History

Background: Epilepsy is the fourth most frequent neurological disorder worldwide. Epilepsy can be diagnosed if someone has two or more spontaneous seizures. Subtypes M1 and M3 of the receptor are affected by pilocarpine, with the M3 receptor having the ability to activate phospholipase C. In this way, the second messenger's inositol triphosphate, diacylglycerol, calcium, and protein kinase are produced. Because of this, M3 cholinergic agonists cause calcium to be upregulated, leading to smooth muscle contraction. Ursodeoxycholic acid is an effective drug for treating cholestatic liver disease. There are a number of interconnected and synergistic ways in which ursodeoxycholic acid affects the liver. Method: Thirty adult male Wistar rats, weighing 200 ± 20 g were utilized in this study Group I(negative Control): Rats will be received of N/S(0.5 ml/kg) Group II(Sco+ LiCa +Pilo): Rats received LiCa; 127 mg/kg, followed by pilocarpine administration (30 mg/kg) .scopolamine (1 mg/kg in rats) is also given to the rats 30 min before pilocarpine administration. Group III (Diazepam ):Epileptic rats treated with diazepam (20 mg/kg )was started 2 h after the beginning of SE.Group IV (min. dose of UDCA): Epileptic rats will be received UDCA 25 mg/kg/day.Group V (max. dose of UDCA ) Epileptic rats will be received UDCA 100 mg/kg/day .Result: Based on measurement of markers: TNF-α, GSH, we reported increase the level of TNF-α & decrease the level of GSH when given pilocarpine, while we found raise in the GSH level & decrease in the level of TNF-α in UDCA treated-group Conclusion: It can be concluded that the UDCA improve the biochemical alterations (decrease GSH & increase TNF ) that occur after S.E and UDCA have the same effect when comparison with diazepam effect.