Galuteolin Inhibited Autophagy for Neuroprotection Against Transient Focal Cerebral Ischemia in Rats
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ORIGINAL PAPER
Galuteolin Inhibited Autophagy for Neuroprotection Against Transient Focal Cerebral Ischemia in Rats Juxun Zhu1,2 · Liyun Wang3,4 · Jinping Zhang1,2 Received: 9 August 2019 / Accepted: 6 August 2020 © Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Galuteolin, a Chinese herbal medicine, purified from Lonicera Japonica. In this study, we aimed to investigate the neuroprotective effect of galuteolin against cerebral ischemia/reperfusion (I/R) injury. We administered galuteolin or galuteolin and rapamycin to rats which had middle cerebral artery occlusion/reperfusion (MCAO/R). A series of characterizations were carried out to monitor the outcomes of galuteolin in I/R rats regarding the infarct volumes, neurological deficits, and brain water, as well as its effect on neuroprotection and autophagy. It was found that galuteolin significantly reduced the infarct volume, brain water content, and the neurological deficits in a dose-dependent manner. Neuron damages were decreased in the hippocampal carotid artery 1 pyramidal layer by galuteolin. The expression levels of neuron-specific enolase (NSE) increased after galuteolin treatment. Galuteolin significantly decreased the expression levels of autophagy-related proteins. In addition, galuteolin decreased rapamycin-related neuron damages and activations of autophagy in I/R rats. Our data suggested that galuteolin can inhibit ischemic brain injuries through the regulation of autophagy-related indicators in I/R. Keywords Galuteolin · Cerebral I/R · MCAO/R · Autophagy · Neuroprotection
Introduction It was widely investigated that hypoxia–ischemia can result in insufficient blood flow to the brain tissues, leading to the apoptosis of neuronal cells, and damages of major organs (Vannucci 1990). It remains to be a leading cause of death * Jinping Zhang [email protected] 1
Department of Neurology, The First Affiliated Hospital of Shandong First Medical University, No. 16766 Jingshi Road, Lixia District, Jinan 250014, Shandong, People’s Republic of China
2
Department of Neurology, Shandong Provincial Qianfoshan Hospital, Shandong University, No. 16766 Jingshi Road, Lixia District, Jinan 250014, Shandong, People’s Republic of China
3
Department of Gastroenterology, The First Affiliated Hospital of Shandong First Medical Universit, No. 16766 Jingshi Road, Lixia District, Jinan 250014, Shandong, People’s Republic of China
4
Department of Gastroenterology, Shandong Provincial Qianfoshan Hospital, Shandong University, No. 16766 Jingshi Road, Lixia District, Jinan 250014, Shandong, People’s Republic of China
and permanent disability all around the world (Rice et al. 1981). The middle cerebral artery occlusion (MCAO) could activate the proliferation, migration, and differentiation of neural stem cells (Longa et al. 1989). However, studies have demonstrated that autophagy, a lysosome-mediated degradation process of cells, is activated after middle cerebral artery occlusion after hypoxia–ischemia (Liu and Levine 2015;
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