Anti-injury Effect Of Scutellarin On The Hypoxic Ischemic Brain Damage Of Neonatal Rats And The Expression Of P38 MAPK

Hypoxia-ischaemia brain damage(HIBD) is neonata brain syndrome in perinatal period, because of cerebral hypoxia ischemia caused by various factors, and can often result in irreversible brain damage and a range of neurological sequelae. Hypoxia-ischaemia brain damage not only serious threat to the health of newborns, but also has high rate of disability and serious complications, which seriously affecting the quality of life of children. To actively explore the effective and safe treament method is a reseach hotspot both at home and abroad, but so far have not yet achieved a breakthrough progress. In recent years, experimental study and clinical treatment of traditional Chinese medicine Chinese on HIBD has attracted more and more people’s attention. Breviscapine is a kind of flavonoid isolated from Erigeron breviscapus, mainly containing scutellarin, a small amount of apigenin-7-O-glucronide and other flavonoids. Scutellarin since the 70’s of the last century for the first time after the separation, has been made into various forms, more for the treatment of diseases of Central nervous system and circulatory system, and has obtained the good clinical curative effect. But the related research of scutellarin in treatment of neonatal HIBD is rare at present. This experiment based on the neonatal rat model of hypoxic ischemic brain damage, through the expression of cell apoptosis and p38 MAPK in the CA1 hippocampus at different time points, to investigate the effect of scutellarin on neonatal HIBD rats and the effect on the expression of p38 MAPK and its mechanism, thereupon then providing a favourable theoretical basis for the clinical treatment of neonatal HIBD.Objective: The research is to study the effects of scutellarin treat hypoxia-ischaemia brain damage in neonatal rats and the expression of p38 MAPK signal pathway following HIBD.Methods: 45 healthy 7-day-old neonatal SD rats were randomly divided into sham operation group, HIBD group, and scutellarin group(25mg/kg). After medication, each group respectively executed 5 rats in 24 h, 3d, 7d, and take brain tissue sliceof. HE staining was used for pathological change of brain tissue was observed; The neuronal apoptosis was detected using TUNEL assay. The highest expression and expressional tendencies of p38 MAPK was determined by the method of immunohistochemistry.Results: HE staining: in sham operation group, cells arranged in neat rows, the body was basically normal, no lack of nerve cells; ligated brain cells of HIBD group arranged in disorder, nuclear pyknosis, dissolved obviously, showing a large number of degeneration and necrosis of neurons; scutellarin group could also be observed degeneration, necrosis of neurons, but the degree was reduce than HIBD group. TUNEL staining: in sham operation group at each time point in hippocampal CA1 area of positive cells expression; HIBD group at each time point, the number of positive cells increased significantly, there was statistical significance difference compared with sham operation group(P<0.05); scutellarin group could observe positive cells decreased, but the positive cells decreased significantly compared with the HIBD group at the same time point, there was statistical significance difference compared with sham operation group(P<0.05). Immunohistochemical staining: The HIBD positive cells in hippocampal CA1 region in group at each time point are widely visible p38 MAPK expression, there are significant differences compared to the sham operation group(P<0.05). The number of positive cells of scutellarin group at each time point in p38 MAPK expression decreased gradually, there was statistical significance difference(P<0.05) compared with HIBD group at the same time points.Conclusion:1.Scutellarin could significantly inhibit the phosphorylation of p38 MAPK after hypoxia ischemia.2.Scutellarin can obviously reduce the apoptosis of hypoxic ischemic brain damage of nerve cells3.Scutellarin might reduce the apoptosis of nerve cells through inhibition the phosphorylation of p38 MAPK after hypoxia ischemia, thus exerting a protective effect on the brain of neonatal rats with HIBD.