Analysis of Intrinsic Apoptosis Pathways in Ischemic Stroke

The intrinsic apoptosis pathway, also known as the mitochondria-mediated apoptotic pathway, plays an important role in the pathology of ischemic stroke. The activation of this pathway mainly originates from intracellular stress signals, such as oxidative stress and Ca2+ imbalance. In ischemic brain injury, the activation of the intrinsic apoptosis pathway occurs as follows.

  • Ischemia leads to an increase in mitochondrial membrane permeability, and apoptosis-promoting factors, such as cytochrome c, are released from mitochondria to the cytoplasm.
  • Cytochrome c binds to procaspase-9, forming an apoptosome complex and activating caspase-9.
  • The activated caspase-9 further acts on the downstream caspase-3 to trigger the final apoptosis.

Inhibition of the intrinsic apoptosis pathway is another important strategy for stroke treatment. It has been found that ischemic brain injury can be attenuated in animal models by modulating the Bcl-2 family, inhibiting cytochrome c release or caspase-9 activation.

Fig. 1. Mitochondria-dependent pathways of apoptosis are important in cerebral ischemia and reperfusion. Fig. 1. Mitochondria-dependent pathways of apoptosis in cerebral ischemia and reperfusion. (Niizuma et al., 2010)

Our Services

At Ace Therapeutics, we provide comprehensive services for analyzing the intrinsic apoptosis pathway in ischemic stroke. Our team of highly skilled scientists utilizes state-of-the-art technology to help clients study the release of pro-apoptotic molecules in mitochondria, including cytochrome C, BID, Bax, cysteine asparaginase. We aim to help clients identify targets for preclinical stroke treatment.

Identification and Validation of Intrinsic Apoptosis Pathways Related Targets for Stroke

We provide high-throughput sequencing to help clients identify potential therapeutic targets associated with intrinsic apoptosis pathways in stroke.

  • ROS
  • Bcl-2 family proteins: such as cytochrome c, AIF, endonuclease G (Endo G), and second mitochondria-derived activator of caspase (Smac)
  • Caspase-9
  • Downstream effector caspases: caspase-3, caspase-6, and caspase-7
  • p53 signaling pathway
  • p53-induced protein with a death domain (PIDD) signaling pathway

Analysis of Intrinsic Apoptosis Pathways in Experimental Stroke Models

We use advanced quantitative methods to measure the levels of key molecules involved in the intrinsic pathway of apoptosis. By analyzing samples from in vitro and animal models of ischemic stroke, we provide precise measurements of apoptotic factors and thus analyze their role in neuronal cell death. Our immunohistochemistry and immunofluorescence techniques enable visualization of the distribution and localization of apoptotic molecules within brain tissue sections. In addition, we offer advanced molecular imaging techniques, such as confocal microscopy and live cell imaging, to visualize the dynamic process of apoptosis in real-time.

Ace Therapeutics not only specializes in the analysis of extrinsic apoptosis pathway in stroke, but also has the ability to explore the molecular mechanisms associated with intrinsic apoptotic pathways. This comprehensive research capability and advanced experimental methods will help clients to better discover and validate new therapeutic targets. If you are interested in our services, please do not hesitate to contact us!

  1. Niizuma, K., et al. (2010). Mitochondrial and apoptotic neuronal death signaling pathways in cerebral ischemia. Biochimica et Biophysica Acta (BBA)-Molecular Basis of Disease, 1802(1), 92-99.
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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