RETRACTED: Activation of the PI3K-Akt pathway promotes neuroprotection of the δ-opioid receptor agonist against cerebral ischemia-reperfusion injury in rat models

Epigallocatechin-3-Gallate Reduces Neuronal Apoptosis in Rats after Middle Cerebral Artery Occlusion Injury via PI3K/AKT/eNOS Signaling Pathway

“…Chen et al [ 27 ] investigated the ischemia/reperfusion mechanism in MCAO rat models and verified that Bcl-2 expression reduced, but Caspase-3 and Bax expression increased. Lv et al [ 15 ] confirmed that δ -opioid receptor agonist improved neuronal apoptosis after cerebral ischemia/reperfusion through PI3K-Akt activation pathway. In the present study, MCAO models were treated with EGCG, and PI3K antagonist LY294002 was injected in the brain.…”

“…After the fixation of the brain slices, the digital camera was taken out, and the area of infarct area was calculated by Image J image analysis software (dyeing weakened area of middle cerebral artery). In order to offset the error of the infarct volume caused by edema after cerebral infarction, using the indirect infarct volume method proposed by Lv et al [ 15 ] measured the area of the ipsilateral noninfarct area and the contralateral area of the infarct in each slice of the brain, respectively. The infarct volume was expressed as the percentage of infarcted volume in the total volume of the contralateral hemisphere, which is calculated by the formula, (contralateral volume of infarct − ipsilateral noninfarct volume)/contralateral volume of infarct × 100%.…”

β-Funaltrexamine Displayed Anti-Inflammatory and Neuroprotective Effects in Cells and Rat Model of Stroke

“…Clinically, cancer patients undergoing intensive morphine treatment have an increased risk of stroke incidence [34]. Accordingly, a growing body of evidence has revealed the neuroprotective effects of the nonselective opioid receptor antagonist naloxone, δ opioid receptor agonists, and κ opioid receptor agonists in rodent models experiencing neurodegeneration [3,7,[9][10][11][24][25][26][35][36][37]. Being a CNS-penetrating compound, the selective µ opioid receptor antagonist β-funaltrexamine is capable of inhibiting LPS-induced neuroinflammation in mice after receiving an intraperitoneal injection [29,30].…”

“…Beyond its effect on the nociceptive/analgesic systems, the opioidergic system also displays effects on physiological and behavioral functions, including respiration, ion channel activity, and immune responses [1,2]. Additionally, alteration in the opioidergic system has been reported in the disease initiation and progression of several acute and chronic diseases, including neurodegenerative diseases [3][4][5][6][7][8][9]. These phenomena highlight the potential pathogenic roles that the opioidergic system may have and candidate targets for intervention with an aim to prevent and/or treat diseases.…”

“…Upon binding with either the µ, δ, or κ opioid receptor, they display shared or distinct biological consequences. For example, the neuroprotective effects of the δ and κ opioid receptor agonists and µ opioid receptor antagonist have been described [7,[9][10][11]. Despite morphine long being known to have immunosuppressive properties in vivo, a chronic morphine infusion causes neuroinflammation [12,13].…”