotting was used to detect the expression of phosphorylated c-Jun N-terminal kinase (p-JNK), glial fibrillary acidic protein (GFAP) and Ionized calcium binding adapter molecule (Iba1) in spinal cord, immunofluorescence assay to detect the Co-localization expression of GFAP and p-JNK, reverse transcription-polymerase chain reaction to detect the mRNA expression of tumor Necrosis Factor-α (TNF- α), interleukin- 6 (IL-6) and interleukin-1 (IL-1β) andenzyme-linked immunosorbent assay to detect the protein expression of TNF- α, IL-6 and IL-1β. Results: The TWL and MWT in group CINP were significantly lower those in the control group from 3 days to 14 days after the first injection of vincristine (P<0.01). The MWT and TWL in group CINP+Tan were significantly higher than those in group CINP +NS (P<0.01). Significant up- regulation was found in group CINP as compared with the control group in protein expression of p-JNK, GFAP, TNF- α, IL-6 and IL-1β and the Mrna expression of TNF- α, IL-6 and IL-1β in spinal cord (P<0.01). Significant down-regulation was observed in group CINP+Tan as compared with the CINP+NS group in the protein expression of p-JNK, GFAP, TNF- α, IL-6, IL-1β and the mRNA expression of TNF- α, IL-6 and IL-1β in the spinal cord (P<0.05). The co-localization expression of GFAP and p-JNK were observed in spinal cord. Conclusion: Tanshinone IIA can inhibit the hyperalgesia of neuropathic pain rats induced by vincristine, and its mechanism may be related to the activation of JNK pathway and inflammation of astrocytes.

Key words： Neuropathic pain Tanshinone IIA Vincristine Phosphorylated c-Jun N-terminal kinase

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http://www.hbyxzzs.cn/EN/10.3969/j.issn.1006-6233.2020.07.001 OR http://www.hbyxzzs.cn/EN/Y2020/V26/I7/1057

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