Epilepsy　is　a　neurological　disorder　involving　mitochondrial　dysfunction　and　neuroinflammation.　This　study　examines　the　relationship　between　NLRP3　inflammasome　activation　and　mitophagy　in　the　temporal　lobe　epilepsy,　which　has　not　been　reported　before.　A　pilocarpine-induced　epileptic　rat　model　was　used　to　assess　seizure　activity　and　neuronal　loss.　Pyroptosis　markers　(NLRP3,　cleaved　Gasdermin　D,　IL-1　beta/IL-18),　and　autophagy/mitophagy　activity　(LC3B-II/I,　BNIP3,　TOMM20/LC3B　colocalization)　were　analyzed　via　immunofluorescence,　Western　blot,　and　transmission　electron　microscopy.　NLRP3　inhibitors　and　anti-IL-1　beta　antibodies　were　administered　to　evaluate　therapeutic　effects.　Epileptic　rats　exhibited　progressive　neuronal　loss　and　seizure　aggravation,　correlating　with　NLRP3　inflammasome　activation　and　pyroptosis.　While　general　autophagy　was　upregulated,　mitophagy　was　selectively　impaired　in　the　hippocampus.　NLRP3　activation　promoted　IL-1　beta　release,　which　suppressed　mitophagy　via　PPTC7　upregulation.　NLRP3　activation　inhibitor　(MCC950)　and　anti-IL-1　beta　treatment　restored　mitophagy　and　reduced　seizures.　NLRP3　inflammasome-driven　pyroptosis　exacerbates　epilepsy　by　impairing　mitophagy　activity　via　IL-1　beta/PPTC7.　Targeted　NLRP3　inhibition　mitigates　this　cascade,　offering　a　promising　strategy　for　refractory　epilepsy.