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Objective The roles of cerebrovascular oxidative stress in vascular functional remodeling have been described in hindlimb-unweighting(HU) rats. However, the underlying mechanism remains to be established. Methods We investigated the generation of vascular reactive oxygen species(ROS), Nox2/Nox4 protein and m RNA levels, NADPH oxidase activity, and manganese superoxide dismutase(Mn SOD) and glutathione peroxidase-1(GPx-1) m RNA levels in cerebral and mesenteric smooth muscle cells(VSMCs) of HU rats. Results ROS production increased in cerebral but not in mesenteric VSMCs of HU rats compared with those in control rats. Nox2 and Nox4 protein and m RNA levels were increased significantly but Mn SOD/GPx-1 m RNA levels decreased in HU rat cerebral arteries but not in mesenteric arteries. NADPH oxidases were activated significantly more in cerebral but not in mesenteric arteries of HU rats. NADPH oxidase inhibition with apocynin attenuated cerebrovascular ROS production and partially restored Nox2/Nox4 protein and m RNA levels, NADPH oxidase activity, and Mn SOD/GPx-1 m RNA levels in cerebral VSMCs of HU rats. Conclusion These results suggest that vascular NADPH oxidases regulate cerebrovascular redox status and participate in vascular oxidative stress injury during simulated microgravity.
Objective The roles of cerebrovascular oxidative stress in vascular functional remodeling have been described in hindlimb-unweighting (HU) rats. However, the underlying mechanism remains to be established. Methods We investigated the generation of vascular reactive oxygen species (ROS), Nox2 / Nox4 protein and m RNA levels, NADPH oxidase activity, and manganese superoxide dismutase (Mn SOD) and glutathione peroxidase-1 (GPx-1) m RNA levels in cerebral and mesenteric smooth muscle cells (VSMCs) of HU rats. Cerebral but not in mesenteric VSMCs of HU rats compared with those in control rats. Nox2 and Nox4 protein and m RNA levels were significantly increased but Mn SOD / GPx-1 m RNA levels decreased in HU rat cerebral arteries but not in mesenteric arteries. oxidases were activated significantly more in cerebral but not in mesenteric arteries of HU rats. NADPH oxidase inhibition with apocynin attenuated cerebrovascular ROS production and partially restored Nox2 / Nox4 protein and m RNA levels, NADPH oxidase activity, and Mn SOD / GPx-1 m RNA levels in cerebral VSMCs of HU rats. Conclusion These results suggest that vascular NADPH oxidases regulate cerebrovascular redox status and participate in vascular oxidative stress injury during simulated microgravity