Neuroprotective Effects of Kukoamine a against Radiation-induced Rat Brain Injury through Inhibition of Oxidative Stress and Neuronal Apoptosis
| Autor: | Hongda Ma, Yaqiong Zhang, Changli Wang, Weihong Meng, Qingchun Zhao, Zhihua Cheng |
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| Rok vydání: | 2016 |
| Předmět: |
Male
Apoptosis Biology Pharmacology medicine.disease_cause Biochemistry Neuroprotection Antioxidants Superoxide dismutase 03 medical and health sciences Cellular and Molecular Neuroscience chemistry.chemical_compound 0302 clinical medicine Western blot medicine Animals Rats Wistar Radiation Injuries Neurons TUNEL assay medicine.diagnostic_test Superoxide Dismutase General Medicine Glutathione Malondialdehyde Disease Models Animal Oxidative Stress Neuroprotective Agents chemistry Brain Injuries 030220 oncology & carcinogenesis biology.protein Spermine Apoptosis Regulatory Proteins 030217 neurology & neurosurgery Oxidative stress |
| Zdroj: | Neurochemical Research. 41:2549-2558 |
| ISSN: | 1573-6903 0364-3190 |
| Popis: | Radiation-induced brain injury (RIBI) is a prominent side effect of radiotherapy for cranial tumors. Kukoamine A (KuA) has the ability of anti-oxidative stress and anti-apoptosis in vitro. The aim of this study was to investigate whether KuA would prevent the detrimental effect of ionizing radiation on hippocampal neurons. For this study, male Wistar rats were received either sham irradiation or whole brain irradiation (30 Gy single dose of X-rays) followed by the immediate injection of either KuA or vehicle intravenously. The dose of KuA was 5, 10 and 20 mg/kg respectively. The protective effects of KuA were assessed by Nissl staining. The levels of oxidative stress marker and antioxidants activities were assayed by kits. TUNEL staining was performed to detect the level of apoptosis in hippocampal neurons. The expression of apoptosis-related proteins as well as the brain-derived neurophic factor (BDNF) was evaluated by western blot. Whole brain irradiation led to the neuronal abnormality and it was alleviated by KuA. KuA decreased malondialdehyde (MDA) level, increased glutathione (GSH) level, superoxide dismutase (SOD) and catalase (CAT) activities, as well as alleviated neuronal apoptosis by regulating the expression of cleaved caspase-3, cytochrome C, Bax and Bcl-2. Additionally, KuA increased the expression of BDNF. These data indicate that KuA has neuroprotective effects against RIBI through inhibiting neuronal oxidative stress and apoptosis. |
| Databáze: | OpenAIRE |
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