The role of proinflammatory cytokines on liver damage after pentylenetetrazole-induced acute and chronic epilepsy models in rats

Abstract Objectives: The mechanisms of acute liver failure resulting from epilepsy are poorly defined and appear to be multifactorial, including hypoxia and steatosis. The role of inflammation on liver damage after seizures is unclear. This study aimed to investigate the relationship between proinflammatory cytokines and liver damage after pentylenetetrazole-induced acute and chronic epilepsy models in rats. Materials and methods: Male Wistar albino adult rats (n = 18), weighing 220–240 g, were used in the experiment. The animals were divided into three groups: (1) Control Group (Control; n = 6); rats were treated with a single dose of saline intraperitoneally (i.p.), (2) Acute Epileptic Model Group (n = 6); rats were treated with a single dose of i.p. PTZ (45 mg/kg), (3) Chronic Epileptic Model Group (n = 6); rats were treated with repeated doses of i.p. PTZ (35 mg/kg) every other day for 15(fifteen) times. Result: There was a significant difference between the control and acute epileptic model in terms of serum AST, TNF-α, IL-1 β and IL-6 parameters (p<0.05). On the other hand, there was a significant difference between the acute and chronic epileptic models in the serum AST, TNF-α and IL-6 parameters (p<0.05). Conclusions: As a result, while liver damage is secondary to hypoxia during epileptic seizures, multifactorial causes are blamed. Proinflammatory cytokines that increase in the liver after these factors may be responsible for liver damage in acute epileptic seizures. Compensation mechanisms such as antioxidant defence mechanism in chronic epileptic seizures may prevent liver damage.