Abstract: Objective To investigate the relationship between peroxisome proliferator activated receptor γ (PPARγ) activation and pyroptosis in rat model of cerebral ischemia-reperfusion injury. Methods Forty male SD rats of SPF were randomly divided into sham operation group, MCAO model group, pioglitazone group and pioglitazone+GW9662 group, 10 rats for each group. Neurological deficits were measured by Zea-Longa score, and infarct sizes were measured by TTC staining. The expressions of PPARγ, caspase-1, Gasdermin D (GSDMD), interleukin (IL) - 1β and IL-18 in ischemic penumbra were observed by Western blot assay. Results The expression level of PPARγ protein was significantly lower 24- h after cerebral ischemia-reperfusion injury in MCAO group than that of sham group (P＜0.05). The values of caspase-1, GSDMD, IL-1β and IL-18 were significantly higher in MCAO group than those in sham operation group (P＜0.05). Meanwhile, the neurological deficits and infarct sizes were significantly higher in MCAO group than those of sham operation group (P＜0.01). The level of PPARγ was significantly increased in PGZ group compared with that of MCAO group (P＜ 0.05), while the caspase-1, GSDMD, IL-1β and IL-18 decreased (P＜0.05). And neurological deficits and infarct sizes decreased significantly (P＜0.01). However, in PGZ+GW9662 group, the effect of PPARγ was reversed. Conclusion At the early stage of rat cerebral ischemia/reperfusion, the activation of PPARγ inhibits the pyroptosis to reduce neuron injury.

Key words: reperfusion injury, pyroptosis, brain injuries, PPAR gamma, Pioglitazone