Low-energy extracorporeal shock wave therapy promotes BDNF expression and improves functional recovery after spinal cord injury in rats.
低能量体外休克治疗促进大鼠脊髓损伤后 BDNF 表达，改善功能恢复
- 作者列表："Matsuda M","Kanno H","Sugaya T","Yamaya S","Yahata K","Handa K","Shindo T","Shimokawa H","Ozawa H","Itoi E
:Low-energy extracorporeal shock wave therapy (ESWT) has been used to treat various human diseases. Previous studies have shown that low-energy ESWT promotes the release of various cell growth factors and trophic factors from the cells surrounding the target lesion. The aim of the current study was to determine whether the application of low-energy ESWT upregulates the expression of brain-derived neurotrophic factor (BDNF) and reduces neural tissue damage and functional impairment using a rat model of thoracic spinal cord contusion injury. We found that low-energy ESWT promoted BDNF expression in the damaged neural tissue. The expression of BDNF was increased in various neural cells at the lesion. Additionally, low-energy ESWT increased the area of spared white matter and the number of oligodendrocytes in the injured spinal cord compared with untreated control animals. There were more axonal fibers around the injured site after the application of low-energy ESWT than control. Importantly, low-energy ESWT improved the locomotor functions evaluated by both the BBB scale and ladder rung walking test in addition to the sensory function measured using a von Frey test. Moreover, the electrophysiological assessment confirmed that the conductivity of the central motor pathway in the injured spinal cord was restored by low-energy ESWT. These findings indicate that low-energy ESWT promotes BDNF expression at the lesion site and reduces the neural tissue damage and functional impairment following spinal cord injury. Our results support the potential application of low-energy ESWT as a novel therapeutic strategy for treating spinal cord injury.
: 低能量体外休克疗法 (ESWT) 已被用于治疗多种人类疾病。已有研究表明，低能量 ESWT 促进靶病变周围细胞释放各种细胞生长因子和营养因子。本研究的目的是确定低能量 ESWT 的应用是否上调脑源性神经营养因子 (BDNF) 的表达并使用大鼠胸脊髓挫伤损伤模型减轻神经组织损伤和功能损伤。我们发现低能量 ESWT 促进受损神经组织中 BDNF 的表达。病变处各神经细胞 BDNF 表达增加。此外，与未治疗的对照动物相比，低能量 ESWT 增加了损伤脊髓中备用白质的面积和少突胶质细胞的数量。应用低能量 ESWT 后损伤部位周围轴突纤维较对照组多。重要的是，低能量 ESWT 除了使用 von Frey 试验测量的感觉功能外，还改善了通过 BBB 量表和梯级步行试验评价的运动功能。此外，电生理评估证实，低能量 ESWT 恢复了损伤脊髓中中枢运动通路的导电性。这些发现表明低能量 ESWT 促进损伤部位 BDNF 表达，减轻脊髓损伤后神经组织损伤和功能损伤。我们的结果支持低能量 ESWT 作为治疗脊髓损伤的新型治疗策略的潜在应用。
METHODS:Objective To clarify the existence of monophasic neuromyelitis optica spectrum disorders (NMOSD) and to identify predictive factors of long-term relapse-free form. Methods We retrospectively analyzed 289 Chinese patients with NMOSD. Selected subjects were divided into three groups based on the time interval between disease onset and the first relapse, if any. Clinical and imaging data were acquired from each patient’s medical record and evaluated as predictive factors for NMOSD. Results In total, none of the participating patients exhibited a monophasic form of NMOSD. Rather, 241 patients were selected for relapse tendency analysis; 143 (59.3%) patients relapsed within the first year, 66 (27.4%) during 1–5 years, and 32 (13.3%) beyond 5 years. Such onset symptoms as optic neuritis (ON) and non-longitudinally extensive transverse myelitis (LETM) were independent prognostic factors for a prolonged remission interval.
METHODS::Neuromyelitis optica spectrum disorders (NMOSD) are an inflammation of the central nervous system associated with autoantibodies to aquaporin-4. We have undertaken a clinic-based survey of NMOSD in the Australia and New Zealand populations with the aim of characterising the clinical features and establishing the value of recently revised diagnostic criteria. Cases of possible NMOSD and age and sex-matched controls with multiple sclerosis (MS) were referred from centres across Australia and New Zealand. Cases were classified as NMOSD if they met the 2015 IPND criteria and remained as suspected NMOSD if they did not. Clinical and paraclinical data were compared across the three groups. NMOSD was confirmed in 75 cases and 89 had suspected NMOSD. There were 101 controls with MS. Age at onset, relapse rates and EDSS scores were significantly higher in NMOSD than in MS. Lesions and symptoms referable to the optic nerve were more common in NMOSD whereas brainstem, cerebellar and cerebral lesions were more common in MS. Longitudinally extensive spinal cord lesions were seen in 48/71 (68%) of cases with NMOSD. Elevations of CSF, white cell count and protein were more common in NMOSD. We have confirmed a clinical pattern of NMOSD that has been seen in several geographical regions. We have demonstrated the clinical utility of the current diagnostic criteria. Distinct patterns of disease are evident in NMOSD and MS, but there remains a large number of patients with NMOSD-like features who do not meet the current diagnostic criteria for NMOSD and remain a diagnostic challenge.
METHODS:Spinal cord injury (SCI) is a traumatic lesion that causes disability with temporary or permanent sensory and/or motor deficits. The pharmacological approach still in use for the treatment of SCI involves the employment of corticosteroid drugs. However, SCI remains a very complex disorder that needs future studies to find effective pharmacological treatments. SCI actives a strong inflammatory response that induces a loss of neurons followed by a cascade of events that lead to further spinal cord damage. Many experimental studies demonstrate the therapeutic effect of stem cells in SCI due to their capacity to differentiate into neuronal cells and by releasing neurotrophic factors. Therefore, they appear to be a valid strategy to use in the field of regenerative medicine. The purpose of this paper is to provide an overview of clinical trials, recorded in clinical trial.gov during 2005−2019, aimed to evaluate the use of stem cell-based therapy in SCI. The results available thus far show the safety and efficacy of stem cell therapy in patients with SCI. However, future trials are needed to investigate the safety and efficacy of stem cell transplantation.