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，从铁死亡角度探讨其在动眼神经功
能重建中的作用机制。方法：108只7周龄雄性SD大鼠随机分为空白组、假手术组、模型组、电针组、诱导剂
组、（电针+诱导剂）组，每组18只，分别于术后1、7、14 d评估，每时间点6只。建立动眼神经损伤模型（假手
术组仅暴露神经）。电针组术后每日电针眼周肌肉20 min，持续14 d。各组于术后1、7、14 d评估一般状态、
动眼神经功能、线粒体超微结构（电镜），并检测铁死亡相关指标；术后 14 d 应用 Western blot 检测 GPX4、
SLC7A11。结果：空白组与假手术组各指标差异无统计学意义。术后第1天，电针组与模型组差异无统计
学意义；术后第7、14天，电针组较模型组各项指标显著改善。模型组较假手术组各时间点损伤显著。模型
组较诱导剂组损伤更轻。术后1 d，（电针+诱导剂）组与诱导剂组无差异；术后7、14 d，（电针+诱导剂）组较
诱导剂组显著改善。术后1 d，模型组线粒体萎缩、嵴减少，电针组损伤较轻，诱导剂组严重损伤，（电针+诱
导剂）组形态异常；术后7 d，模型组线粒体显著萎缩、嵴缺失，电针组损伤，诱导剂组持续肿胀破裂，（电针+
诱导剂）组较诱导剂组有部分恢复但仍异常；术后14 d，模型组线粒体仍萎缩、嵴缺失，电针组线粒体接近正
常，诱导剂组进行性肿胀破裂，（电针+诱导剂）组较诱导剂组显著改善但仍有缺陷（膜修复不全、嵴紊乱）。
结论：眶内电针可能通过调节Fe2+
、MDA、GSH、GPX4、SLC7A11表达，改善线粒体结构，减轻铁死亡，促进
大鼠动眼神经功能恢复。
To observe the effect of intraorbital electroacupuncture on nerve function in a rat model
of oculomotor nerve injury and explore its underlying mechanism in oculomotor nerve functional reconstruction
from the perspective of ferroptosis. Methods: A total of 108 7-week-old male Sprague-Dawley (SD) rats were
randomly divided into six groups: blank group, sham-operation group, model group, electroacupuncture group,
inducer group, and (electroacupuncture + inducer) group, with 18 rats in each group. Assessments were
conducted at postoperative days 1, 7, and 14, with 6 rats evaluated at each time point. An oculomotor nerve
injury model was established (the sham-operation group only involved exposure of the nerve). The
electroacupuncture group received daily electroacupuncture stimulation of the periorbital muscles for 20 minutes
for 14 consecutive days postoperatively. General condition, oculomotor nerve function, and mitochondrial
ultrastructure (examined via electron microscopy) were evaluated in each group at postoperative days 1, 7, and
14, along with the detection of ferroptosis-related indicators. At postoperative day 14, Western blot analysis was
performed to detect GPX4 and SLC7A11. Results: There were no significant differences in all indicators
between the blank group and the sham-operation group. On postoperative day 1, no significant differences were
observed between the electroacupuncture group and the model group. However, on postoperative days 7 and 14,
all indicators in the electroacupuncture group showed significant improvement compared to the model group.
The model group exhibited significant injury at all time points compared to the sham-operation group. The injury
in the model group was less severe than that in the inducer group. On postoperative day 1, there were no
differences between the (electroacupuncture + inducer) group and the inducer group. On postoperative days 7
and 14, the (electroacupuncture + inducer) group showed significant improvement compared to the inducer
group. On postoperative day 1, the model group exhibited mitochondrial atrophy and reduced cristae, while the
electroacupuncture group showed milder injury, the inducer group exhibited severe injury, and the
(electroacupuncture + inducer) group showed morphological abnormalities. On postoperative day 7, the model
group demonstrated significant mitochondrial atrophy and cristae loss, the electroacupuncture group showed
injury, the inducer group exhibited persistent swelling and rupture, and the (electroacupuncture + inducer) group
showed partial recovery compared to the inducer group but still exhibited abnormalities. On postoperative day
14, the model group still showed mitochondrial atrophy and cristae loss, the electroacupuncture group had mitochondria close to normal,
the inducer group exhibited progressive swelling and rupture, and the (electroacupuncture + inducer) group showed significant
improvement compared to the inducer group but still had defects (incomplete membrane repair and disordered cristae). Conclusion:
Intraorbital electroacupuncture may promote the recovery of oculomotor nerve function in rats by regulating the expression of Fe2+
, MDA,
GSH, GPX4, and SLC7A11, improving mitochondrial structure, and reducing ferroptosis.
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