[Exploration of the mechanism of electroacupuncture at "Jiaji" (EX-B2) in treating neuronal apoptosis in rats with spinal cord injury based on the JAK2/STAT3 pathway]
- PMID: 40551645
- DOI: 10.13702/j.1000-0607.20240070
[Exploration of the mechanism of electroacupuncture at "Jiaji" (EX-B2) in treating neuronal apoptosis in rats with spinal cord injury based on the JAK2/STAT3 pathway]
Abstract
Objectives: To observe the effect of electroacupuncture (EA) at "Jiaji" (EX-B2) on inhibiting neuronal apoptosis in rats with spinal cord injury based on the Janus tyrosine kinase (JAK)/signal transducer and activator of transcription (STAT) signaling pathway, so as to explore the underlying mechanism of EA in the treatment of spinal cord injury.
Methods: A total of 36 SD rats were randomly divided into sham operation group, spinal cord injury group, and Jiaji EA group, with 12 rats in each group. The spinal cord injury model was established using Allen's method. The Jiaji EA group was treated with EA at EX-B2 (once a day, 30 min each time, for a total of 14 d). After the treatment, the Basso Beattie Bresnahan (BBB) score was used to evaluate the hindlimb motor function of rats in each group. HE staining was used to observe the morphological changes of spinal cord tissues. TUNEL staining was used to observe the pathological changes and neuronal apoptosis rate of the spinal cord. Western blot was used to detect the relative expression levels of phosphorylated (p)-JAK2, p-STAT3, B-cell lymphoma-2 (Bcl-2), Bcl-2 associated X protein (Bax), and Caspase-3 proteins in the spinal cord.
Results: Compared with the sham operation group at the same time point, the BBB score decreased (P<0.01), the spinal cord tissue structure in the injury area was disordered, the cell body shrank, and the neuronal apoptosis rate increased (P<0.01), the expression levels of p-JAK2, p-STAT3, Bax, and caspase-3 proteins increased (P<0.01) while the expression level of Bcl-2 protein decreased (P<0.01) in rats of the spinal cord injury group. Compared with the spinal cord injury group, the BBB score increased on the 7th and 14th day of intervention (P<0.01), the spinal cord tissue structure tended to be normal, the degree of neuronal damage was reduced, and the apoptosis rate decreased (P<0.01), the expression levels of p-JAK2, p-STAT3, Bax, and caspase-3 proteins decreased (P<0.01, P<0.05), while the expression level of Bcl-2 protein increased (P<0.05) in rats of the Jiaji EA group.
Conclusions: EA at EX-B2 can improve the motor function of rats with spinal cord injury, up-regulate the expressions of anti-apoptotic factors, down-regulate the expressions of pro-apoptotic factors, and reduce neuronal apoptosis in spinal cord injury. The mechanism may be related to the inhibition of the activation of the JAK2/STAT3 signaling pathway.
目的: 基于Janus酪氨酸蛋白激酶(JAK)/信号转导及转录激活因子(STAT)信号通路观察电针“夹脊”对脊髓损伤大鼠神经元凋亡的影响,探讨电针治疗脊髓损伤的可能机制。方法: 将36只SD大鼠随机分为假手术组、脊髓损伤组、夹脊电针组,每组12只。采用Allen’s法制备脊髓损伤模型。夹脊电针组给予电针“夹脊”治疗(每日1次,30 min/次,共14 d)。治疗结束后对各组大鼠进行BBB评分评估大鼠后肢运动功能;HE染色观察脊髓组织形态;TUNEL染色观察脊髓病理改变及神经元凋亡率;Western blot法检测脊髓磷酸化(p)-JAK2、p-STAT3、B细胞淋巴瘤-2(Bcl-2)、Bcl-2相关X蛋白(Bax)、天冬半胱氨酸特异性蛋白酶-3(Caspase-3)蛋白的相对表达量。结果: 与同时间点假手术组比较,脊髓损伤组BBB评分降低(P<0.01);损伤区脊髓组织结构紊乱,胞体皱缩,神经元凋亡率升高(P<0.01);p-JAK2、p-STAT3、Bax、Caspase-3蛋白表达水平升高(P<0.01),Bcl-2蛋白表达水平降低(P<0.01)。与脊髓损伤组比较,夹脊电针组大鼠干预第7、14天时BBB评分升高(P<0.01);脊髓组织结构趋于正常,神经元受损程度减轻,神经元凋亡率下降(P<0.01);p-JAK2、p-STAT3、Bax、Caspase-3蛋白表达水平降低(P<0.01,P<0.05),Bcl-2蛋白表达水平升高(P<0.05)。结论: 电针“夹脊”可改善脊髓损伤大鼠运动功能,上调抗凋亡因子的表达,下调促凋亡因子的表达,减少损伤脊髓中神经元的凋亡,其机制可能与抑制JAK2/STAT3信号通路的激活有关。.
Keywords: Apoptosis; Electroacupuncture; Janus tyrosine kinase (JAK)/signal transducer and activator of transcription (STAT) signaling pathway; Jiaji (EX-B2); Spinal cord injury.
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