Activation of PDGFR and ROS in early brain injury in rats after subarachnoid hemorrhage
Objective To investigate the effects of inhibiting the activation of platelet-derived growth factor receptor (PDGFR) and reactive oxygen species (ROS) on early brain damage (EBI) after subarachnoid hemorrhage (SAH), and explore their possible acting mechanism in the process. Methods Adult male SD ra...
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Editorial Office of Journal of Army Medical University
2022-06-01
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Series: | 陆军军医大学学报 |
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Online Access: | http://aammt.tmmu.edu.cn/Upload/rhtml/202202166.htm |
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author | LIAO Yisi HUANG Jiashang XIE Yanfeng SHI Quanhong DAN Wei |
author_facet | LIAO Yisi HUANG Jiashang XIE Yanfeng SHI Quanhong DAN Wei |
author_sort | LIAO Yisi |
collection | DOAJ |
description | Objective To investigate the effects of inhibiting the activation of platelet-derived growth factor receptor (PDGFR) and reactive oxygen species (ROS) on early brain damage (EBI) after subarachnoid hemorrhage (SAH), and explore their possible acting mechanism in the process. Methods Adult male SD rats were randomly divided into sham operation group, SAH group, PDGF receptor inhibition group and ROS inhibition group, with 12 rats in each group. The rat model of SAH was established by intravascular puncture. In 1 h later, the rats in the treatment groups were injected with corresponding drugs by intraperitoneal injection. At 24 and 48 h after operation, animal mortality and body weight changes were observed, brain dysfunction was evaluated with neurobehavioral assessment, and brain water content was measured to evaluate blood-brain barrier permeability. Western blot analysis was used to detect the changes of PDGFR and phosphorylated PDGFR and the expression of p-JNK and p-MMP-9 after SAH. The oxidation products of lipids and proteins, malondialdehyde (MDA) and ROS were also detected. Results Both inhibiting the activation of PDGFR and scavenging ROS reduced brain water content after SAH (P < 0.05), decreased the expression of MMP-9 (P < 0.05), improved the neurological function score (P < 0.05), reduced the production of ROS and MDA (P < 0.05), and decreased the phosphorylation of JNK and c-Jun. Inhibiting the generation of ROS suppressed the activation of PDGFR to a certain extent, and inhibiting the activation of PDGFR also reduced the generation of ROS to a certain extent (P < 0.05). Conclusion After SAH in rats, ROS is involved in the activation of PDGFR, and its activation can further aggravate free radical damage. The JNK-MMP-9 pathway is indeed an important pathway that causes blood-brain barrier disruption in EBI.
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first_indexed | 2024-12-12T13:44:40Z |
format | Article |
id | doaj.art-a0225600d22f4094baa326ac298e5eb9 |
institution | Directory Open Access Journal |
issn | 2097-0927 |
language | zho |
last_indexed | 2024-12-12T13:44:40Z |
publishDate | 2022-06-01 |
publisher | Editorial Office of Journal of Army Medical University |
record_format | Article |
series | 陆军军医大学学报 |
spelling | doaj.art-a0225600d22f4094baa326ac298e5eb92022-12-22T00:22:42ZzhoEditorial Office of Journal of Army Medical University陆军军医大学学报2097-09272022-06-0144121243124810.16016/j.2097-0927.202202166Activation of PDGFR and ROS in early brain injury in rats after subarachnoid hemorrhageLIAO Yisi0HUANG Jiashang1XIE Yanfeng2SHI Quanhong3DAN Wei4Department of Neurosurgery, the First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, ChinaDepartment of Neurosurgery, the First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, ChinaDepartment of Neurosurgery, the First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, ChinaDepartment of Neurosurgery, the First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, ChinaDepartment of Neurosurgery, the First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, ChinaObjective To investigate the effects of inhibiting the activation of platelet-derived growth factor receptor (PDGFR) and reactive oxygen species (ROS) on early brain damage (EBI) after subarachnoid hemorrhage (SAH), and explore their possible acting mechanism in the process. Methods Adult male SD rats were randomly divided into sham operation group, SAH group, PDGF receptor inhibition group and ROS inhibition group, with 12 rats in each group. The rat model of SAH was established by intravascular puncture. In 1 h later, the rats in the treatment groups were injected with corresponding drugs by intraperitoneal injection. At 24 and 48 h after operation, animal mortality and body weight changes were observed, brain dysfunction was evaluated with neurobehavioral assessment, and brain water content was measured to evaluate blood-brain barrier permeability. Western blot analysis was used to detect the changes of PDGFR and phosphorylated PDGFR and the expression of p-JNK and p-MMP-9 after SAH. The oxidation products of lipids and proteins, malondialdehyde (MDA) and ROS were also detected. Results Both inhibiting the activation of PDGFR and scavenging ROS reduced brain water content after SAH (P < 0.05), decreased the expression of MMP-9 (P < 0.05), improved the neurological function score (P < 0.05), reduced the production of ROS and MDA (P < 0.05), and decreased the phosphorylation of JNK and c-Jun. Inhibiting the generation of ROS suppressed the activation of PDGFR to a certain extent, and inhibiting the activation of PDGFR also reduced the generation of ROS to a certain extent (P < 0.05). Conclusion After SAH in rats, ROS is involved in the activation of PDGFR, and its activation can further aggravate free radical damage. The JNK-MMP-9 pathway is indeed an important pathway that causes blood-brain barrier disruption in EBI. http://aammt.tmmu.edu.cn/Upload/rhtml/202202166.htmsubarachnoid hemorrhageearly brain injuryplatelet-derived growth factorreactive oxygen species |
spellingShingle | LIAO Yisi HUANG Jiashang XIE Yanfeng SHI Quanhong DAN Wei Activation of PDGFR and ROS in early brain injury in rats after subarachnoid hemorrhage 陆军军医大学学报 subarachnoid hemorrhage early brain injury platelet-derived growth factor reactive oxygen species |
title | Activation of PDGFR and ROS in early brain injury in rats after subarachnoid hemorrhage |
title_full | Activation of PDGFR and ROS in early brain injury in rats after subarachnoid hemorrhage |
title_fullStr | Activation of PDGFR and ROS in early brain injury in rats after subarachnoid hemorrhage |
title_full_unstemmed | Activation of PDGFR and ROS in early brain injury in rats after subarachnoid hemorrhage |
title_short | Activation of PDGFR and ROS in early brain injury in rats after subarachnoid hemorrhage |
title_sort | activation of pdgfr and ros in early brain injury in rats after subarachnoid hemorrhage |
topic | subarachnoid hemorrhage early brain injury platelet-derived growth factor reactive oxygen species |
url | http://aammt.tmmu.edu.cn/Upload/rhtml/202202166.htm |
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