Reduction of inflammatory response after ischemia-reperfusion injury in rats with panax notoginseng saponins by regulating nucleotide-bound oligomerized domain-like receptor protein 1(NLRP1)/Caspase-1 signaling via Cezanne

Acute ischemic stroke (AIS) is featured as damage of blood-brain barrier in severe cases, which leads to brain tissue damage. Panax notoginseng saponins (PNS), because of its anti-inflammatory effect, can reduce the inflammatory response caused by ischemia-reperfusion, thereby reducing the degree of damage to the blood-brain barrier. Studies on AIS have confirmed that, Cazenne has an anti-inflammatory effect, but specific mechanism by which PNS regulates Cazenne to reduce the inflammatory response after cerebral ischemia-reperfusion injury (IRI) is still unclear. Therefore, this study explored PNS’ role in inhibiting the inflammatory response after cerebral IRI through Cezanne. Sprague-Dawley (SD) rats were randomly grouped and then assigned into sham operation group (sham), model group (MCAO), model+PNS (MCAO+PNS), model+PNS+Cezanne silencing lentivirus (MCAO+PNS+shCezanne), and model+PNS+empty carrier (MCAO+PNS+shNC). Neurological function was scored by mNSS while cerebral infarction volume was tested by TCC staining. The brain was tested by dry and wet method, while levels of inflammatory factors and NLRP1 and Caspase-1 were detected by ELISA, Western blot, and Cazenne expression was detected by immunofluorescence. PNS reduced the expression of pro-inflammatory factors in MCAO rats, by mainly downregulating NLRP-1 and Caspase-1. By upregulating Cezanne and inflammatory factors downstream NLRP1/Caspase-1 pathway was inhibited, thereby improving the inflammation in the rats after IRI. PNS inhibited the activity of NLRP1/Caspase-1 signaling pathway through Cezanne, thereby reducing inflammatory factors in the brain after cerebral IRI, and reducing inflammatory response.