Liu Yaru, Jin Guilin, Feng Mingke
School of Acupuncture-Moxibustion and Tuina, Beijing University of Chinese Medicine, Beijing, China.
University of Tibetan Medicine, Lhasa, China.
Heliyon. 2024 Nov 17;10(23):e40443. doi: 10.1016/j.heliyon.2024.e40443. eCollection 2024 Dec 15.
Apoptosis induced by cerebral ischemia-reperfusion is one of the key pathological processes of nerve injury. Tibetan golden acupuncture (GA) is a common treatment for ischemic brain injury in Tibetan. The aim of this study was to explore whether GA prevents cerebral ischemia-reperfusion-induced apoptosis in mice by blocking the JNK/caspase-3 pathway.
In experiment I, 36 mice were randomly divided into a Sham group, CI/RI group, CI/RI + GA group. Morris water maze tests, TdT-mediated dUTP-biotin nick end labeling (TUNEL) staining and flow cytometry (FCM) were used to evaluate the effect of the GA intervention on CI/RI. In experiment II, 30 mice were randomly divided into a Sham group, CI/RI group, CI/RI + GA group, CI/RI + SP group and CI/RI + SP + EA group. Western blotting was used to detect protein expression of key factors in the JNK signaling pathway in the hippocampus.
After 7 and 14 interventions, behavioral evaluations in CI/RI + GA group was significantly different from those in CI/RI groups (p < 0.01), pathological injury and apoptosis were significantly reduced (p < 0.01). Compared with CI/RI group, the expression of P-JNK/JNK, Cleaved caspase-3/caspase-3, Bax, and Bad proteins in CI/RI + GA group, CI/RI + SP and CI/RI + SP + GA groups were significantly decreased (p < 0.01). The expression of B-cell lymphoma 2 (Bcl-2) was significantly increased (p < 0.01, p < 0.05).
GA can restore neurological dysfunction and inhibit hippocampal neuronal apoptosis in CI/RI mice, at least partially through inhibition of the JNK/Caspase-3 signaling pathway and regulation of apoptosis signals.
脑缺血再灌注诱导的细胞凋亡是神经损伤的关键病理过程之一。藏医金针疗法（GA）是藏医治疗缺血性脑损伤的常用方法。本研究旨在探讨GA是否通过阻断JNK/半胱天冬酶-3信号通路来预防小鼠脑缺血再灌注诱导的细胞凋亡。
在实验I中，将36只小鼠随机分为假手术组、脑缺血再灌注组（CI/RI组）、脑缺血再灌注+GA组。采用Morris水迷宫试验、TdT介导的dUTP生物素缺口末端标记法（TUNEL）染色和流式细胞术（FCM）评估GA干预对脑缺血再灌注的影响。在实验II中，将30只小鼠随机分为假手术组、脑缺血再灌注组、脑缺血再灌注+GA组、脑缺血再灌注+SP组和脑缺血再灌注+SP+EA组。采用蛋白质免疫印迹法检测海马中JNK信号通路关键因子的蛋白表达。
干预7天和14天后，脑缺血再灌注+GA组的行为学评估结果与脑缺血再灌注组相比有显著差异（p<0.01），病理损伤和细胞凋亡明显减少（p<0.01）。与脑缺血再灌注组相比，脑缺血再灌注+GA组、脑缺血再灌注+SP组和脑缺血再灌注+SP+GA组中P-JNK/JNK、裂解的半胱天冬酶-3/半胱天冬酶-3、Bax和Bad蛋白的表达显著降低（p<0.01）。B细胞淋巴瘤2（Bcl-2）的表达显著增加（p<0.01，p<0.05）。
GA可以恢复脑缺血再灌注小鼠的神经功能障碍并抑制海马神经元凋亡，至少部分是通过抑制JNK/半胱天冬酶-3信号通路和调节凋亡信号来实现的。
