Effect of Bouvardia ternifolia Root Extract on Brain Structures, Oxidative Stress, and p53 Expression in a Rat Model...

Background/Objectives: Cerebral ischemia and reperfusion injury, induced by bilateral common carotid artery occlusion and reperfusion (BCCAO/R), cause extensive neuronal damage and cognitive impairment. Bouvardia ternifolia (BtD), a plant known for its anti-inflammatory and neuroprotective effects, may offer therapeutic benefits against ischemic injury. This study aimed to evaluate the neuroprotective effects of BtD root extract on neuronal integrity, oxidative stress, and p53 protein expression following global cerebral ischemia in rats. Methods: Adult male Sprague Dawley rats were subjected to the BCCAO/R procedure for 60 min, followed by six days of reperfusion. Experimental groups included BCCAO/R+BtD, BCCAO/R+silymarin (reference control), BCCAO/R+vehicle, and sham controls. Neuronal morphology in the cortex, striatum, hippocampus, and cerebellum was assessed histologically. Oxidative stress markers, including reactive oxygen species (ROS), lipid peroxidation (LPO), reduced glutathione (GSH), and superoxide dismutase (SOD), were measured, along with the expression of p53 protein. Results: Treatment with BtD significantly decreased oxidative stress markers-LPO (82.2%), ROS (88.2%), GSH (66.5%), and SOD (54%)-and reduced p53 expression levels by 75%. Histological evaluation revealed that neurons in the BCCAO/R+BtD and BCCAO/R+silymarin groups maintained normal morphology, characterized by elongated cells and well-defined nuclei. In contrast, the BCCAO/R+vehicle group exhibited marked neuronal damage, including pyknosis, nuclear fragmentation, and interstitial edema, particularly in the hippocampal CA1 and cortical regions. BtD treatment significantly preserved neuronal structure and enhanced antioxidant defenses. Conclusions:Bouvardia ternifolia extract demonstrates neuroprotective potential in cerebral ischemia by maintaining neuronal architecture, reducing oxidative stress, and modulating p53 expression, supporting its therapeutic relevance in ischemia-reperfusion injury.