Rhubarb extract has a protective role against radiation-induced brain injury and neuronal cell apoptosis.
Oxidative stress caused by ionizing radiation is involved in neuronal damage in a number of disorders, including trauma, stroke, Alzheimer's disease and amyotrophic lateral sclerosis. Ionizing radiation can lead to the formation of free radicals, which cause neuronal apoptosis and have important roles in the development of some types of chronic brain disease. The present study evaluated the effects of varying concentrations (2, 5 and 10 µg/ml) of ethanolic rhubarb extract on the neuronal damage caused by irradiation in primary neuronal cultures obtained from the cortices of rat embryos aged 20 days. Brain damage was induced with a single dose of γ-irradiation that induced DNA fragmentation, increased lactate dehydrogenase release in neuronal cells and acted as a trigger for microglial cell proliferation. Treatment with rhubarb extract significantly decreased radiation-induced lactate dehydrogenase release and DNA fragmentation, which are important in the process of cell apoptosis. The rhubarb extract exhibited dose-dependent inhibition of lactate dehydrogenase release and neuronal cell apoptosis that were induced by the administration of ionizing radiation. The effect of a 10 µg/ml dose of rhubarb extract on the generation of reactive oxygen species (ROS) induced by radiation was also investigated. This dose led to significant inhibition of ROS generation. In conclusion, the present study showed a protective role of rhubarb extract against irradiation-induced apoptotic neuronal cell death and ROS generation.
Department of Neurology, Zhongshan City People's Hospital, Zhongshan, Guangdong 528403, P.R. China.
Kui
K
Lu
Department of Neurology, First Affiliated Hospital of Sun Yat‑sen University, Guangzhou, Guangdong 510080, P.R. China.
Cheng
C
Zhang
Department of Neurology, Zhongshan City People's Hospital, Zhongshan, Guangdong 528403, P.R. China.
Wenjun
W
Wu
Department of Neurology, Zhongshan City People's Hospital, Zhongshan, Guangdong 528403, P.R. China.
Min
M
Zhou
Department of Neurology, Sun Yat‑sen Memorial Hospital of Sun Yat‑sen University, Guangzhou, Guangdong 510120, P.R. China.
Yamei
Y
Tang
Department of Neurology, Sun Yat‑sen Memorial Hospital of Sun Yat‑sen University, Guangzhou, Guangdong 510120, P.R. China.
Ying
Y
Peng
D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D001930:Brain Injuries / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D002478:Cells, Cultured; D053938:DNA Fragmentation / Q000187:drug effects; D005260:Female; D005720:Gamma Rays / Q000009:adverse effects; D009474:Neurons / Q000187:drug effects / Q000378:metabolism / Q000473:pathology / Q000528:radiation effects; D018696:Neuroprotective Agents / Q000737:chemistry / Q000494:pharmacology*; D018384:Oxidative Stress / Q000187:drug effects; D010936:Plant Extracts / Q000737:chemistry / Q000494:pharmacology*; D011832:Radiation Injuries / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D011837:Radiation-Protective Agents / Q000737:chemistry / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism; D012250:Rheum / Q000737:chemistry*
D018696:Neuroprotective Agents; D010936:Plant Extracts; D011837:Radiation-Protective Agents; D017382:Reactive Oxygen Species