Objective: To observe the effect of electroacupuncture (EA) on neurological function, the expressions of phosphorylated c-Jun amino terminal kinase (p-JNK) and Beclin-1 in rats with traumatic brain injury (TBI), so as to explore the underlying mechanism of EA in the treatment of TBI.
Methods: A total of 64 SD rats were randomly divided into blank, sham, modeling groups, with 8 rats in the blank group and the sham group and 48 rats in the modeling group. The modified Feeney free-fall impact method was used to establish the TBI rat model. After modeling, rats of the modeling group were randomly divided into model and EA groups, which were further divided into 3 d, 7 d and 14 d subgroups with 8 rats in each group. Rats in the EA group were treated with acupuncture at "Baihui" (GV20, retained for 15 min), "Shuigou" (GV26, stabbed for 20 s), "Neiguan" (PC6) and "Zusanli" (ST36) of the right side. EA (2 Hz, 1 mA) was applied to PC6 and ST36 for 15 min. The above treatments were performed once a day, and different subgroups were continuously stimulated for 3, 7 and 14 days, respectively. The neurological impairment was evaluated by modified neurological severity score(mNSS). The pathological morphological changes and the protein expressions of p-JNK and Beclin-1 in the injured area of the brain were detected by Nissl staining and immunohistochemistry, separately.
Results: After modeling, the mNSS and the protein expressions of p-JNK and Beclin-1 were increased (P< 0.05) on day 3, 7 and 14 in the model group relative to the sham group. The Nissl bodies were reduced or even dissolved and neurons were seriously damaged in the model group on the 3rd day, which were mildly repaired on day 7 and 14. Following acupuncture interventions, compared with the model group, the mNSS on day 7 and 14 and the protein expressions of p-JNK and Beclin-1 on day 3, 7 and 14 were decreased (P< 0.05)in the EA group. The status of Nissl bodies and neurons in the EA group was better at all time points than that in the model group. There were no significant differences in the above indicators between the blank group and the sham group.
Conclusion: EA can significantly improve the neurological function of TBI model rats, which may be related to its effects in down-regulating the protein expressions of p-JNK and Beclin-1 in the injured area of the brain.
目的：观察电针对创伤性颅脑损伤(TBI)大鼠神经功能和磷酸化c-Jun 氨基末端激酶(p-JNK)、Beclin-1表达的影响，探讨电针治疗TBI的可能机制。方法：将64只6周龄SD大鼠随机分为空白组、假手术组各8只，其余大鼠采用改良Feeney自由落体撞击法复制TBI模型并随机均分为模型组、电针组，进一步分为3、7、14 d 3个亚组，每组8只。电针组大鼠予“百会”“水沟”、右侧“内关”“足三里”针刺干预，“百会”留针15 min, “水沟”点刺20 s，“内关”“足三里”两穴分别连接电针治疗仪的正极与负极，断续波，频率2 Hz，电流强度约1 mA，每次电针干预时长为15 min。采用mNSS评分评定各组大鼠神经功能缺损情况，Nissl染色法观察大鼠脑组织病理形态改变，免疫组织化学染色法检测大鼠损伤区脑组织p-JNK、Beclin-1蛋白表达。结果：与空白组和假手术组比较，模型组大鼠3、7、14 d时mNSS评分均升高(P<0.05)；与同时点模型组比较，电针组干预7、14 d时mNSS评分降低(P<0.05)。与空白组和假手术组比较，模型组大鼠3 d时尼氏小体减少甚至溶解消失，神经元受损严重，7、14 d时尼氏小体逐渐增加，神经元形态有所恢复；电针组大鼠神经元修复状况在各时点都优于模型组。与空白组和假手术组比较，模型组大鼠各时点损伤区脑组织p-JNK、Beclin-1蛋白表达均升高(P<0.05)；与模型组比较，同时点电针组大鼠损伤区脑组织p-JNK、Beclin-1蛋白表达均降低(P<0.05)。结论：电针可明显改善TBI大鼠神经功能损伤，促进大鼠损伤脑组织修复，其机制可能与下调损伤脑组织中p-JNK、Beclin-1蛋白的表达有关。.
Keywords: Autophagy; Beclin-1; Electroacupuncture; Neural function; Traumatic brain injury; c-Jun amino terminal kinase.