Neuroprotection and neuroregeneration are two of the most promising disease-modifying ther-apies for the incurable and widespread Parkinson’s disease. In Parkinson’s disease, progressive degeneration of nigrostriatal dopaminergic neurons causes debilitating motor symptoms. Neu-rotrophic factors play important regulatory roles in the development, survival and maintenance of speciifc neuronal populations. These factors have the potential to slow down, halt or reverse the loss of nigrostriatal dopaminergic neurons in Parkinson’s disease. Several neurotrophic fac-tors have been investigated in this regard. This review article discusses the neurodevelopmental roles and therapeutic potential of three dopaminergic neurotrophic factors: glial cell line-derived neurotrophic factor, neurturin and growth/differentiation factor 5.

Type 2 diabetes is a risk factor for Alzheimer’s disease and Parkinson’s disease. Insulin signaling in the brains of people with Alzheimer’s disease or Parkinson’s disease is impaired. Preclinical studies of growth factors showed impressive neuroprotective effects. In animal models of Alz-heimer’s disease and Parkinson’s disease, insulin, glia-derived neurotrophic factor, or analogues of the incretin glucagon-like peptide-1 prevented neurodegenerative processes and improved neuronal and synaptic functionality in Alzheimer’s disease and Parkinson’s disease. On the basis of these promising ifndings, several clinical trials are ongoing with the ifrst encouraging clinical results published. This gives hope for developing effective treatments for Alzheimer’s disease and Parkinson’s disease that are currently unavailable.

Wistar rats were intragastrical y perfused with Chinese medicines used for tonifying the kidney. These included 0.180 g/mL of Herba Epimedi (Epimedium), Semen Cuscutae (Dodder Seed), or Herba Cistanches (Desertliving Cistanche), 0.04 mg/mL monoamine oxidase-B inhibitor selegiline, or distil ed water for 14 consecutive days to prepare drug-containing serum or blank serum. MES23.5 cells in the logarithmic phase were cultured in media supplemented with 15%drug-containing serum for 24 hours, fol owed by incubation in culture solution containing 100μmol/L H2O2 for 3 hours. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and flow tometry results showed that al drug-containing serums improved the survival rate of H 2 O 2-injured MES23.5 cells, inhibited pro-apoptotic FasL and caspase-3 expression, promoted anti-apoptotic Bcl-2 expression. However, drug-containing serums had little influence on Fas expression in H 2 O 2-injured MES23.5 cells. Enzyme-linked immunosorbent assay results showed that serum containing Herba Cistanches or Herba Epimedi increased the expression of nerve growth factor, brain-derived neurotrophic factor, and glial cellline-derived neurotrophic factor in injured MES23.5 cells;serum containing Semen Cuscutae only increased brain-derived neurotrophic factor expres-sion; while expression of the above neurotrophic factors remained the same in cells treated with serum containing selegiline. These findings indicate that Chinese medicines used to tonify the kid-ney can protect nerve cells by regulating the expression of apoptosis-related factors and neuro-trophic factors in MES23.5 cells.

神经营养因子与周围神经再生

人们对神经营养因子在促进周围神经元的存活,维持周围神经元的数目方面的作用进行了大量研究.神经损伤后,给予外源性神经营养因子,能够产生与靶器官源性的神经营养因子相似的作用.周围神经再生过程中,神经营养因子NGF、NT-3和BDNF对背根节初级感觉神经元和脊髓运动神经元的存活及其表型的表达具有明确的选择性作用.其他神经营养因子,如CNTF、GDNF、LIF、GGF等,对神经元细胞也具有不同作用.本文将就神经营养因子对治疗周围神经损伤及周围神经疾病的潜在作用作一综述.

AIM: It is well known that different injuries will result in different consequences. In this paper, we investigated the morphological change of spinal cord following crushed, hemi-sectioned and transected injury. METHODS: Sixty Wistar rats were randomly divided into 4 groups: intact group, crushed spinal cord injury group (cSCI), hem-sectioned SCI group (hSCI) and transitioned SCI group (tSCI). The models of SCI were established by the method in our laboratory. The animals in each group were sacrificed respectively at 24 hours, 7 and 24 days after operation. The L2 spinal cord which located in the caudal of injury site was taken respectively from each animal in each group and sectioned into frozen sections (20 μm). The sections were stained by hematoxylin and observed under light microscope. The number of neurons in dorsal and ventral horn was also counted. RESULTS: In cSCI group, some neurons appear to atrophy compared with that of intact group, but the number of neurons did not decrease apparently than that of intact group (P＞0.05). Comparatively, some cavities were observed in dorsal and ventral horn in hemi-sectioned and transitioned SCI group. And the number of neurons in dorsal horn and ventral horn decreased greatly at 24 hours, 7 and 21 days compared with intact group (P＜0.05). The results indicated that the decrease of neuronal number in dorsal horn and ventral horn after injury resulted from hSCI and tSCI, but not from cSCI. As a result, some different strategies should be considered for different injuries. For example, some neurotrophic factors may be useful in cSCI, but, many neurons have disappeared following hSCI and tSCI, therefore, other strategies that increase the number of neurons should be considered too. CONCLUSION: Our results provide the important morphological evidences on the change of spinal cord following cSCI, hSCI and tSCI. The data will be useful in treatment of SCI in the future.