Analysis of Autophagy-Inflammation-Related Signaling Pathways in Stroke

Under stress conditions such as starvation and hypoxia, autophagy can be activated to provide cells with nutrients and energy. In the early stage of cerebral ischemia, 5'-AMP-activated protein kinase (AMPK) can activate autophagy and inhibit NF-κB and the inflammatory vesicle NLRP3, thereby reducing inflammation. Appropriate autophagy has a protective effect on ischemic neural tissues, whereas excessive autophagy may lead to cell death. Inflammatory response plays an important role in neuronal cell survival and recovery of neural tissue after ischemia. Many studies have identified an interaction between autophagy and inflammation in the pathogenesis of ischemic stroke. The autophagy-inflammation pathway may provide a new direction for the treatment of ischemic stroke.

Fig. 1. The autophagy-inflammation pathway provides a new direction for the treatment of ischemic stroke.Fig. 1. A mechanism of the cellular inflammatory response after cerebral ischemia. (Mo et al., 2020)

Our Services

Ace Therapeutics is a leading company in the field of stroke research, providing reliable analytical services to study autophagy-inflammation-related signaling pathways in stroke. Our integrated approach combines cutting-edge technology, state-of-the-art equipment, and a team of highly skilled experts to explore the onset and regulation of autophagy and inflammation in neural tissues after ischemia, helping our clients develop neuroprotective strategies for stroke.

To simulate the complex pathophysiology of stroke, we utilize in vitro models of stroke to study the molecular mechanisms of autophagy and inflammation in a controlled environment. In vivo models, including transgenic mice and animal models of stroke, allow for a more comprehensive understanding of the interactions between autophagy and inflammation throughout the organism. Our experts use these models to analyze the role of autophagy in the pathogenesis of ischemic stroke, focusing on the following targets:

  • AMPK
  • ULK1, VPS34, and Beclin-1
  • Rapamycin kinase (mTOR)
  • Mitogen-activated protein kinases (MAPK), especially p38 MAPK
  • NF-κB
  • NLRP3
  • Inflammatory factors: IL-6, TNF-α

Our Methods

  • Transcriptome analysis: We utilize high-throughput transcriptome analyses, such as RNA sequencing (RNA-seq), to examine gene expression profiles associated with autophagy and inflammation in stroke. By comparing the transcriptomes of ischemic brain tissue with control samples, we can identify differentially expressed genes involved in autophagy and inflammatory pathways.
  • Proteomic analysis: Our proteomic analysis service enables comprehensive analysis of protein expression and post-translational modifications associated with autophagy and inflammation in stroke. Using advanced mass spectrometry techniques, we can identify and quantify proteins involved in autophagy, inflammatory signaling pathways, and their crosstalk.
  • Immunohistochemical analysis: We employ immunohistochemical analysis to study the spatial distribution and cellular localization of autophagy and inflammation markers in animal models of stroke.

Ace Therapeutics provides comprehensive autophagy-inflammation-related signaling pathways analysis services to explore new direction for the treatment of ischemic stroke. If you are interested in our services, please do not hesitate to contact us!

  1. Mo, Y., et al. (2020). Autophagy and inflammation in ischemic stroke. Neural Regeneration Research, 15(8), 1388-1396.
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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