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目的探讨氯胺酮对糖尿病周围神经病变大鼠的脊髓保护作用。方法成年雌性W istar大鼠70只,随机留取10只为正常对照组(A组),腹腔注射生理盐水(3 m.lkg-1.d-1);其余大鼠用链脲菌素(STZ)制造糖尿病模型,得到48只糖尿病大鼠。将其随机等分为2组:B组为糖尿病对照组(n=24):腹腔注射与A组等体积的生理盐水;C组为氯胺酮治疗组(n=24):腹腔注射氯胺酮10 m.gkg-1(1 m.gm l-1);于治疗后第1、3、5及8周分别进行行为学测定,记录机械痛觉;于第8周测定并记录神经传导速度;取脊髓切片,应用免疫组化方法和图象分析系统检测TNFα-在脊髓背角的表达情况,同时用尼氏染色法观察脊髓的病理形态学改变。结果与A组比较,B组、C组大鼠脊髓背角组织中TNF-a的表达显著升高(P<0.01);与B组比较,C组的TNFα-表达显著降低(P<0.01),并且减轻了糖尿病慢性神经触诱发痛(P<0.01)。结论糖尿病大鼠周围神经病变引起的神经痛与脊髓背角促炎性细胞因子TNFα-有关。而氯胺酮可明显抑制脊髓背角TNFα-的表达,减轻糖尿病神经痛。
Objective To investigate the protective effects of ketamine on spinal cord injury in diabetic peripheral neuropathy rats. Methods Seventy adult Wistar rats were randomly divided into normal control group (A group) and normal saline (3 m.lkg-1.d-1). The remaining rats were treated with streptozotocin STZ) to create a diabetic model, resulting in 48 diabetic rats. The rats in group B were randomly divided into 2 groups: group B was diabetic control group (n = 24): intraperitoneal injection of equal volume of saline and group A were treated with ketamine (n = 24): intraperitoneal injection of ketamine 10 m. g kg-1 (1 m.gm l-1). Behavioral tests were performed at 1, 3, 5 and 8 weeks after treatment to record the mechanical allodynia. The nerve conduction velocity was measured and recorded at the 8th week. Immunohistochemistry and image analysis system were used to detect the expression of TNFα in spinal dorsal horn. The pathological changes of spinal cord were observed by Nissl staining. Results Compared with group A, the expression of TNF-a in dorsal horn of spinal cord in group B and group C was significantly increased (P <0.01); Compared with group B, the expression of TNFα in group C was significantly decreased (P <0.01) , And alleviated the chronic neurotrauma in diabetic patients (P <0.01). Conclusion Neuralgia induced by peripheral neuropathy in diabetic rats is related to TNFα, a proinflammatory cytokine in spinal dorsal horn. Ketamine can significantly inhibit spinal dorsal horn TNFα expression, reduce diabetic neuralgia.