[Animal Modeling]-Neuroprotective effect and mechanism of nanoliposomal quercetin on cerebral ischemia-reperfusion injury

  Objective: To study the neuroprotective effect and mechanism of nanoliposome quercetin (nLQ) on focal cerebral ischemia-reperfusion injury in rats.

  Method: 80 male SD rats were randomly divided into sham operation group, model group, nLQ low-dose group, medium-dose group and high-dose group, each with 16 rats. The rat middle artery cerebral ischemia-reperfusion model was prepared with an improved suture method. At 48 hours after cerebral ischemia and reperfusion in each group, the behavioral scores of rats were observed by the neurological deficit scoring method, and the 2,3,5-triphenyltetrazolium chloride (TTC) staining experiment was performed to determine the cerebral infarct volume. Determination of water content in brain tissue by dry and wet weight method; determination of serum tumor necrosis factor-α (TNF-α) and interleukin 10 (IL-10) by enzyme-linked immunosorbent assay (ELISA) method; detection of brain tissue by flow cytometry Apoptosis of nerve cells; Western blotting was used to detect changes in the expression of B lymphoma 2 gene (Bcl-2) and Bcl-2 related X protein (Bax). versus

  Result: Compared with the model group, the neurological symptoms of rats in the low, medium and high dose nLQ groups were significantly improved, the behavior score was significantly reduced, and the cerebral infarction volume was significantly reduced. Significantly reduced, serum TNF-α and II-10 levels were significantly reduced, apoptosis rate was significantly reduced, the expression level of apoptosis-related protein Bcl-2 was significantly increased, and the expression level of Bax was significantly reduced (P\u003c0.05 or P\ u003c0.01), and there is a dose-effect relationship.

   Conclusion: nLQ has an excellent protective effect on focal cerebral ischemia-reperfusion injury in rats. The mechanism that nLQ improves the symptoms of nervous system defects and reduces neuronal apoptosis and blood may be related to the reduction of inflammatory response factor TNF-α.