Picroside II Exerts a Neuroprotective Effect by Inhibiting mPTP Permeability and EndoG Release after Cerebral...

Area of Science:

• Neuroscience
• Cell Biology
• Pharmacology

Background:

• Cerebral ischemia/reperfusion (I/R) injury is a critical condition linked to mitochondrial dysfunction.
• Mitochondrial membrane permeability plays a key role in the pathogenesis of I/R injury.

Purpose of the Study:

• To investigate the neuroprotective effects of picroside II (Picr) in a rat model of cerebral I/R injury.
• To elucidate the mechanisms by which Picr affects mitochondrial permeability transition pore (mPTP) and endonuclease G (EndoG) release.

Main Methods:

• Rats underwent 2 hours of cerebral ischemia followed by 24 hours of reperfusion.
• Neurobehavioral function, infarct volume, and reactive oxygen species (ROS) were assessed.
• Mitochondrial permeability transition pore (mPTP) permeability, apoptosis, and protein expression (EndoG, VDAC1) were analyzed.

Main Results:

• Picr treatment significantly reduced neurological deficit scores (mNSS), infarct volume, and ROS levels.
• Picr decreased mPTP permeability, apoptosis, and the cytoplasmic/nuclear release of EndoG.
• Downregulation of voltage-dependent anion channel 1 (VDAC1) expression was observed in the Picr group.

Conclusions:

• Picroside II demonstrates significant neuroprotective effects against cerebral I/R injury in rats.
• Picr attenuates I/R injury by downregulating VDAC1, reducing mPTP permeability, and inhibiting EndoG release from mitochondria.