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Growing evidence implicates that processes mediated by cytokines, growth factors, and the plasminogen activation (PA) system play crucial roles in pathogenesis of epilepsy and its comorbidities. Using the lithium-pilocarpine rat model, we investigated mRNA expression patterns of PA system components (tPA/PAI-1/uPAR), pro-inflammatory cytokines (IL-1β/TNF-α), and TGF-β1 during latent (7 days) and chronic (5 months) periods after status epilepticus (SE). Our results revealed region-specific dysregulation of the PA system that persisted into the chronic period, with tPA (<i>Plat</i>) transiently upregulated in dorsal hippocampus during the latent phase while uPAR (<i>Plaur</i>) exhibited sustained elevation in entorhinal cortex into the chronic period. TGF-β1 (<i>Tgfb1</i>) exhibited widespread upregulation across all examined brain regions during the latent period, remaining elevated in the ventral hippocampus 5 months after SE. Notably, latent-phase neuroinflammation showed cortical specificity, with IL-1β (<i>Ilb1</i>) expression increased in the frontal cortex while the hippocampal expression remained unchanged. Additionally, we investigated the development of depressive-like behavior in rats in the chronic period after SE using sucrose preference test. Rats displaying anhedonia (reduced sucrose preference) exhibited significantly higher <i>Tgfb1</i> and <i>Tnf</i> expression in the ventral hippocampus and entorhinal cortex compared to non-anhedonic and control rats in the chronic period after SE. Our findings demonstrate persistent, region-specific transcriptional changes in the PA system following SE, with upregulation of <i>Tgfb1</i> and <i>Tnf</i> associated with more severe functional outcome in the chronic period after SE.