ABSTRACT
Objective To investigate the effect of propofol on the learning and memory function in neonatal rats under hypoxic conditions. Methods Eighty-four 7-day-old SD rats were randomly divided into 6 groups (n = 14 each): propofol + 18% oxygen (propofol-hypoxia, group PH), propofol + air (group PA), propofol +100% oxygen (propofol-oxygen, group PO), 0.9% normal saline (NS) + 18% oxygen (group CH), NS + air (group CA), NS + 100% oxygen (group CO). The rats received injection of intraperitoneal propofol 50 mg/kg or NS 5.0 ml/kg once a day for 7 consecutive days and they were exposed to 18% oxygen, air or 100% oxygen at the end of each injection. SaO2 and respiratory rate (RR) were monitored and recorded after administration. The rats were returned to the cage after recovery of the righting reflex. Six rats in each group were sacrificed 24 h after the 7th injection, and the brain tissues were taken to observe the apoptosis in hippocampal neurons. Morris water maze test was used to test the learning and memory function 2 weeks after administration in the other rats. Results RR was significantly lower and the escape latency at T1.2 longer in group PO than in group CO (P ＜ 0.05). RR and SaO2 were significantly decreased, apoptotic index was increased, the escape latency was prolonged and the frequency of crossing the original platform was reduced in group PA compared with group CA, and in group PH compared with group CH (P ＜ 0.05). Compared with group PO, SaO2 was significantly decreased, apoptotic index was increased, the escape latency was prolonged and the frequency of crosing the original platform was reduced in group PA (P ＜ 0.05). Conclusion Propofol induces apoptosis in hippocampal neurons and decreases the learning and memory function in neonatal rats under hypoxic conditions.
ABSTRACT
Objective To investigate the effects of penehyclidine hydrochloride (PHCD) pretreatment on expression of NF-κB and iNOS in rats with LPS-induced brain injury. Methods One hundred and five male SD rats weighing 200-220 g were randomly divided into 5 groups (n=21 each): group Ⅰ normal saline (NS);group Ⅱ LPS (L);group Ⅲ,Ⅳ,Ⅴ PHCD 0.05, 0.15, 0.45 mg/kg (D1,2,3). The animals were anesthetized with chloral hydrate 350 mg/kg. Brain injury was induced by intra-arterial LPS 150 μg administered via left internal carotid artery in group Ⅱ-Ⅴ. In group Ⅲ,Ⅳ, and Ⅴ PHCD 0.05, 0.15 and 0.45 mg/kg were given intraperitoneally (IP) at 10 min before intra-arterial LPS. The animals were decapitated at 4, 6 and 12 h after administration of PHCD (n=7 at each time point in each group). The brains were immediately removed for determination of water content, expression of NF-κB and iNOS protein and examination with light and electron microscope. Results Water content of the brain and expression of NF-κB and iNOS protein were significantly higher in group L, D1, D2 and D3 than in group NS and were significantly lower in group D2 and D3 than in group L. Intra-arterial LPS produced severe damage to the brain which was significantly attenuated by PHCD in group D2 and D3. Conclusion PHCD 0.15,0.45 mg/kg pretreatment can attenuate LPS-induced brain injury by inhibiting the up-regulation of expression of NF-κB and iNOS.
ABSTRACT
Objective:To investigate the effects of Penehyclidinehydrochloride(PHCD) on endotoxin-induced cerebral edema.Methods:one handred and five S-D male rats(200～220g)were randomly divided into 5 groups(n=21):groupC control;groupL LPS;group DL,DM and DH received intraperitoneal PHCD 0.05,0.15 or 0.45mg/kg 10min before lipopolysaccharide(LPS) administration.Cerebral edema was induced by internal carotid arterial LPS 150?g.Seven animals each group were decapitated at 4、6 and 12h after operation and their brains were immediately removed for determination of water content of brain and microscopic examination.Results:Administration of LPS caused severe brain damage and significantly increased water content of the brain.The LPS-induced changes were mitigated by pretreatment with different doses of PHCD in groupDM and DH,but there was no significant difference between the two groups.Conclusion:Pretreatment with PHCD can attenuate LPS-induced cerebral edema.