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目的:探讨中药复方益糖康对链脲佐菌素(STZ)致糖尿病模型大鼠背根神经节(DRG)中电压门控性钠离子通道亚型1.7(Nav1.7)蛋白及mRNA表达的影响。方法:将健康雄性Wistar大鼠40只,体重200～250 g,随机分为空白对照组、模型组和益糖康组,其中,模型组和益糖康组采用STZ 55 mg.kg-1ip复制糖尿病大鼠模型,然后分别给予安慰剂和益糖康(4g.kg-1)5 mL.d-1ig。每周测血糖1次,随时剔除血糖低于16.7 mmol.L-1的大鼠。6周后,采集大鼠背根神经节(DRG)标本,用免疫组化和RT-PCR方法分别检测其钠离子通道Nav1.7蛋白和mRNA表达水平。结果:动物给药6周后处死前血糖:空白对照组(6.73±0.9)mmol.L-1,模型组(20.12±1.3)mmol.L-1,益糖康组(19.34±1.2)mmol.L-1,模型组与空白对照组比较有显著差异(P<0.01),益糖康组与模型组比较无显著差异。Nav1.7蛋白表达的灰度值:空白对照组149.41±5.71,模型组104.53±9.02,益糖康组132.57±6.13,模型组与空白对照组比较其表达水平显著上调(P<0.01),益糖康组与模型组比较其表达水平显著降低(P<0.01)。Nav1.7 mRNA表达的积分吸光度比值:空白对照组0.114±0.018,模型组0.215±0.043,益糖康组0.128±0.025,模型组与空白对照组比较其表达水平显著上调(P<0.01),益糖康组与模型组比较其表达水平显著降低(P<0.01)。结论:中药复方益糖康可能对Nav1.7通道有阻断作用,是其改善糖尿病痛性神经病症状的机制之一。
Objective: To investigate the expression of voltage-gated Na (superscript +) channel subtype 1.7 (Nav1.7) protein and mRNA in dorsal root ganglion (DRG) of diabetic rats induced by streptozotocin (STZ) influences. Methods: Forty healthy male Wistar rats weighing 200-250 g were randomly divided into blank control group, model group and Yixikang group. The model group and Yixikang group were treated with STZ 55 mg.kg-1 ip Diabetic rat model, and then given placebo and Yixikang (4g.kg-1) 5mL.d-1ig. Blood sugar was measured once a week, and rats with blood glucose lower than 16.7 mmol.L-1 were removed at any time. Six weeks later, DRG specimens of rats were collected, and the expression of Nav1.7 protein and mRNA in sodium channel were detected by immunohistochemistry and RT-PCR respectively. Results: The blood glucose of the rabbits was lower than that of the control group (6.73 ± 0.9) mmol.L-1, the model group (20.12 ± 1.3) mmol.L-1, and the group of Yixikang (19.34 ± 1.2) mmol. L-1, there was a significant difference between the model group and the blank control group (P <0.01). There was no significant difference between the Yixikang group and the model group. The gray value of Nav1.7 protein expression was 149.41 ± 5.71 in the blank control group, 104.53 ± 9.02 in the model group and 132.57 ± 6.13 in the Yixikang group. The expression level of Nav1.7 protein was significantly up-regulated compared with the blank control group (P <0.01) Compared with model group, the expression level of Tangkang group was significantly lower (P <0.01). The integral absorbance ratio of Nav1.7 mRNA expression was 0.114 ± 0.018 in the blank control group, 0.215 ± 0.043 in the model group and 0.128 ± 0.025 in the Yixikang group. The expression level of Nav1.7 mRNA was significantly up-regulated in the model group compared with the blank control group (P <0.01) Compared with model group, the expression level of Tangkang group was significantly lower (P <0.01). Conclusion: Yikangkang, a traditional Chinese medicine compound, may block the Nav1.7 channel and is one of the mechanisms of its improvement on the symptoms of diabetic pain neuropathy.