目的：神经元凋亡是缺氧缺血性脑损伤(HIBD)过程中重要的病理改变,有研究证明地塞米松预处理对新生大鼠缺氧缺血性脑损伤起有效的保护作用,而中药黄芩苷的部分药理作用与地塞米松类似。该文旨在探讨黄芩苷对新生大鼠HIBD神经凋亡的影响。方法：健康6日龄SD新生大鼠被随机分为空白对照组、HIBD组、黄芩苷后处理组、黄芩苷预处理组、地塞米松后处理组、地塞米松预处理组。在6日龄行预处理,7日龄制作新生大鼠HIBD模型,10日龄时处死,取脑组织标本。用干湿法检测各组脑组织含水量,用TUNEL法测定细胞凋亡数,观察脑组织形态学改变。结果：HIBD组动物脑组织含水量,细胞凋亡数较空白对照组均明显升高。黄芩苷、地塞米松预处理组脑组织含水量分别为(87.4±0.7)%,(87.3±0.5)%,较HIBD组(88.9±1.7)%下降,且具有统计学意义(P<0.05),细胞凋亡数分别为102±47;75±26,较HIBD组的251±28显著减少(P<0.05),而黄芩苷、地塞米松后处理组以上指标未见明显改善(P>0.05)。空白对照组脑组织结构正常,HIBD组可见明显的神经元丢失变性,而黄芩苷、地塞米松预处理组神经元损伤明显减轻,黄芩苷、地塞米松后处理组神经元损伤未见减轻。结论：黄芩苷及地塞米松预处理对新生大鼠HIBD产生保护作用,能减少神经元凋亡,而后处理无效。

OBJECTIVE: Previous research suggests that dexamethasone (Dex) pretreatment protects neonatal rats against hypoxic-ischemic brain damage (HIBD). Some of the pharmacological effects of baicalin (a traditional Chinese medicine extracted from Scutellaria baicalensis Georgi) are similar to Dex. This study was designed to explore the effect of baicalin on the neuronal apoptosis following HIBD in neonatal rats. METHODS: Six-day-old Sprague-Dawley rats were randomly assigned into Control (without HI), HIBD, Dex-pretreatment and post-treatment, Baicalin-pretreatment and-post-treatment groups. HIBD was induced by ligating the left common carotid artery, followed by exposure to hypoxia. In the pretreatment groups either baicalin (16 mg/kg) or Dex (0.1 mg/kg) was administered to the rats 24 hrs before HIBD; in the post-treatment groups baicalin or Dex was given 30 minutes after HIBD. The rat pups were sacrificed on postnatal day 10, and brain tissues were harvested. Brain water content was determined, morphological changes were observed under a light microscope, and neuronal apoptosis was measured by terminal deoxynucleotidyl transferase mediated dUTP biotin nick end labeling (TUNEL) staining. RESULTS: The brain water content and the number of apoptotic cells were significantly higher in the HIBD group than those of the Control group (P<0.05). Both baicalin and Dex pretreatment decreased the brain water content from 88.9±1.7 % (HIBD group) to 87.4±0.7% (baicalin) or 87.3±0.6% (Dex) (P<0.05) and the number of apoptotic cells were reduced from 251 ± 28 (HIBD group) to 102 ± 47 (baicalin) or 75 ± 26 (Dex) (P<0.05). Baicalin and Dex post-treatment had no effects on the brain water content and the number of apoptotic cells. Loss and degeneration of neurons could be observed in the HIBD group. Baicalin and Dex pretreatment significantly alleviated neuronal injury, but post-treatment did not. CONCLUSIONS: Pretreatment with baicalin, as with Dex, has a protective effect against HIBD in neonatal rats, but baicalin or Dex post-treatment do not reverse the neuronal injuries.