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Curcumin Could Prevent the Development of Chronic Neuropathic Pain in Rats with Peripheral Nerve Injury

机译:姜黄素可预防周围神经损伤大鼠的慢性神经性疼痛的发展

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Background: Peripheral nerve injury results in chronic neuropathic pain characterized by allodynia and/or spontaneous pain. It has been suggested that activation of mitogen-activated protein kinases such as extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) contribute to theneuropathic pain.Objectives: We investigated if curcumin could prevent the development of neuropathic pain in rats with chronic constriction injury (CCI) of the sciatic nerve. Methods: The animals were divided into 3 groups. In the curcumin treatment group (n = 10), curcumin (50 mg/kg/d PO) was administered once daily from 1 day before CCI to 7 days after CCI. The rats in the sham group (n = 10) and CCI group (n = 10) received a control vehicle. The mechanical allodynia was assessed using von Frey at 1, 3, 5, and 7 days after nerve injury. Western blots were used to evaluate the levels of p-ERK, p-JNK, and phosphorylation of NR1 (p-NRl) subunits of N-methyl-D-aspartate in the spinal dorsal root ganglion. Results: In the CCI group, mechanical allodynia was observed during 7 days after nerve injury. However, curcumin treatment reversed the mechanical allodynia 7 days after nerve ligation. There were no differences in the expression of p-ERK, p-JNK, and p-NRl between the sham and curcumin groups. However, the expression of p-ERK, p-JNK, and p-NRl in the CCI group were higher than the sham group and curcumin group, respectively (P < 0.05). Conclusions: Treatment with curcumin during the early stages of peripheral neuropathy can prevent the development of chronic neuropathic pain.
机译:背景:周围神经损伤导致慢性神经性疼痛,其特征在于异常性疼痛和/或自发性疼痛。有人提出,诸如细胞外信号调节激酶(ERK)和c-Jun N端激酶(JNK)等促分裂原活化蛋白激酶的激活可导致神经性疼痛。坐骨神经慢性压迫性损伤(CCI)大鼠的疼痛。方法:将动物分为3组。在姜黄素治疗组(n = 10)中,从CCI前1天到CCI后7天每天一次给予姜黄素(50 mg / kg / d PO)。假手术组(n = 10)和CCI组(n = 10)的大鼠接受了对照载体。在神经损伤后第1、3、5和7天使用von Frey评估机械性异常性疼痛。 Western印迹用于评估脊髓背根神经节中p-ERK,p-JNK的水平以及N-甲基-D-天冬氨酸的NR1(p-NR1)亚基的磷酸化。结果:在CCI组中,神经损伤后7天观察到机械性异常性疼痛。但是,姜黄素治疗可在神经结扎后7天逆转机械性异常性疼痛。在假手术组和姜黄素组之间,p-ERK,p-JNK和p-NR1的表达没有差异。然而,CCI组中p-ERK,p-JNK和p-NR1的表达分别高于假手术组和姜黄素组(P <0.05)。结论:姜黄素在周围神经病变的早期治疗可以预防慢性神经性疼痛的发展。

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