Significance of Suppression of Cerebral Gluconeogenesis in the Protective Value of Exercise Post Conditioning Towards Ischemic Injury in Rats

  • Asha K Assistant Professor, Department of Life Science, School of Sciences, JAIN (Deemed-to-be University), Karnataka, India
  • Kiran Nagar Professor, Department of Ayurveda, Sanskriti University, Mathura, Uttar Pradesh, India
  • Mayur Porwal Associate Professor, College of Pharmacy, Teerthanker Mahaveer University, Moradabad, Uttar Pradesh, India
Keywords: phosphoenolpyruvate carboxykinase (PCK), Endoplasmic retinal (ER), ischemia/reperfusion (I/R), microscopic endothelial cells (MEC)


The practice of exercise before a stroke lowers neurovascular damage and improves functional results. In order to determine the extent to which regulation of gluconeogenesis was related to how much brain damage post-stroke exercise training (PostE) prevented, this research set out to investigate these questions. Middle Cerebral Artery (MCA) blockage for 72 hours ensued by 24 hours of resuscitation in young rats. After 24 hours after a reperfusion PostE's treadmill exercise was started. Infarct quantity, neurological deficits at one and three days after reperfusion as well as apoptosis of cells was used to gauge the extent of the brain injury. Oxaloacetate (OAA), glucose, lactate, pyretic acid, phosphoenolpyruvate (PEP), and ROS were quantified by ELISA, and immunofluorescence was used to the critical enzyme phosphoenolpyruvate carboxykinase (PCK)-1/2's site and production. By using Western blot, we were able to identify upstream pathways such as forehead 3-kinase (PI3K)/Akt, p-PI3K/Akt, transcription factor (FoxO1), and all of them. Additionally, immunofluorescence was used to find p-FoxO1 expressed in the cytoplasm. PostE is superior to non-exercise control. Subsequently one and three days, there were smaller brain infarction sizes, neurological problems, and cell death. On both days, OAA was higher in postE groups and lower affects the expression of tissue PCKs, PEP, pyretic acid, lactate, ROS, glucose. The workout environment also drastically reduced PCK-1/2 expressions. Additionally, PostE dramatically increased the expression of phosphorylated PI3K, AKT, and FoxO1 proteins at one and three days. In this work, PostE suppressed gluconeogenesis and decreased brain damage after stroke in conjunction with increased PI3K/AKT/FoxO1 signalling. These findings imply that FoxO1 control of gluconeogenesis is a factor in post-stroke brain protection.


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How to Cite
Asha K, Kiran Nagar, & Mayur Porwal. (2023). Significance of Suppression of Cerebral Gluconeogenesis in the Protective Value of Exercise Post Conditioning Towards Ischemic Injury in Rats. Revista Electronica De Veterinaria, 24(2), 208 - 221. Retrieved from