Cerebral ischemia (CI) can lead to ischemic stroke. The most effective therapy for cerebral ischemic stroke is the early restoration of blood reperfusion. However, reperfusion after CI can result in cerebral ischemia reperfusion (CI/R) injury. This study aimed to detect the effect of eriocitrin on cerebral I/R injury and investigate the underlying mechanism.

Our results indicated that Eriocitrin attenuated oxidative injury and inflammatory response in rats with CI/R via the Nrf2/HO-1/NQO1/NF-κB signaling pathway.

Seventy male Sprague-Dawley (SD) rats were randomly divided into 5 groups: the control group, the cerebral I/R group, the I/R + eriocitrin 8 mg/kg group, the I/R + eriocitrin 16 mg/kg group, and the I/R + eriocitrin 32 mg/kg group. Different doses of eriocitrin or 0.5% carboxymethyl cellulose sodium were administrated to the rats once daily for 7 days before middle cerebral artery occlusion (MCAO). PCR staining was performed to observe cerebral infarction. Hematoxylin and eosin (H&E) staining was carried out to observe the damage to the brain tissue. Terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) was used to detect apoptosis. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the relative mRNA levels of related molecules. Western blot was used to detect the expression of related proteins. The detection kits were used to detect superoxide dismutase (SOD) and lactic dehydrogenase (LDH) activity, and malondialdehyde (MDA) content respectively. Enzyme-linked immunosorbent assay (ELISA) was used to detect TNF-radiation, interleukin-6 (IL-6), and interleukin-10 (IL-10).

The results showed that Eriocitrin significantly reduced the cerebral infarct volume, cerebral water content, and cerebral indexes. Eriocitrin treatment alleviated pathological injury, promoted cell proliferation, and inhibited cell apoptosis. Eriocitrin upregulated SOD activity and downregulated MDA and LDH content. Eriocitrin also effectively decreased the levels of IL-6 and tumor necrosis factor-α (TNF-α), but increased the content of IL-10 in serum and brain tissues. Furthermore, Eriocitrin increased the phosphorylation of nuclear factor erythroid 2-related factor (Nrf2), as well as the expressions of heme-oxygenase-1 (HO-1) and quinine oxidoreductase 1 (NQO1). Moreover, Eriocitrin decreased the phosphorylation of nuclear factor-κB (NF-κB) p65. Conclusions: Our results indicated that Eriocitrin attenuated oxidative injury and inflammatory response in rats with CI/R via the Nrf2/HO-1/NQO1/NF-κB signaling pathway.