RETRACTED: Oleocanthal protects against neuronal inflammation and cardiopulmonary bypass surgery-induced brain injury in rats by regulating the NLRP3 pathway

Abstract

Background: Open heart surgery is performed with the aid of cardiopulmonary bypass (CPB) techniques that may cause neuronal injuries. Objective: This study investigated the potential protective effect of oleocanthal pre-treatment against CPB-induced cerebral injury. Methods: Oleocanthal 30 mg/kg i.p. was administered 3 h before CPB induction in the treated group. Behavioral neurological scores and cerebral injury were assessed to determine the effects of oleocanthal, based on oxidative stress and serum mediators of inflammation by enzyme-linked immunosorbent assay (ELISA). Quantitative Polymerase Chain Reaction (qRT-PCR) was used to estimate the mRNA expression of Toll-like receptor 4 (TLR4) and Interleukin 1 Receptor Associated Kinase 4 (IRAK4) proteins in the cerebral tissue of rats CPB-induced injury. Western blot assay and histopathology were also performed. Results: The findings suggest that pre-treatment with oleocanthal reduced neurological dysfunction and cerebral injury. Parameters of oxidative stress and cytokine levels were reduced in the serum of the oleocanthal treated group compared with the CPB-only group. Pre-treatment with oleocanthal ameliorated the expression of TLR-4, IRAK4, and Zonula occludens-1 (ZO-1) proteins in the cerebral tissue of the CPB-injured rats. Conclusions: The results revealed that treatment with oleocanthal protected against cerebral damage by controlling microglia inflammation through the TLR-4 pathway.

Oleacein Attenuates Lipopolysaccharide-Induced Inflammation in THP-1-Derived Macrophages by the Inhibition of TLR4/MyD88/NF-κB Pathway

“…Several research groups reported the anti-oxidant and anti-inflammatory activities of oleocanthal and oleuropein [30][31][32][33][34][35][36][37], while those of OLC are still poorly defined. Recently, it has been shown that OLC exerts anti-inflammatory effects in human adipocytes challenged with TNF-α, a prototypic inflammatory stimulus, which could aid to explain the cardiometabolic benefit of EVOO consumption [32].…”

Biochemical Changes in Cardiopulmonary Bypass in Cardiac Surgery: New Insights

“…These regulatory mechanisms of vasoconstriction are deregulated, to a greater or lesser extent, during and after the cardiopulmonary bypass ends (Figure 3). The passage of blood through CPB stimulates the activation of the complement cascade, production of ROS species and release of inflammatory mediators, such as the triad of cytokines, interleukin-1 (IL-1), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) [45,[75][76][77][78]. All this inflammatory biochemistry is capable of acting in specific areas of the brain such as the locus coeruleus and the paraventricular nucleus of the hypothalamus, where the cells responsible for the hypothalamic-pituitary-adrenal axis are located; they stimulate these regions and lead to a reduction and desensitization of the alpha-1 adrenergic receptor and an increase in the inflammatory state, thus forming a cycle that is difficult to overcome (11).…”