Tamibarotene Improves Hippocampus Injury Induced by Focal Cerebral Ischemia-Reperfusion via Modulating PI3K/Akt Pathway in Rats.

Goal: The present study aimed to examine whether Am80 (tamibarotene) protects the hippocampus against cerebral ischemia-reperfusion (I/R) injury and whether phosphoinositide-3-kinase/Akt (PI3K/Akt) pathway mediates this effect.

Materials And Methods: Rats were subjected to 90 minutes of middle cerebral artery occlusion followed by 24 hours of reperfusion. The animals were randomly divided into 7 groups: sham-operated group; I/R group; groups pretreated with 2 mg/kg, 6 mg/kg, and 10 mg/kg of Am80; Am80 (6 mg/kg) combined with the selective PI3K inhibitor wortmannin (0.

Correction to: All-Trans Retinoic Acid Ameliorates the Early Experimental Cerebral Ischemia-Reperfusion Injury in Rats by Inhibiting the Loss of the Blood-Brain Barrier via the JNK/P38MAPK Signaling Pathway.

The original version of this article unfortunately contained a mistake. The affiliation of the author Lu Xu has been submitted and published incorrectly and has been corrected with the erratum.

All-Trans Retinoic Acid Ameliorates the Early Experimental Cerebral Ischemia-Reperfusion Injury in Rats by Inhibiting the Loss of the Blood-Brain Barrier via the JNK/P38MAPK Signaling Pathway.

All-trans retinoic acid (ATRA) influences the outcomes of cerebral ischemic reperfusion (CIR) injury, but the mechanism remains unclear. The present study aimed to investigate the effects of ATRA on loss of the blood brain barrier (BBB) following CIR and to explore the possible mechanisms. Transient middle cerebral artery occlusion was performed on male SD rats to construct an in vivo CIR model.

Neuroprotective Effect of β-Caryophyllene on Cerebral Ischemia-Reperfusion Injury via Regulation of Necroptotic Neuronal Death and Inflammation: and .

Necrotic cell death is a hallmark feature of ischemic stroke and it may facilitate inflammation by releasing intracellular components after cell-membrane rupture. Previous studies reported that β-caryophyllene (BCP) mitigates cerebral ischemia-reperfusion (I/R) injury, but the underlying mechanism remains unclear. We explored whether BCP exerts a neuroprotective effect in cerebral I/R injury through inhibiting necroptotic cell death and inflammation.

β-Caryophyllene Pretreatment Alleviates Focal Cerebral Ischemia-Reperfusion Injury by Activating PI3K/Akt Signaling Pathway.

β-Caryophyllene (BCP) has been reported to be protective against focal cerebral ischemia-reperfusion (I/R) injury by its anti-oxidative and anti-inflammatory features. Recent study demonstrates that the BCP exhibits potential neuroprotection against I/R injury induced apoptosis, however, the mechanism remains unknown. Therefore, we investigate the underlying anti-apoptotic mechanism of BCP pretreatment in I/R injury.

β-Caryophyllene/Hydroxypropyl-β-Cyclodextrin Inclusion Complex Improves Cognitive Deficits in Rats with Vascular Dementia through the Cannabinoid Receptor Type 2 -Mediated Pathway.

This work was conducted to prepare β-caryophyllene-hydroxypropyl-β-cyclodextrin inclusion complex (HPβCD/BCP) and investigate its effects and mechanisms on cognitive deficits in vascular dementia (VD) rats. First, HPβCD/BCP was prepared, optimized, characterized, and evaluated. HPβCD/BCP and AM630 were then administered to VD rats to upregulate and downregulate the cannabinoid receptor type 2 (CB2).

β-Caryophyllene protects in vitro neurovascular unit against oxygen-glucose deprivation and re-oxygenation-induced injury.

β-Caryophyllene (BCP) mediates neuroprotection in cerebral ischemic animals. The neurovascular unit (NVU) acts as an intricate network to maintain the neuronal homeostatic microenvironment. However, the effects exerted by BCP on NVU remain unclear.