Pinocembrin pretreatment counteracts the chlorpyrifos-induced HO-1 downregulation, mitochondrial dysfunction, and inflammation in the SH-SY5Y cells

Can Propolis Be a Useful Adjuvant in Brain and Neurological Disorders and Injuries? A Systematic Scoping Review of the Latest Experimental Evidence

“…In addition, it inhibited apoptosis by reducing the expression of genes associated with apoptosis signaling pathways; protein-coding gene Bax, cytochrome-c, cas-3, cas-8, and p53 genes [24,25]. It was also evident that propolis protected cell membranes and prevented further deterioration of the tissue morphology associated with toxicity [23,26,28,33,35,37].…”

“…The therapeutic properties of propolis and its bioactive compounds appear to be due to their anti-inflammatory properties. In animals and cell cultures which were subjected to chemical and radiation toxicity, propolis was consistently demonstrated to reduce the expression of inflammatory and oxidative markers such as malonaldehyde (MDA), tumor necrosis factor-α (TNF-α), nitric oxide (NO), and inducible nitric oxide synthase (iNOS), while increasing and maintaining antioxidant parameters, namely superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR), and glutathione (GSH) [23,27,[29][30][31][32]34,36]. In addition, it inhibited apoptosis by reducing the expression of genes associated with apoptosis signaling pathways; protein-coding gene Bax, cytochrome-c, cas-3, cas-8, and p53 genes [24,25].…”

The SH-SY5Y human neuroblastoma cell line, a relevant in vitro cell model for investigating neurotoxicology in human: Focus on organic pollutants

“…CPF causes mitochondrial damage: mitochondrial swelling and alterations in the pattern of the crests [83] and mitochondrial fragmentation [62,81,91]. Moreover, CPF decreases the mitochondrial membrane potential [79-82, 91, 92], disrupts the activity of complex I-III and V [92] and decreases ATP levels [79,80,82,92]. Recently, the effects of CPF treatment (50 and 100 µM for 5d) on mitochondria have been linked to a loss of coenzyme Q 10 status, and posttreatment of cells with coenzyme Q 10 partially recovered the effects of CPF on cell viability, and the decreased activities of citrate synthase and of complexes II/III [89].…”

“…J o u r n a l P r e -p r o o f 12 Beside the disruption of mitochondria functions, the involvement of inflammatory processes in CPF-triggered apoptosis was also observed, as CPF treatment increased the amount of cyclooxygenase-2 (COX-2), tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β) and NF-B proteins [80,84,85]. The mitogen-activated protein kinases (MAPK) c-jun N-terminal kinase (JNK) and p38 MAPK seem to be implicated in the inflammation process and generation of ROS since the use of specific inhibitors of these kinases attenuates COX-2 expression and ROS production [84].…”

Activation of Sirtuin-1 by Pinocembrin Treatment Contributes to Reduced Early Brain Injury after Subarachnoid Hemorrhage

“…Pinocembrin, a natural compound distributed in propolis, shows immunomodulatory, anti-inflammatory, antifree radical, and anticytotoxicity properties [9]. A great deal of research has demonstrated the promising effects of pinocembrin against various CNS diseases including ischemic brain injury, hemorrhagic brain injury, traumatic brain injury, psychiatric disorders, and neurodegenerative disorders [9][10][11][12]. In a model of intracerebral hemorrhage, pinocembrin significantly mitigated hemorrhagic brain injury by suppressing toll-like receptor 4 and reducing M1 microglia [9].…”