Objective To investigate the effects of cordyceps polysaccharides (CSP) on ischemic stroke (IS) in rat models via the interleukin (IL)-23/IL-17 pathway.Methods Rats were randomly assigned to the sham operation group, model group, NXTJN group, low-dose CSP group, and high-dose CSP group. The rat model of IS was established using the middle cerebral artery occlusion (MCAO) method, and the change in cerebral blood flow was monitored with the laser speckle imaging for three days after the operation. The Bederson scores and the modified neurological severity (mNSS) scores were employed to assess the neurological function of rats. The pathomorphological changes in the brain tissues of rats were observed by Hematoxylin-Eosin (HE) and Nissl staining. Western blotting was used to detect the proteins involved in the IL-23/IL-17 pathway in brain tissues, including IL-23, IL-23R, IL-17, ACT1, and TRAF6.Results The neurological function scores in all groups with rat models were significantly higher than those in the sham operation group (P < 0.05). However, there were no statistically significant differences among the groups with rat models (P > 0.05). The neurological function scores at 3 days post-modeling were significantly lower in the NXTJN group compared to the model group (P < 0.05). Similarly, the scores in the low-dose and high-dose CSP groups were significantly lower than those in the model group (P < 0.05). Compared with the sham operation group, rat models exhibited significantly reduced cerebral blood flow on the affected side, with large ischemic areas and a lower ratio of blood flow value on the affected side to that on the unaffected side (P < 0.05). In comparison to the model group, the NXTJN group, low-dose CSP group, and high-dose CSP group showed increased blood flow on the affected side, reduced ischemic areas, and a higher ratio of blood flow value on the affected side to that on the unaffected side (P < 0.05). The HE staining results showed that the brain tissues of the sham operation group exhibited orderly cell arrangement, normal morphology, intact cytoplasmic structure with light staining, large and clear nuclei, and complete nucleoli. In contrast, the ischemic penumbra region of the model group showed irregular cell distribution, disordered cell arrangement, cellular nuclear shrinkage or disappearance, extensive cell necrosis, and severe tissue structural damage. Compared with the model group, the NXTJN group, low-dose CSP group, and high-dose CSP group showed reduced cellular damage, fewer necrotic cells, and partial restoration of tissue morphology. The Nissl staining results showed that the sham operation group had abundant neurons and Nissl bodies with normal morphology, orderly cell arrangement, and no necrotic cells. Compared to the sham operation group, the model group exhibited deformed neurons, disorganized cell arrangement, loose stroma, a reduced number of Nissl bodies and marginalization of their distribution. In comparison to the model group, the NXTJN group, low-dose CSP group, and high-dose CSP group demonstrated improved cellular conditions, an increased number of Nissl bodies, more regular cell morphology, and relatively orderly cell arrangement. The relative expression levels of IL-23, IL-23R, IL-17, ACT1, and TRAF6 proteins were higher in the model group compared to the sham operation group. In contrast, these expression levels were lower in the low-dose and high-dose CSP groups compared to the model group (P < 0.05).Conclusions This experiment confirms that CSP has a certain protective effect on MCAO rats and may be achieved by regulating the IL-23/IL-17 pathway.