Analysis of Neuroinflammatory Mechanisms in Stroke

Neuroinflammation is an inflammatory response in the brain and is a key component of stroke pathology. The course of neuroinflammation is determined by the site, duration, and course of nerve injury. Brain damage after ischemic stroke leads to necrosis and apoptosis. A variety of immune cells are activated, including microglia, macrophages, and T lymphocytes. In addition, inflammation in the brain exacerbates the release of multiple cytokines as well as interferons or chemokines in the damaged brain tissue and peripheral blood, leading to the breakdown of the blood-brain barrier (BBB). These cytokines are important mediators in the course of the stroke-induced immune-inflammatory response, participating in the progression of cerebral infarction and influencing the severity and outcome of the disease. In conclusion, understanding the mechanisms of neuroinflammation can help to develop new diagnostic, prognostic, and neuroprotective strategies for post-stroke inflammation.

Fig. 1. Schematic representation of post-ischemic inflammatory response in stroke. (Jayaraj et al., 2019)

Our Services

At Ace Therapeutics, we specialize in analyzing the neuroinflammatory mechanisms of stroke. Our team of experts employs state-of-the-art technology and expertise to unravel the complex interactions that occur within the neurovascular unit during stroke pathogenesis. We aim to help clients develop stroke therapies that target neuroinflammation.

Our services cover a wide range of approaches, including molecular analysis, cellular studies, and advanced imaging techniques. We can analyze the neuroinflammatory process and BBB destruction in stroke involving multiple signaling pathways.

• Analysis of Cytokines in Stroke
• Analysis of Chemokines in Stroke
• Analysis of HMGB1 Signaling Pathway in Ischemic Stroke
• Analysis of MAPK Signaling Pathway in Stroke
• Analysis of MMP Signaling Pathway in Stroke
• Analysis of Sphingosine-1-Phosphate Signaling in Stroke
• Molecular Mechanism Analysis of Inflammasomes in Stroke
• Analysis of Microglial Phagocytosis in Ischemic Stroke

Our Methods

In Vivo Neuroinflammation Assays

We can examine various inflammatory mediators (cytokines, chemokines, adhesion molecules, and inflammatory vesicles), signaling pathways, and gene expression profiles associated with neuroinflammation in stroke in animal models of stroke. We utilize cutting-edge imaging technologies to visualize and quantify neuroinflammatory processes in vivo. These non-invasive imaging techniques help clients assess changes in blood-brain barrier integrity, inflammatory cell infiltration, and spatial distribution of inflammatory markers.

In Vitro Neuroinflammation Assays

We use advanced cellular techniques, including primary cell cultures and co-culture systems, to mimic stroke. By studying the behavior and responses of different cell types (e.g., microglia, astrocytes, neurons, and endothelial cells), we can analyze neuroinflammatory in vitro.

Why Choose Us

• Our expertise spans multiple disciplines, including neuroscience, immunology, molecular biology, and imaging, allowing us to analyze neuroinflammation from multiple perspectives.
• By harnessing the power of advanced technology, we can provide our clients with reliable data that facilitates a deeper understanding of the neuroinflammatory processes underlying stroke pathology.
• Our flexibility and adaptability ensure that we deliver personalized, high-quality results that meet our clients' expectations.

Ace Therapeutics actively collaborates with leading academic institutions, research organizations, and pharmaceutical companies to advance their understanding of the neuroinflammatory mechanisms underlying stroke. Through our comprehensive analysis 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. Jayaraj, R. L., et al. (2019). Neuroinflammation: friend and foe for ischemic stroke. Journal of neuroinflammation, 16, 1-24.