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Updated: May 1, 2026
Experimental Models to Study the Neuroprotection of Acidic Postconditioning Against Cerebral Ischemia
Published on: July 31, 2017
Neuroprotective mechanism of ischemic postconditioning in mice: a possible relationship between protein kinase C and
1Department of Pharmaceutical Sciences and Drug Research, Punjabi University, Patiala, India.
Background:
The present study was conducted to pharmacologically investigate the role of protein kinase C (PKC) pathway in neuroprotective mechanism of ischemic postconditioning (iPoCo) and determine the influence of nitric oxide (NO) signaling in PKC-mediated effects.
Materials And Methods:
Bilateral carotid artery occlusion of 12 min followed by reperfusion for 24 h was used to produce ischemia and reperfusion (I/R)-induced cerebral injury in male Swiss mice. Memory was assessed using Morris water maze test. Degree of motor incoordination was evaluated using inclined beam-walk test, rota-rod test, and lateral push test. Cerebral infarct size was measured using triphenyltetrazolium chloride staining. Brain acetylcholinesterase activity, thiobarbituric acid reactive species, nitrite/nitrate, and reduced glutathione levels were also estimated.
Results:
Bilateral carotid artery occlusion followed by reperfusion produced significant rise in cerebral infarct size, acetylcholinesterase activity, and thiobarbituric acid reactive species levels along with the fall in nitrite/nitrate and glutathione levels. A significant impairment of memory and motor coordination was also noted. iPoCo consisting of three episodes of 10 s carotid artery occlusion and reperfusion significantly attenuated infarct size, memory impairment, motor incoordination, and altered biochemicals. iPoCo-induced neuroprotective effects were significantly abolished by chelerythrine (a nonselective PKC inhibitor). L-Arginine, an NO precursor significantly attenuated I/R-induced injury and mimicked the neuroprotective effect of postconditioning. Furthermore, this protective effect of L-arginine on I/R injury and iPoCo was abolished when it was coadministered with chelerythrine.
Conclusions:
It may be concluded that neuroprotective mechanism of iPoCo involves PKC mediated pathway with NO signaling as an essential step.
Insights
Ischemic postconditioning (iPoCo) protects the brain via the protein kinase C (PKC) pathway. Nitric oxide (NO) signaling is crucial for these neuroprotective effects against ischemic injury.
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Investigates the role of protein kinase C (PKC) in neuroprotection.
- Examines the influence of nitric oxide (NO) signaling in PKC-mediated effects.
Purpose of the Study:
- To pharmacologically elucidate the neuroprotective mechanisms of ischemic postconditioning (iPoCo).
- To determine the involvement of the PKC pathway and NO signaling in iPoCo's protective effects.
Main Methods:
- Induced cerebral injury in mice via carotid artery occlusion and reperfusion.
- Assessed neuroprotection using behavioral tests (memory, motor coordination) and biochemical markers (infarct size, oxidative stress, neurotransmitters).
- Utilized PKC inhibitor (chelerythrine) and NO precursor (L-arginine) to investigate pathway involvement.
Main Results:
- iPoCo significantly reduced infarct size, improved memory and motor coordination, and normalized biochemical markers.
- PKC inhibition abolished iPoCo's neuroprotective effects.
- L-arginine mimicked iPoCo's protection, but this effect was blocked by chelerythrine, indicating NO's role in PKC-mediated protection.
Conclusions:
- Neuroprotection by iPoCo involves the PKC pathway.
- Nitric oxide (NO) signaling is an essential component of the PKC-mediated neuroprotective mechanism of iPoCo.
