Experimental Study On Effecting Of Panax Notoginseng Saponin On Apoptosis Rate And Brain Derived Neumtrophic Factor In Brain Injury Of Neonatal Rat Model With Asphyxia

Objective To study the protective effect of Panax Notoginseng Saponin in the hypoxic-ischemic brain injury through establishing the classic neonatal rat model with neonatal rat atmospheric Asphyxia model. Through testing the changes of apoptosis rate and the expression of BDNF, we can learn that PNS plays a protective role by increasing BDNF's expression, and reducing brain cell apoptosis rate of neonatal asphyxia brain tissue. And study the effective time window of the treatment of neonatal brain damage, verify the protective effect of Panax Notoginseng Saponin in hypoxic-ischemic brain injury. To Seek a new theoretical foundation for the treatment and diagnosis of hypoxic-ischemic myocar-dial injury in neonatal asphyxia.Methods887-day-old newborn SD rats were randomly divided into the control group, saline-treated group and PNS-treated group. Right after hypoxic-ischemic insult, PNS or normal saline solution were injected intraperitoneally. Normal Saline-treated group or PNS-treated group were also randomly divided into saline or PNS-treated for6hours(group6h),24hours(group24h),48hours(group48h),72hours(group72h),7days(group7d). The newborn rats of PNS-treated group were given l00mg/kg PNS by intraperitoneal injection as soon as the neonatal rat model with neonatal rat atmospheric Asphyxia model were established, the same dose of PNS was repeated by intraperitoneal injection every12hours. The newborn rats of Normal Saline-treated group were given the same volume of normal saline by intraperitoneal injection every12hours At the end of the study, group I of neonatal rats were broken ends and taken the brain together, group II and III were given the same treatment respectively in6hours,24hours,48hours,72hours,7days after asphyxia, and then were fixed, paraffin-embedded and made into paraffin sections. And take the steps of HE staining, TUNEL and immunohistochemical,to detect the brain apoptosis rate and expression of BDNF. At last the data were processed with SPSS17.0statistical method.Results (1) Compared with the group I, the apoptosis rate and the level of BDNF was time-dependently increased in saline-treated group between6hours and48hours, Reach the peak In48hours, The level of BDNF in3days decreased significantly,7days returned to normal; the apoptosis rate of longer duration,7days was higher than that of normal.(2)Contrast with GroupIIIand II, Group III the apoptosis rate of Group III is low, group III1except the group (P>0.05), the level of BDNFof group III was high than group II(P<0.05), Group III cell apoptosis rate and BDNF expression at day7were not returned to normal.(3) Contrast with GroupIIIand I, the apoptosis rate and expression of BDNF were significantly increased (P<0.05), and reached the peak in48hours,7days did not return to normal.Conclusions These findings suggest that(1)PNS can attenuate brain injury induced by brain ischemia.(2)In hypoxic-ischemic brain injury, the levels of BDNF reached peak at48hour, without PNS intervention, BDNF in7days back to normal; but the rate of apoptosis in7days is still higher than the normal control group, PNS treatment of asphyxia caused by hypoxia ischemia injury should be extended to7days later. In conclusion, the results show, l00mg/kg Panax Notoginseng Saponin can increase asphyxia caused by hypoxic-ischemic brain damage in the expression of BDNF, their common action, reduce the rate of neuronal apoptosis, on asphyxia in neonatal rats with hypoxic ischemic brain injury has a protective effect, and drug intervention should at least be maintained until7days after asphyxia, or even more.