Effects of hydroxysafflor yellow A on the experimental traumatic brain injury in rats
Effects of hydroxysafflor yellow A on the experimental traumatic brain injury in rats
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DOI：
10.1080/10286020903510636
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发表时间：
2010-01-01
影响因子：
1.7
通讯作者：
Dai, Hai-Bin
中科院分区：
文献类型：
--
作者：
Bie, Xiao-Dong;Han, Jue;Dai, Hai-Bin
探讨羟基红花黄色素A(HSYA)对创伤性脑损伤的治疗作用。将大鼠分为4组：对照组、脑创伤组、脑损伤+HSYA组、脑损伤+尼莫地平组。静脉注射生理盐水、HSYA或尼莫地平。分别于伤前30min和伤后6h注射。观察脑挫伤体积、线粒体ATPase活性、脑组织丙二醛(MDA)含量及血浆组织纤溶酶原激活物(t-PA)和纤溶酶原激活物抑制物-1(PAI-1)含量。结果表明，HSYA在4 mg/kg剂量下对小鼠的抑制率为59.2%。颅脑损伤48h后，Na+，K+-ATPase、Ca2+-ATPase和Mg2+-ATPase活性分别下降至对照组的31%、35%和38%。HSYA使这些ATPase活性分别增加162、96和131%。HSYA还能提高脑挫伤大鼠右侧顶叶挫伤灶附近的超氧化物歧化酶活性，降低丙二醛含量。伤后12h，HSYA组大鼠海马区t-PA活性升高64.64%，PAI-1活性降低71.88%，MMP9表达降低49.11%。综上所述，HSYA可能为改善颅脑损伤后的预后提供了一种潜在的治疗策略。
This paper explores the effects of hydroxysafflor yellow A (HSYA) on traumatic brain injury (TBI). Rats were divided into four groups: control, TBI, TBI combined with HSYA, and TBI combined with nimodipine. Saline, HSYA, or nimodipine was i.v. injected at 30min before and 6h after the onset of TBI. The contusion volume of brain, mitochondrial ATPase activity, brain malondialdehyde (MDA) content, and the concentrations of tissue plasminogen activator (t-PA) and plasminogen activator inhibitor-1 (PAI-1) in the blood plasma were investigated. The results showed that the inhibitory rate of HSYA at a dose of 4mg/kg was 59.2% compared with the TBI group. After the insult by TBI for 48h, the activity of Na+, K+-ATPase, Ca2+-ATPase, and Mg2+-ATPase decreased to 31, 35, and 38% of control group. HSYA increased these ATPase activities by 162, 96, and 131% of TBI group. HSYA also increased superoxide dismutase activity and decreased MDA content in the right parietal lobe adjacent to contusion foci in TBI rats. HSYA enhanced the t-PA activity by 64.64%, decreased the PAI-1 activity by 71.88%, and decreased the MMP-9 expression to 49.11% in the hippocampus of the TBI group at 12h. In conclusion, HSYA may exert a potential therapeutic strategy to improve the outcome following TBI injury.