TABLE 1.
Possible mechanisms involved in epilepsy.
| Component | Specific factors | References |
|---|---|---|
| Neurotransmitters | Imbalance of Glu and GABA | Hirose (2014) |
| Synapses and Receptor | GABA-A, NMDA, 5-HT, AMPA receptor, acetylcholine receptor Enzyme, modulator, transporter, axonal burst bud | Hirose (2014); Paoletti et al. (2013); Thijs et al. (2019) |
| Ion channels | Sodium channel; Potassium channel; HCN channel; Calcium channel; Chloride channel | Alexander et al. (2016); Contet et al. (2016); Duflocq et al. (2008); Tang et al. (2016) |
| Inflammatory cytokines | IL-1β, IL-2, IL-4, IL-6, IL-10, TNF-α, cyclooxygenase-2, Platelet-activating factor, Prostaglandin E2, Adhesion molecules, MMP-9; TLR-1, -2, -3; Chemokines were increased | Godhwani and Bahna (2016); Kumar et al. (2019) |
| Immune system | Both cellular and humoral immunity are affected. Increasing IgA, IgG, CD8, CD54; Decreasing CD3, CD4, CD4/CD8 | Ravizza et al. (2006); Roseti et al. (2015); Liu et al. (2015) |
| Glial cell | Astrocytes and microglia proliferated and the ability of astrocytes to absorb potassium ions decreased | Bark et al. (2018) |
| Oxidative stress and apoptosis | ROS was increased, the ratio of Bcl-2/Bax was decreased, and the expression levels of apoptotic proteins cytochrome C and Caspase-3 were significantly increased | Liang et al. (2012); Kudin et al. (2002) |
| Mitochondrial dysfunction | Increasing Ca2+ and ATP consumption | Rowley and Patel (2013); Liang et al. (2012); Kudin et al. (2002); Smith and Patel (2017) |
| Genetic factors | SCN1A, SCN2A, SCN8A and other mutations | Pal et al. (2010) |
| Glycogen metabolism | Decreased glycogen degradation, abnormal expression of glucocorticoid | Walls et al. (2009) |
MMP-9, Matrix metalloproteinase-9; TLR, Toll-like receptors.