Compound C对布比卡因神经毒性损伤的影响与机制

Effect and mechanism of Compound C on the neurotoxic injury of Bupivacaine

目的研究Compound C对布比卡因神经毒性损伤的影响及作用机制。方法健康雄性SD大鼠18只,随机分为3组,每组6只。对照组(N组):鞘内注射生理盐水30μl,腹腔注入生理盐水;2%布比卡因组(B组):鞘内注射2%布比卡因30μl,腹腔注入生理盐水;2%布比卡因+Compound C组(B+C组):鞘内注射2%布比卡因30μl,腹腔注入Compound C 20 mg/kg。各组大鼠处理后2 h、3 h、4 h、1 d和2 d利用弗莱毛测痛法测量机械痛阈,并进行下肢运动功能(MF)评分。处理3 d处死各组大鼠,采用荧光定量PCR检测各组大鼠背根神经节中单磷酸腺苷活化蛋白激酶(AMPK)的表达。结果鞘内注射布比卡因30 min后,B组和B+C组的MF评分较N组明显增高(P<0.05),4 h后B组和B+C组运动功能恢复正常。在鞘内注射布比卡因1 d后,B组的机械痛阈低于B+C组和N组(P<0.05)。荧光定量PCR结果显示,B+C组AMPK表达低于B组及N组(P<0.05)。结论 Compound C可减轻布比卡因神经毒性损伤作用,其机制可能是通过抑制AMPK的表达从而保护神经组织细胞。

Objective To investigate the effect of Compound C on neurotoxicity injury of Bupivacaine and mechanism.Methods Eighteen normal male SD rats were divided into 3 groups randomly,6 rats in each group.Normal group（group N）：the rats were received intrathecal injection with normal 30 μl and intraperitoneal injection with normal saline;2%Bupivacaine group（group B）：the rats were received intrathecal injection with 2% Bupivacaine 30 μl and intraperitoneal injection with normal saline.2% Bupivacaine combined with Compound C group（group B＋C）：the rats were received intrathecal injection with 2% Bupivacaine 30 μl combined with intraperitoneal injection with 20 mg/kg Compound C.The thresholds of mechanical pain were measured by using Von-Frey hair at 2 h,3 h,4 h,1 d,and 2 d after treatment,and motor function（MF） score was performed.The rats were sacrificed 3 d after treatment and the expression of AMPK in the dorsal root ganglia of rats was examined by fluorescent quantitation PCR.Results 30 min after intrathecal injection with Bupivacaine,compared with the group N,the MF scores of the group B and group B ＋C were increased obviously（P〈0.05）,and the MF scores of the group B and group B＋C were recovered 4 h after treatment.1 d After intrathecal in jection with Bupivacaine,the thresholds of mechanical pain decreased in group B,compared with those of group B＋C and group N（P〈0.05）.The fluorescent quantitation PCR results indicated that,the expressions of AMPK in group B＋C was lower than that of the group B and group N（P〈0.05）.Conclusion Compound C can attenuate the neurotoxicity injury of Bupivacaine,and the mechanism may be that it inhibited the expression of AMPK and protected the neural cells.