Aerobic exercise delays retinal ganglion cell death after optic nerve injury
Aerobic exercise delays retinal ganglion cell death after optic nerve injury
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有氧运动可延缓视神经损伤后视网膜神经节细胞死亡
DOI：
10.1016/j.exer.2020.108240
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发表时间：
2020-11-01
影响因子：
3.4
通讯作者：
Zhong, Yong-Mei
中科院分区：
文献类型：
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作者：
He, Yuan-Yuan;Wang, Lu;Zhong, Yong-Mei
有氧运动已被证明在预防神经系统疾病和改善认知功能方面发挥着至关重要的作用。本研究观察了跑台训练对成年大鼠视神经切断后视网膜神经节细胞(RGCs)的影响。每周在跑步机上运动5d(30min/d，以9m/min的速度运动)，或将对照组大鼠运动3周后置于静态跑步机上，切断大鼠左侧视神经。手术后，大鼠又进行了一周的运动。失活动大鼠视神经切断后5天和7天，视网膜节细胞存活率分别为67%和39%。然而，运动大鼠在轴突切断后5天(74%存活率)和7d(48%存活率)RGCs显著增加。此外，运动后视网膜脑源性神经营养因子(BDNF)蛋白水平较非活动大鼠视神经切断后显著上调。通过腹腔注射BDNF原肌球蛋白受体激酶(TrkB)受体拮抗剂ANA-12阻断运动中的BNDF信号，可使运动大鼠视网膜神经节细胞的数量减少到静止状态的水平，有效地取消了运动对视网膜神经节细胞的保护作用。结果提示，跑台训练通过上调BDNF的表达，有效地挽救视神经切断后视网膜神经节细胞的退行性变。
Aerobic exercise has been shown to play a crucial role in preventing neurological diseases and improving cognitive function. In the present study, we investigated the effect of treadmill training on retinal ganglion cells (RGCs) following optic nerve transection in adult rats. We exercised the rats on a treadmill for 5 d/week (30 min/d at a rate of 9 m/min) or placed control rats on static treadmills After 3 weeks of exercise, the left optic nerve of each rat was transected. After the surgery, the rat was exercised for another week. The percentages of surviving RGCs in the axotomized eyes of inactive rats were 67% and 39% at 5 and 7 days postaxotomy, respectively. However, exercised rats had significant more RGCs at 5 (74% survival) and 7 days (48% survival) after axotomy. Moreover, retinal brain-derived neurotrophic factor (BDNF) protein levels were significantly upregulated in response to exercise compared with those in the axotomized eyes of inactive rats. Blocking BNDF signaling during exercise by intraperitoneal injections of ANA-12, a BDNF tropomyosin receptor kinase (TrkB) receptor antagonist, reduced the number of RGCs in exercised rats to the level of RGCs in the inactive rats, effectively abolishing the protection of RGCs afforded by exercise. The results suggest that treadmill training effectively rescues RGCs from neurodegeneration following optic nerve transection by upregulating the expression of BDNF.