ROCK2 regulates autophagy in the hippocampus of rats after subarachnoid hemorrhage
Autor: | Zhiyong Zhang, Aijun Fu, Yang Chen, Gang Liu, Xiaoliang Li, Linlin Sun, Yude Ma |
---|---|
Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
medicine.medical_specialty Subarachnoid hemorrhage Hippocampus Sham group Rats Sprague-Dawley 03 medical and health sciences 0302 clinical medicine Western blot Downregulation and upregulation Internal medicine Immunochemistry Autophagy Medicine Animals cardiovascular diseases ROCK2 rho-Associated Kinases medicine.diagnostic_test business.industry General Neuroscience Subarachnoid Hemorrhage medicine.disease nervous system diseases Rats 030104 developmental biology Endocrinology business 030217 neurology & neurosurgery |
Zdroj: | Neuroreport. 29(18) |
ISSN: | 1473-558X |
Popis: | The role of autophagy in subarachnoid hemorrhage (SAH) remains unclear. This study aimed to investigate the role of ROCK2 in the regulation of hippocampus autophagy after SAH. Thirty-six Sprague-Dawley rats were randomly divided into three groups - the sham group, the SAH group, and the SAH+ ROCK2 inhibitor group (or the drug group) - and analyzed through a behavior test. The hippocampus tissues were analyzed using immunochemistry and western blot analysis. We observed injured morphology in the hippocampus and impaired learning and memory ability in the rats in the SAH group, accompanied by upregulated ROCK2 expression and increased beclin-1 and LC3-II expression. Compared with the SAH group, we observed normal morphology in the hippocampus and better learning and memory ability in the rats in the drug group, accompanied by downregulated ROCK2 expression and increased beclin-1 and LC3-II expression. SAH activates autophagy in the hippocampus, but this could be inhibited by ROCK2. Inhibition of ROCK2 promotes autophagy and reduces the injury in the hippocampus, leading to the recovery of learning and memory ability following SAH. ROCK2 may represent a new target for the treatment of SAH. |
Databáze: | OpenAIRE |
Externí odkaz: |