Molecular Mechanism Analysis of Oxidative Stress in Stroke

Oxidative stress is caused by reactive oxygen species (ROS) during cerebral ischemia, potentially leading to cell death and ultimately brain death after reperfusion. Especially during reperfusion, superoxide anion radicals, hydroxyl radicals, and nitric oxide (NO) are produced, which can cause lipid peroxidation, inflammation, and apoptosis. The cerebral vasculature is a major target of oxidative stress, which plays a key role in the pathogenesis of ischemic brain injury following cerebrovascular attacks. In addition, mitochondrial dysfunction is caused after stroke, and oxidative stress further aggravates mitochondrial damage. Actively protecting mitochondrial function, resisting oxidation, scavenging free radicals, and mitigating oxidative stress have become effective strategies to save neurons from the pathological process of cerebral ischemia-reperfusion.

Fig. 1. Oxidative stress plays a key role in the pathogenesis of ischemic brain injury following cerebrovascular attacks.Fig. 1. Therapeutic opportunities throughout the time-course of oxidative stress development in ischemic stroke. (Qin et al., 2022)

Our Services

Ace Therapeutics provides molecular mechanism analysis services focused on oxidative stress in stroke, assisting clients in the development of novel pharmaceuticals. Our team of highly skilled researchers and scientists can use state-of-the-art technologies and methods to reveal the complex interactions between ROS production, antioxidant defense systems, and cell damage in stroke.

Analysis of Molecular Mechanisms of Oxidative Stress in Stroke

We can analyze the following signaling pathways associated with mitochondrial dysfunction and oxidative stress in in vitro and in vivo models of stroke.

Development of Potential Biomarkers for Oxidative Stress in Stroke

We can help clients develop a range of biomarkers to assess levels of oxidative stress and evaluate disease progression in stroke.

  • Biomolecules damaged by ROS: malondialdehyde (MDA), oxidized low-density lipoprotein (oxLDL), 8-isoprostaglandin-F-2 (8-iso-PGF2), a biomarker of lipid peroxidation, 8-hydroxy-2-deoxyguanosine (8-OHdG), a biomarker of DNA oxidation, etc.
  • Enzymes and molecules associated with the antioxidant defense system: superoxide dismutase (SOD), glutathione peroxidase (GPX), thioredoxin (Trx), gammaglutamyltransferase (GGT), vitamins A (retinol), C (ascorbic acid, AA), and carotenoids, etc.

Why Choose Us

  • Our team of experienced researchers and scientists with deep expertise in the field of stroke ensures that results are analyzed and interpreted with the highest quality.
  • We utilize cutting-edge technologies and methods to investigate the complex molecular mechanisms behind oxidative stress in stroke.
  • Our services provide a comprehensive understanding of oxidative stress in stroke by analyzing a wide range of biomarkers, signaling pathways, and cellular processes.
  • By fostering collaboration, we aim to accelerate the development of innovative antioxidant therapies for stroke.

Through our comprehensive analytical services, multidisciplinary approach, and state-of-the-art facilities, we strive to be your trusted partner. Contact us to move your stroke program forward!

  1. Rodrigo, R., et al. (2013). Oxidative stress and pathophysiology of ischemic stroke: novel therapeutic opportunities. CNS & Neurological Disorders-Drug Targets (Formerly Current Drug Targets-CNS & Neurological Disorders), 12(5), 698-714.
All of our services are intended for preclinical research use only and cannot be used to diagnose, treat or manage patients.
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