The Role of Mitochondria in Brain Cell Protection from Ischaemia by Differently Prepared Propolis Extracts

Abstract

Mitochondria are both the primary targets and mediators of ischaemic damage in brain cells. Insufficient oxygen causes reactive oxygen species that damage the mitochondria, leading to the loss of functionality and viability of highly energy-demanding neurons. We have recently found that aqueous (AqEP), polyethylene glycol-aqueous (Pg-AqEP) and ethanolic propolis extracts (EEP) can modulate mitochondria and ROS production in C6 cells of astrocytic origin. The aim of this study was to investigate the effect of the extracts on viability, mitochondrial efficiency and superoxide generation, and inflammatory cytokine release in primary rat cerebellar neuronal-glial cell cultures affected by ischaemia (mimicked by hypoxia +/− deoxyglucose). AqEP and Pg-AqEP (15–60 µg/mL of phenolic compounds, or PC) significantly increased neuronal viability in ischaemia-treated cultures, and this was accompanied by a reduction in mitochondrial superoxide levels. Less extended protection against ischaemia-induced superoxide production and death was exhibited by 2 to 4 µg/mL of PC EEP. Both Pg-AqEP and Ag-EP (but not EEP) significantly protected the cultures from hypoxia-induced elevation of TNF-α, IL-1β and IL-6. Only Pg-AqEP (but not AqEP or EEP) prevented hypoxia-induced loss of the mitochondrial basal and ATP-coupled respiration rate, and significantly increased the mitochondrial respiratory capacity. Summarising, the study revealed that hydrophilic propolis extracts might protect brain cells against ischaemic injury by decreasing the level of mitochondrial superoxide and preventing inflammatory cytokines, and, in the case of Pg-AqEP, by protecting mitochondrial function.

Propofol via Antioxidant Property Attenuated Hypoxia-Mediated Mitochondrial Dynamic Imbalance and Malfunction in Primary Rat Hippocampal Neurons

“…Furthermore, our data suggested intracellular ROS played a critical role, since both antioxidant and ROS scavenger reduced ROS (Figure 3) and abolished hypoxia-induced mitochondrial malfunction (Figure 3). The pivotal role of ROS during hypoxia-induced mitochondrial malfunction was also supported by previous publications, which demonstrated that hypoxia may impair mitochondrial function through inducing oxidative stress in rat cardiomyocytes [28], human renal tubular cells [29], murine fibroblasts [30], rat cerebral neuronal glial cells [31], and primary rat hippocampal neurons [32]. ), while reduced the phosphorylated of Drp1 at ser 637 (p-Drp1 ser637 ), which were both attenuated by propofol, α-tocopherol, and ebselen.…”

Antineuroinflammatory Effect of Amburana cearensis and Its Molecules Coumarin and Amburoside A by Inhibiting the MAPK Signaling Pathway in LPS-Activated BV-2 Microglial Cells

“…As DEAC's main bioactive markers CM and AMB showed a promising antiinflammatory effect, we then further described the mechanisms underlying DEAC-mediated attenuation of inflammation in BV-2 cells. There are several published works describing A. cearensis or its active principles' antiinflammatory or antioxidant activities [10,11,15,17,29,[39][40][41]. However, these studies are mainly confined to just showing their effects without further investigating the molecular mechanism underlying them.…”

In Vitro and In Silico Anti-Glioblastoma Activity of Hydroalcoholic Extracts of Artemisia annua L. and Artemisia vulgaris L.

“…Rat glioma C6 cells were purchased from the Cell Lines Service GmbH, Eppelheim, Germany. For the cytotoxicity control of tested extracts or chlorogenic acid, a rat cerebellar neuronal-glial cell culture was used from postnatal 5–7-day-old Wistar rats [ 65 , 66 ]. Cell cultures were seeded in culture flasks containing Dulbecco’s Modified Eagle Medium (DMEM) with 10% of fetal bovine serum, 100 U/mL penicillin, and 100 µg/mL streptomycin.…”