目的探讨双黄连注射液对大鼠急性乌头碱中毒脑损伤的干预作用。方法将200只SD大鼠分为空白对照组、双黄连对照组、乌头碱中毒组,双黄连干预A组,双黄连干预B组,每组40只。乌头碱中毒组及双黄连干预组以20μg/kg乌头碱一次性尾静脉注射染毒,注射后2~3 min内给双黄连干预组注射双黄连(A组30 mg/kg、B组60 mg/kg);空白对照组及双黄连对照组按体质量予尾静脉注射等量生理盐水(2 ml/kg)后,给双黄连对照组注射双黄连(60 mg/kg)。给药后1、6、12、24 h用高效液相法测定脑组织谷氨酸(Glu)、γ氨基丁酸(GABA),采用TUNEL法检测神经元凋亡情况。结果与空白对照组相比,乌头碱中毒组Glu含量、神经元凋亡数目显著升高,大鼠脑皮质GABA含量在染毒后1 h明显下降(P均均<0.05)。与乌头碱中毒组相比,双黄连干预A、B组GABA含量明显升高,Glu含量明显降低,脑皮质凋亡细胞数目显著降低(P<0.05)。各组相比,乌头碱中毒组在注射乌头碱后12 h时脑额叶皮质光病理学损伤最为明显,双黄连干预A、B组脑皮质损伤较乌头碱中毒组有所改善。结论双黄连可显著抑制兴奋性递质Glu含量提高GABA含量,拮抗神经细胞凋亡,从而起到一定程度的拮抗急性乌头碱所致脑损害。 Objective To investigate the effects of Shuanghuanglian Injection on acute cerebral injury induced by aconitine in rats. Methods 200 SD rats were divided into blank control group, Shuanghuanglian control group, aconitine poisoning group, Shuanghuanglian intervention group A and Shuanghuanglian intervention group B, 40 rats in each group. Aconitine intoxication group and Shuanghuanglian intervention group were treated with 20μg / kg aconitine once a single intravenous injection. Shuanghuanglian was injected into Shuanghuanglian intervention group within 2 ~ 3 minutes after injection (group A, 30 mg / kg, group B 60 mg / kg). Shuanghuanglian control group was injected with Shuanghuanglian (60 mg / kg) after injection of equal volume of normal saline (2 ml / kg) into the tail vein of the control group and shuanghuanglian control group. At 1, 6, 12 and 24 h after administration, glutamate (Glu) and gamma aminobutyric acid (GABA) were measured by high performance liquid chromatography. Neuronal apoptosis was detected by TUNEL method. Results Compared with the blank control group, the content of Glu and neuron apoptosis in aconitine poisoning group were significantly increased. The content of GABA in cerebral cortex of aconitine poisoning group obviously decreased at 1 hour (P <0.05). Compared with aconitine poisoning group, Shuanghuanglian intervention group A, B GABA content was significantly increased, Glu content was significantly reduced, the number of apoptotic cells in the cerebral cortex significantly reduced (P <0.05). Compared with each group, aconitine poisoning group had the most obvious light pathology of cerebral frontal cortex after 12h injection of aconitine, and the cerebral cortex injury of group A and group B was better than aconitine poisoning group. Conclusion Shuanghuanglian can significantly inhibit the content of Glu in excitatory neurotransmitter, increase the content of GABA and antagonize the apoptosis of nerve cells, which can antagonize aconitine-induced brain damage to a certain extent.