The neuroprotective attributes of chlorogenic acid (CGA) have been delineated in prior literature, yet its precise role in addressing encephalopathy associated with sepsis remains to be elucidated. The primary objective of this study was to delineate the neurocognitive effects of CGA and to ascertain the underlying mechanisms of its action in a caecal ligation and puncture (CLP)-induced model of sepsis. Male Sprague-Dawley rats were subjected to sepsis via the CLP procedure and subsequently segregated into distinct cohorts: (1) CLP + CGA; (2) CLP + saline; (3) sham + CGA; and (4) sham + saline. The experimental paradigm entailed the intraperitoneal administration of 30 mg/kg CGA. In the novel object recognition assay, septic rats manifested discernible deficits in memory retention, as evidenced by their diminished ability to recognize novel objects during both acute and protracted assessments. Contrastingly, CGA administration efficaciously attenuated these cognitive shortcomings, signifying an enhancement in mnemonic function. Concurrently, in the open field assessment, CGA-treated rats mirrored the behavioural patterns exhibited by sham-operated counterparts, alluding to the preservation and potential augmentation of cognitive faculties. Collectively, these observations underscore the putative therapeutic efficacy of CGA in ameliorating cognitive dysfunctions and mnemonic deficits engendered by sepsis.