眶内电针通过调控CASR介导的NLRP3炎症小体活化促进大鼠动眼神经损伤修复的机制研究OA
Mechanistic Study of Intraorbital EA in Promoting Repair of Oculomotor Nerve Injury in Rats via Regulation of CASR-Mediated NLRP3 Inflammasome Activation
目的:观察眶内电针对动眼神经损伤模型大鼠神经功能的影响,从炎症反应角度探讨其在动眼神经功能重建中的作用机制.方法:将90只SD大鼠随机分为假手术组、模型组、电针组、抑制剂组和电针+抑制剂组,每组18只(分3、7及14 d 3个亚组,每组各6只).采用眶内夹闭法造模,电针组对大鼠上直肌、下直肌及内直肌进行干预(20 min/d,14 d).对大鼠一般状态、动眼神经功能(瞳孔直径、眼球偏斜距离)进行评分,HE染色法检测动眼神经形态,Western blotting法检测CASR、NLRP3、IL-1β及IL-18表达情况,RT-qPCR法检测ASC、Caspase-1等因子表达情况.结果:与假手术组比较,模型组一般状态、动眼神经功能及各因子指标比较,差异具有统计学意义(P＜0.01);与模型组比较,电针组术后3 d仅炎症指标改善,差异具有统计学意义(P＜0.05),7 d及14 d后上述各指标均显著改善,差异具有统计学意义(P＜0.01),抑制剂组各时间点各指标比较,差异具有统计学意义(P＜0.05或P＜0.01);与电针组比较,术后3 d电针+抑制剂组大鼠一般状态比较,差异无统计学意义(P＞0.05),其余各时间点各指标比较,差异均具有统计学意义(P＜0.01).HE染色显示模型组神经纤维紊乱、髓鞘脱落,而各治疗组髓鞘再生、结构修复.结论:眶内电针可能通过调控CASR介导的NLRP3炎症小体活化促进大鼠动眼神经损伤修复.
Objective:To observe the effects of intraorbital electro-acupuncture(EA)on neurological function in rat model of oculomotor nerve injury and to explore its underlying mechanisms in oculomotor nerve functional reconstruction from the perspective of inflammatory responses.Methods:90 SD rats were randomly divided into the sham operation group,the model group,the EA group,the inhibitor group,and the EA plus inhibitor group,with 18 rats in each group.Each group was further subdivided into three time-point subgroups(3,7,and 14 days),with 6 rats in each subgroup.An oculomotor nerve injury model was established using the intraorbital clamping method.In the EA group,EA was applied to the superior rectus,inferior rectus,and medial rectus muscles for 20 min per day for 14 days.General conditions and oculomotor nerve function(including pupil diameter and ocular deviation distance)were assessed.HE staining was performed to observe the morphological changes of the oculomotor nerve.Western blotting was used to determine the protein expressions of CASR,NLRP3,IL-1β,and IL-18,while RT-qPCR was employed to measure the mRNA expressions of ASC,Caspase-1,and related factors.Results:Compared with the sham operation group,the model group showed significant differences in general conditions,oculomotor nerve function,and the expressions of related factors(P＜0.01).Compared with the model group,the EA group showed improvement in inflammatory markers only at 3 days post-treatment(P＜0.05),while at 7 and 14 days post-treatment,all assessed indicators were significantly improved(P＜0.01).In the inhibitor group,all indicators at each time point were significantly different compared with the model group(P＜0.05,P＜0.01).Compared with the EA group,at 3 days post-treatment,the EA plus inhibitor group showed no significant difference in general conditions(P＞0.05),while all other indicators at subsequent time points were significantly improved(P＜0.01).HE staining revealed disorganized nerve fibers and demyelination in the model group,whereas the treatment groups demonstrated remyelination and structural restoration of the oculomotor nerve.Conclusion:Intraorbital EA may promote repair of oculomotor nerve injury in rats by regulating CASR-mediated NLRP3 inflammasome activation.
方姗姗;李元;姚冰;刘同岩;周凌云
哈尔滨医科大学,黑龙江哈尔滨 150081||哈尔滨医科大学附属第一医院,黑龙江哈尔滨 150001哈尔滨医科大学附属第一医院,黑龙江哈尔滨 150001哈尔滨医科大学,黑龙江哈尔滨 150081||哈尔滨医科大学附属第一医院,黑龙江哈尔滨 150001黑龙江中医药大学,黑龙江哈尔滨 150040哈尔滨医科大学,黑龙江哈尔滨 150081||哈尔滨医科大学附属第一医院,黑龙江哈尔滨 150001
医药卫生
动眼神经损伤CASR眶内电针NLRP3修复机制
Oculomotor nerve injuryCASRIntraorbital electro-acupunctureNLRP3Repair mechanism
《针灸临床杂志》 2026 (6)
67-74,8
国家自然科学基金(82074524,81674052).
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