杏丁、神经生长因子、高压氧对新生大鼠缺氧缺血性脑损伤保护作用的比较研究

目的比较银杏叶提取物杏丁注射液(XGD)、神经生长因子(NGF)、高压氧(HBO)对新生大鼠缺氧缺血性脑损伤(HIBD)的保护作用,并作疗效上的比较。方法夹闭妊娠大鼠子宫血管,制成HIBD新生鼠模型,治疗组给予腹腔注射XGD或NGF或HBO治疗,在生后不同时间比较脑组织含水量、一氧化氮(NO)含量、神经细胞凋亡以及脑部病变情况。结果治疗组的一氧化氮含量明显降低,神经细胞凋亡及脑部病变情况与对照组比较差异显著(P<0.05),脑组织含水量XGD及HBO治疗组明显降低,与对照组比较差异显著(P<0.05),而NGF治疗组脑组织含水量无明显降低。结论XGD、NGF、HBO均对HIBD有保护作用,NGF不能减轻脑水肿。     

妥泰对新生大鼠缺氧缺血性脑损伤保护作用的研究

1　材料和方法　 5 6只 7日龄 Wistar大鼠随机分为对照组(1 4只 )、缺氧缺血 (HI)组 (1 8只 )、妥泰一次给药组 (1 8只 )和多次给药组 (6只 )。结扎右侧颈总动脉、吸入 8% (体积分数 )氧气 2 h制成 HI模型 ,对照组仅分离右侧颈总动脉 ,不结扎、不缺氧。一次给药组于 HI后即刻按体重经胃管注入妥泰 2 0 0 mg/kg,多次给药组首剂 2 0 0 mg/kg,1 2 h后 5 0mg/(kg·d) ,分 2次给药 ,连用 5 d。HI组及对照组注入等量生理盐水。模型制作后 2 4h取右侧前脑组织 ,干湿重法计算脑含水量 [(湿重 -干重 ) /湿重× 1 0 0 % ],原子吸收分光光谱法测脑…     

17β-雌二醇对新生大鼠缺氧缺血性脑损伤的保护作用

目的　研究 17β 雌二醇 (17β E2 )对新生大鼠缺氧缺血脑损伤 (HIBD)后谷氨酸 (Glu)释放的影响 ,探讨 17β E2 是否对HIBD有保护作用。方法　 7日龄Wistar大鼠随机分为三组 ,A、B组为分别在HIBD模型制作前、后腹腔注射 17β E2 (10 0 μg·kg-1) ,C组在HIBD模型制作前腹腔注射等量的生理盐水。注射17β E2 后的不同时间取血检测 17β E2 的浓度。HIBD后 4h处死大鼠 ,用氨基酸分析仪检测脑组织匀浆上清液中Glu的含量。结果　 17β E2 血浓度在注射后 5min达到高峰 ,随后下降。A、B组较C组Clu含量明显下降 (P <0 .0 5 ) ,A、B两组Glu含量没有显著差异 (P >0 .0 5 )。结论　 17β E2 能明显降低HIBD后Glu的释放 ,减轻神经元损伤     

新生大鼠缺氧缺血脑损伤后bcl-x mRNA的表达

目的　探讨新生大鼠脑缺氧缺血后死亡相关基因 bcl- x m RNA表达的变化及其与脑缺氧缺血所致细胞凋亡的关系。方法　通过建立新生大鼠缺氧缺血性脑病动物模型 ,应用快速竞争性 RT- PCR技术对缺氧缺血后不同时间点的缺血侧大脑组织中 bcl- x m RNA的表达进行半定量分析 ,并在相同缺血基础上观察缺氧 1.5小时、2 .5小时和 3.5小时对 bcl- x m RNA表达的影响。结果　缺氧缺血后 ,新生大鼠脑 bcl- xs(bcl-x短型 ) m RNA的表达自缺氧结束后即刻即有明显增强 ,2 4小时达高峰 ,此后逐渐下降 ,7天时回复至正常基线水平。随着缺氧时间的延长即缺氧程度的加重 ,bcl- xs m RNA的表达有增强趋势 ,缺氧 1.5小时组、2 .5小时组及 3.5小时组之间 bcl- xs m RNA表达水平的差异均具显著性意义 (P<0 .0 1)。bcl- xs m RNA的表达高峰与缺氧缺血后脑细胞凋亡的高峰时相相吻合。缺氧缺血对 bcl- xl(bcl- x长型 ) m RNA的表达无影响。结论缺氧缺血可诱导新生大鼠脑 bcl- xs m RNA表达增强。在一定范围内 ,其表达强度与缺氧程度成正相关。 bcl-xs过表达在缺氧缺血后脑细胞凋亡的调控过程中起着一定的作用     

新生大鼠缺氧缺血性脑损伤时Bcl-2和P53蛋白的表达

目的研究Bcl-2的P53蛋白在新生儿缺氧缺血性脑损伤(HIBD)中的表达及与细胞凋亡的关系。方法将新生7日龄Wistar大鼠制成HlBD模型,应用免疫组织化学-SP法及原位缺口末端标记(TUNEL)研究Bcl-2和P53蛋白在新生大鼠及缺氧缺血(HI)后脑中表达及与凋亡的关系。结果新生大鼠HIBD时凋亡与坏死并存,以凋亡为主。Bcl-2免疫蛋白在正常新生大鼠脑内广泛表达(+～++++);Hl后脑病变处Bcl-2免疫强度明显下降(-～+);P53蛋白在正常新生大鼠脑内基本无表达;HI后病变部位散在分布阳性凋亡细胞。结论Hl后Bcl-2免疫表达减弱,P53的免疫表达增强,提示Bcl-2可抑制凋亡,P53可能促进凋亡。     

血红素氧合酶-1/一氧化碳系统在新生大鼠缺氧缺血性脑损伤中的作用

目的 观察新生大鼠缺氧缺血性脑损伤(HIBD)后血红素氧合酶-1/一氧化碳系统(HO-1/CO)变化,探讨其在HIBD中的作用.方法 7日龄Wistar新生大鼠按随机数字表法分为假手术组(Sham组)、缺氧缺血组(HIBD组)及HO抑制剂锌原卟啉组(Znpp组),每组6只.采用实时荧光定量PCR法、硫代巴比妥酸法(TBA法)、流式细胞术(FCM)和双波长定量测定法分别检测脑组织中HO-1 mRNA的表达、丙二醛(MDA)含量、脑组织细胞凋亡率及血中CO浓度.结果 与Sham组比较,HIBD组、Znpp组HO-1 mRNA表达均增强(分别为0.166±0.042、2.289±0.333、1.839±0.322),CO浓度升高[分别为(0.460±0.009)%、(1.026±0.145)%、(0.735±0.079)%],差异有统计学意义(P＜0.05);但与HIBD组比较,Znpp组HO-1 mRNA表达明显减少,CO浓度降低,差异有统计学意义(P＜0.05).与Sham组比较,HIBD组、Znpp组MDA含量及细胞凋亡率均明显升高[MDA含量分别为(1.016±0.210)nmol/mg prot、(1.945±0.312)nmol/mg prot、(3.202±0.693)nmol/mg prot,凋亡率分别为(0.108±0.009)%、(1.412±0.307)%、(2.458±0.565)%],差异有统计学意义(P＜0.05);与HIBD组比较,Znpp组MDA含量及细胞凋亡率明显增高,差异有统计学意义(P＜0.05).结论 缺氧缺血性脑损伤后HO-1/CO系统可能在脑损伤的恢复中起到一定的保护作用.     

尼莫地平对大鼠脑损伤后血脑屏障保护作用的定量研究

<正> 脑损伤后血脑屏障(BBB)通透性增加,脑水肿的发生、发展,加剧脑继发性损害。细胞内钙离子增加,超载是BBB通透性增加的直接原因。伊文兰与血浆蛋白结合的特性,用于定性观察血脑屏障通透性变化。本文采用分光光度计法,检测大鼠脑损伤后皮质、海马伊文氏兰含量,定量评价钙离子拮抗剂尼莫地平对血脑屏障的保护作用。 材料方法:雄性SD大鼠48只,体重250±30g,随机分为正常对照组、假手术组、脑损伤组和治疗组。每组12只。 脑损伤模型采用改良的Feeney’s自由落     

不同途径应用胰岛素样生长因子1对新生大鼠缺氧缺血性脑损伤的影响

目的 研究不同途径应用胰岛素样生长因子1（IGF-1）对新生大鼠缺氧缺血性脑损伤（HIBD）的影响。方法 40只新生大鼠分为4组：HIBD模型对照组（对照组）、静脉注射组、经鼻腔滴入组和假手术组：给药组于缺氧后分别给予尾静脉注射和经鼻腔滴入IGF-1 2．5μg（溶于生理盐水0．1ml中）;对照组于HIBD后给予等量的生理盐水尾静脉注射;假手术组仅分离颈总动脉,不结扎不缺氧。24h后处死取脑组织,免疫组化法观察脑组织caspase-3的表达,组织学方法观察脑组织病理改变情况。结果 与对照组相比,给药各组caspase-3表达减少（均P〈0．01）,神经细胞总数增加（均P〈0．01）,变性／坏死神经细胞数减少（均P〈0．01）,结论 静脉注射和鼻腔滴入IGF-1均可能通过降低HIBD脑组织中caspase-3表达,从而对HIBD脑组织损伤产生保护作用。     

下调lncRNA-MALAT1表达对新生大鼠缺氧缺血性脑损伤的保护作用

目的 探讨小图lncRNA-MALAT1表达对新生大鼠缺氧缺血性脑损伤（HIBD）的影响。方法 取SPF级7 d龄SD大鼠40只,随机分为假手术组、模型组、lncRNA对照组、silncMALAT1组,每组10只。Rice-Vannucci法建立新生大鼠HIBD模型,造模后2 h,侧脑室分别注射生理盐水、生理盐水、空载体重组腺病毒液、silncMALAT1各5μl。造模后7 d,Morris水迷宫试验评估空间学习和记忆能力,TUNEL染色检测海马组织神经元凋亡,PCR和免疫印迹法检测海马组织BDNF/TrkB信号通路mRNA和蛋白表达变化。结果 模型组造模失败2只,lncRNA组失败2只,silncMALAT1组失败1只,造模成功率为83.33%。下调lncRNAMALAT1表达,明显增加新生大鼠学习和记忆能力（P<0.05）,明显减少海马组织神经元凋亡率（P<0.05）,明显下调BDNF/TrkB mRNA和蛋白表达水平（P<0.05）。结论 下调lncRNA-MALAT1表达可减轻新生大鼠HIBD,其机制可能与抑制BDNF/TrkB信号通路、减轻海马组织神经元凋亡...     

白细胞介素1β多克隆抗体对新生大鼠缺氧缺血性脑损伤的作用

目的：研究白细胞介素－（ＩＬ）１β多克隆抗体对新生大鼠缺氧缺血性脑损伤（ＨＩＢＤ）后对损伤大脑的保护效应。方法：制备左脑ＨＩＢＤ的新生大鼠模型,于ＨＩＢＤ前后分别腹腔注射一定浓度的ＩＬ－１β多克隆抗体,观察用药前后损伤大脑脑水含量及组织病理学变化。结果：ＨＩＢＤ前后腹腔注射ＩＬ－１β多克隆抗体可明显降低脑水含量（Ｐ＜０．０１）,但对其相应ｍＲＮＡ转录无影响。组织病理学观察发现用药组大脑水肿明显减轻,神经元死亡明显减少。结论：ＩＬ－１β多克隆抗体可以拮抗ＩＬ－１β的炎性作用,对ＨＩＢＤ大脑有保护效应。     

Resatorvid protects against hypoxic-ischemic brain damage in neonatal rats

Secondary brain damage caused by hyperactivation of autophagy and inflammatory responses in neurons plays an important role in hypoxic-ischemic brain damage(HIBD).Although previous studies have implicated Toll-like receptor 4(TLR4)and nuclear factor kappa-B(NF-κB)in the neuroinflammatory response elicited by brain injury,the role and mechanisms of the TLR4-mediated autophagy signaling pathway in neonatal HIBD are still unclear.We hypothesized that this pathway can regulate brain damage by modulating neuron autophagy and neuroinflammation in neonatal rats with HIBD.Hence,we established a neonatal HIBD rat model using the Rice-Vannucci method,and injected 0.75,1.5,or 3 mg/kg of the TLR4 inhibitor resatorvid(TAK-242)30 minutes after hypoxic ischemia.Our results indicate that administering TAK-242 to neonatal rats after HIBD could significantly reduce the infarct volume and the extent of cerebral edema,alleviate neuronal damage and neurobehavioral impairment,and decrease the expression levels of TLR4,phospho-NF-κB p65,Beclin-1,microtubule-associated protein l light chain 3,tumor necrosis factor-α,and interleukin-1βin the hippocampus.Thus,TAK-242 appears to exert a neuroprotective effect after HIBD by inhibiting activation of autophagy and the release of inflammatory cytokines via inhibition of the TLR4/NF-κB signaling pathway.This study was approved by the Laboratory Animal Ethics Committee of Affiliated Hospital of Yangzhou University,China(approval No.20180114-15)on January 14,2018.     

拉莫三嗪对新生鼠缺氧缺血性脑损伤的神经保护作用

目的研究拉莫三嗪(LTG)对缺氧缺血性脑损伤(HIBD)新生大鼠的神经保护作用,以及不同用药剂量和用药时间对该作用的影响。方法7日龄SD大鼠126只,除假手术组(14只)外均行左侧颈总动脉离断并置入密闭缺氧箱,制备HIBD动物模型。LTG治疗A组(56只)术后3h分别给予LTG5、10、20、40mg/kg,治疗B组(42只)术前1h和术后3、6h给予LTG20mg/kg腹腔注射,缺血缺氧组(14只)无治疗。用酶标法、免疫组化和原位末端标记(TUNEL)法,分别检测HIBD24h后血清神经元特异性烯醇化酶(NSE)浓度、大脑皮层NSE阳性细胞数以及大脑皮层和齿状回TUNEL阳性细胞数。结果与缺氧缺血组比较,10、20、40mg/kg LTG组TUNEL阳性细胞数显著减少;20mg/kg和40mg/kg LTG治疗组血清NSE的浓度显著降低[缺血缺氧组:(103·3±3·3)μg/ml,20mg/kg组:(51·2±2·5)μg/ml,40mg/kg组:(32·4±1·7)μg/ml],皮层NSE阳性细胞数则显著增高,40mg/kg组(78·3±6·5)比20mg/kg组(63·4±6·6)改变更显著。术前1h与术后3、6h给药组的血清NSE的浓度均显著降低,NSE及TUNEL阳性细胞数均显著性增高,术前1h组改变较术后3、6h给药组显著,3h与6h给药组间差异无统计学意义。结论LTG对HIBD新生大鼠可产生神经保护作用,作用疗效与用药时间和剂量有关。     

Estrogen inhibits lipid peroxidation after hypoxic-ischemic brain damage in neonatal rats

Sprague-Dawley neonatal rats within 7 days after birth were used in this study. The left common carotid artery was occluded and rats were housed in an 8% O2 environment for 2 hours to establish a hypoxic-ischemic brain damage model. 17β-estradiol (1 × 10-5 M) was injected into the rat abdominal cavity after the model was successfully established. The left hemisphere was obtained at 12, 24, 48, 72 hours after operation. Results showed that malondialdehyde content in the left brain of neonatal rats gradually increased as modeling time prolonged, while malondialdehyde content of 17β-estrodial-treated rats significantly declined by 24 hours, reached lowest levels at 48 hours, and then peaked at 72 hours after injury. Nicotinamide-adenine dinucleotide phosphate histochemical staining showed the nitric oxide synthase-positive cells and fibers dyed blue/violet and were mainly distributed in the cortex, hippocampus and medial septal nuclei. The number of nitric oxide synthase-positive cells peaked at 48 hours and significantly decreased after 17β-estrodial treatment. Our experimental findings indicate that estrogen plays a protective role following hypoxic-ischemic brain damage by alleviating lipid peroxidation through reducing the expression of nitric oxide synthase and the content of malondialdehyde.     

Omi/HtrA2在缺氧缺血性脑损伤新生大鼠顶叶皮质中的表达变化

目的 观察缺氧缺血性脑损伤(HIBD)新生大鼠顶叶皮质中Omi/HtrA2的表达变化,进而探讨其在HIBD中的可能作用. 方法 将新生7d龄SD大鼠按完全随机数字表法分为假手术组和模型组(制作新生大鼠HIBD模型),并按术后观察时间点不同进一步分为6h、12h、24 h、72 h4个亚组.分别于术前及缺氧后1h对大鼠进行行为学检查;不同时间点处死后观察每只大鼠的脑组织大体形态,并采用免疫组化染色和Western blotting检测病变侧脑组织中Omi/HtrA2蛋白的表达变化. 结果 (1)行为学检查:术前每只大鼠翻身能力、夹尾右旋测定均正常.术后假手术组测定结果同前.模型组大鼠中18只不能翻身,20只出现夹尾右旋,还有14只表现为不能翻身和夹尾右旋同时存在.(2)脑大体形态观察;模型组大鼠结扎侧半球脑组织受损严重,24h时苍白、水肿明显,体积明显大于对侧.假手术组大鼠大脑半球左右对称,未见任何病理变化.(3)Western blotting 结果:模型组Omi/HtrA2蛋白的表达水平在各时间点均较假手术组明显升高,差异均有统计学意义(P＜0.05).Omi/HtrA2在HIBD后6h开始表达,24 h达高峰,随后开始下降.(4)免疫组化染色结果:模型组病变侧大脑皮层Omi/HtrA2阳性细胞数在HIBD后24 h达到高峰,随后降低,与假手术组在各时间点比较差异均有统计学意义(P＜0.05). 结论 新生大鼠HIBD后病变侧大脑皮层Omi/HtrA2的表达水平明显升高,并具有时间差异性,表明其参与了HIBD的病理过程,可能在HIBD诱导的细胞凋亡中发挥重要作用.     

Hyperbaric oxygen treatment promotes neural stem cell proliferation in the subventricular zone of neonatal rats with hypoxic-ischemic brain damage

Hyperbaric oxygen therapy for the treatment of neonatal hypoxic-ischemic brain damage has been used clinically for many years, but its effectiveness remains controversial. In addition, the mechanism of this potential neuroprotective effect remains unclear. This study aimed to investigate the influence of hyperbaric oxygen on the proliferation of neural stem cells in the subventricular zone of neonatal Sprague-Dawley rats (7 days old) subjected to hypoxic-ischemic brain damage. Six hours after modeling, rats were treated with hyperbaric oxygen once daily for 7 days. Immunohistochemistry revealed that the number of 5-bromo-2′-deoxyuridine positive and nestin positive cells in the subventricular zone of neonatal rats increased at day 3 after hypoxic-ischemic brain damage and peaked at day 5. After hyperbaric oxygen treatment, the number of 5-bromo-2′- deoxyuridine positive and nestin positive cells began to increase at day 1, and was significantly higher than that in normal rats and model rats until day 21. Hematoxylin-eosin staining showed that hyperbaric oxygen treatment could attenuate pathological changes to brain tissue in neonatal rats, and reduce the number of degenerating and necrotic nerve cells. Our experimental findings indicate that hyperbaric oxygen treatment enhances the proliferation of neural stem cells in the subventricular zone of neonatal rats with hypoxic-ischemic brain damage, and has therapeutic potential for promoting neurological recovery following brain injury.     

Gastrodin protects neonatal rat brain against hypoxic-ischemic encephalopathy Acute therapeutic drug effects

BACKGROUND:Pharmacological experiments have demonstrated that gastrodin has a protective effect on neonatal rat brain subjected to hypoxia-ischemia; however,the underlying mechanism has not been fully elucidated. OBJECTIVE:The aim of this study was to investigate the acute therapeutic effects of gastrodin by observing prostaglandin B2 and 6-keto-prostaglandin F 1 a in brain issue of neonatal rats that received gastrodin injections immediately after hypoxia-ischemia.DESIGN:Single-factor design.SETTING:Department of Pediatrics,Affiliated Hospital of Yanbian University. MATERIALS:This study was performed in the Laboratory of the Department of Pediatrics,Affiliated Hospital of Yanbian University(key laboratory of provincial Health Department)from April to December 2003.Fifty-five Wistar rats of either gender,aged 7 days,were provided by the Laboratory Animal Center of Affiliated Hospital of Yanbian University.The rats were randomly divided into normal control(n＝10), model(n＝15),gastrodin-treated(n＝15),and Danshen-treated(n＝15)groups.The protocol was performed in accordance with guidelines from the Institute of Health Sciences for the use and care of animals.The following reagents were.used:Gastrodin(Sancai Medicine Group Co.,Ltd.,Zhongshan,Guangdong Province,China;component:gastrodin),Danshen(Conba Stock Company,Jinhua,Zhengjiang Province,China; component:salvia miltiorrhiza),and reagent kits for 125I-prostaglandin B2 and 125I-6-prostaglandin F 1 a (Research and Development Center for Science and Technology,General Hospital of Chinese PLA). METHODS:Rats in the normal control group received no treatment.Rats in the remaining 3 groups were anesthetized,followed by ligation of the left common carotid artery.One hour later,the rats were placed in a closed hypoxic box and allowed to inhale 8% oxygen-air(2.0-3.0 L/min)for 2 hours to develop hypoxic-ischemic encephalopathy.Immediately after lesion,rats in the gastrodin and Danshen-treated groups were intraperitoneally injected with 1 g gastrodin(10 mL/kg)and 15 g Danshen(15 mL/kg),respectively.MAIN OUTCOME EASURES:Forty-eight hours after lesion,the left brain hemisphere was removed and homogenized to test the levels of prostaglandin B2 and 6-keto-prostaglandin F 1 a by radioimmunoassay. RESULTS:Forty successfully lesioned neonatal rats from the model,gastrodin-treated,and Danshen-treated groups,and ten rats from the control group,were included in the final analysis.Levels of prostaglandin B2 and 6-keto-prostaglandin F 1 a in brain tissue of neonatal rats were significantly higher in the model group than in the control group(both P＜0.01).Levels of prostaglandin B2 and 6-keto-prostaglandin F 1 a were significantly lower in the gastrodin-treated and the Danshen-treated groups compared to the model group(all P＜0.01).However,there were no significant differences in levels of prostaglandin B2 and 6-keto-prostaglandin F 1 a between the gastrodin-treated and the Danshen-treated groups(P＞0.05).CONCLUSION:Gastrodin decreased prostaglandin and thromboxan levels in neonatal rat brains subjected to hypoxia-ischemia.     

Neuroprotective effects of sodium orthovanadate after hypoxic-ischemic brain injury in neonatal rats

Sodium orthovanadate (SOV), a competitive inhibitor of protein tyrosine phosphatases, is neuroprotective in adult animals following an ischemic event. The present study evaluated whether SOV might be protective in a rat pup hypoxic-ischemic (HI) model. Seven-day-old rat pups had the right carotid artery permanently ligated followed by 140 min of hypoxia (8% oxygen). SOV 1.15, 2.3, 4.6, 9.2 or 18.4 mg/kg and vehicle were administered by i.p. injection at 5 min after reoxygenation. Brain damage was evaluated by weight loss of the right hemisphere at 22 days after hypoxia and by gross and microscopic morphology. SOV lowered blood glucose at doses of 1.15, 2.3 and 4.6 mg/kg and induced toxic effects at 9.2 mg/kg. The doses of 2.3 and 4.6 mg/kg of SOV significantly reduced brain weight loss (p < 0.05), but treatment with 1.15 or 9.2 mg/kg did not. SOV 4.6 mg/kg also improved the histopathologic score and diminished the HI induced reduction of Akt and ERK-1/2 phosphorylation in the cortex (p < 0.05) and increased the density of BrdU-positive cells in the subventricular zone (p < 0.01). In conclusion, SOV has neuroprotective effects in the neonatal rat HI model partially mediated by activating Akt and ERK-1/2 pathways.     

Gastrodin protects neonatal rat brain against hypoxic-ischemic encephalopathy★ Acute therapeutic drug effects

BACKGROUND： Pharmacological experiments have demonstrated that gastrodin has a protective effect on neonatal rat brain subjected to hypoxia-ischemia; however, the underlying mechanism has not been fully elucidated.
OBJECTIVE： The aim of this study was to investigate the acute therapeutic effects of gastrodin by observing prostaglandin B2 and 6-keto-prostaglandin F 1 a in brain tissue of neonatal rats that received gastrodin injections immediately after hypoxia-ischemia. DESIGN： Single-factor design.
SETTING： Department of Pediatrics, Affiliated Hospital of Yanbian University.
MATERIALS： This study was performed in the Laboratory of the Department of Pediatrics, Affiliated Hospital of Yanbian University （key laboratory of provincial Health Department） from April to December 2003. Fifty-five Wistar rats of either gender, aged 7 days, were provided by the Laboratory Animal Center of Affiliated Hospital of Yanbian University. The rats were randomly divided into normal control （n =10）, model （n = 15）, gastrodin-treated （n = 15）, and Danshen-treated （n = 15） groups. The protocol was performed in accordance with guidelines from the Institute of Health Sciences for the use and care of animals. The following reagents were. used： Gastrodin （Sancai Medicine Group Co., Ltd., Zhongshan, Guangdong Province, China; component： gastrodin）, Danshen （Conba Stock Company, Jinhua, Zhengjiang Province, China; component： salvia miltiorrhiza）, and reagent kits for ^125I-prostaglandin B2 and ^125I-6-prostaglandin F l a （Research and Development Center for Science and Technology, General Hospital of Chinese PLA）.
METHODS： Rats in the normal control group received no treatment. Rats in the remaining 3 groups were anesthetized, followed by ligation of the left common carotid artery. One hour later, the rats were placed in a closed hypoxic box and allowed to inhale 8% oxygen-air （2.0 3.0 L/min） for 2 hours to develop hypoxic-ischemic encephalopathy. Immediately after lesion, rats