Abstract
Background Buyang Huanwu decoction (BYHWD), an important traditional Chinese medicine (TCM), has been used clinically for centuries for the treatment of various diseases. The study aims to explore the BYHWD effects on angiogenesis and neuroprotection after cerebral ischemia/reperfusion (CI/R) injury in rats and to explore the underlying angiogenic roles and mechanisms of BYHWD in hydrogen peroxide (H2O2) induced oxidative stress in human umbilical vein endothelial cells (HUVECs) model. Methods The effects of BYHWD on neurological function were screened by measuring neurological deficits, spatial memory function, and angiogenesis (by microvascular density (MVD) and cerebral blood flow (CBF)) after CI/R injury in middle cerebral artery occlusion (MCAO) in vivo in rats. In vitro, we examined the angiogenic roles and mechanisms of action of BYHWD in an H2O2-induced oxidative stress HUVECs model by measuring cell viability, apoptosis, vascular tube formation, intracellular ROS generation, NADPH oxidase (Nox) activity, and Nox4 protein expression. Results BYHWD significantly improved neurological function, including neurological deficits and spatial learning and memory, and significantly increased MVD and CBF in the ischemic penumbra after CI/R injury in rats. BYHWD significantly increased cell viability, inhibited apoptosis, induced vascular tube formation, decreased intracellular ROS generation, and reduced Nox activity and Nox4 protein expression in H2O2-treated HUVECs in a dose-dependent manner. Conclusions Our study demonstrates that BYHWD promotes neurological function recovery and increases angiogenesis. BYHWD exerts angiogenic effects against cerebral ischemic injury through the downregulation of Nox4, which results in the reduction of ROS generation.
Highlights
Cerebral ischemic stroke remains the main cause of morbidity and mortality in adults worldwide
After 1–4 weeks of administration of Buyang Huanwu decoction (BYHWD), the neurological deficit in both low- and high-dose treatment groups was statistically lower (P < 0.01) than that of vehicle-treated rats, and the neurological deficit decreased gradually during the 4 w of administration of BYHWD (Figure 1). e results showed that BYHWD improved the neurological deficit after focal cerebral ischemia in a dosedependent manner
Effects of BYHWD on Spatial Acquisition after Focal CI. e Morris Water Maze (MWM) experiment was carried out to evaluate spatial learning and memory function. e time taken to find the platform became gradually shorter in all groups during the training of the spatial memory task
Summary
Cerebral ischemic stroke remains the main cause of morbidity and mortality in adults worldwide. Previous studies have indicated that secondary brain injury is aggravated by ROS-induced apoptosis of vascular endothelial cells (VECs) after cerebral ischemic stroke [6, 7]. E study aims to explore the BYHWD effects on angiogenesis and neuroprotection after cerebral ischemia/reperfusion (CI/R) injury in rats and to explore the underlying angiogenic roles and mechanisms of BYHWD in hydrogen peroxide (H2O2) induced oxidative stress in human umbilical vein endothelial cells (HUVECs) model. We examined the angiogenic roles and mechanisms of action of BYHWD in an H2O2-induced oxidative stress HUVECs model by measuring cell viability, apoptosis, vascular tube formation, intracellular ROS generation, NADPH oxidase (Nox) activity, and Nox protein expression. BYHWD significantly increased cell viability, inhibited apoptosis, induced vascular tube formation, decreased intracellular ROS generation, and reduced Nox activity and Nox protein expression in H2O2-treated HUVECs in a dose-dependent manner. BYHWD exerts angiogenic effects against cerebral ischemic injury through the downregulation of Nox, which results in the reduction of ROS generation
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