Effects of hydroxysafflor yellow A on the experimental traumatic brain injury in rats

被引:33
作者
Bie, Xiao-Dong [2 ]
Han, Jue [3 ]
Dai, Hai-Bin [1 ]
机构
[1] Zhejiang Univ, Dept Pharm, Affiliated Hosp 2, Coll Med, Hangzhou 310009, Zhejiang, Peoples R China
[2] Zhejiang Univ, Dept Tradit Chinese Med, Affiliated Hosp 2, Coll Med, Hangzhou 310009, Zhejiang, Peoples R China
[3] Zhanongkou Community Med Care Ctr, Hangzhou 310004, Zhejiang, Peoples R China
关键词
hydroxysafflor yellow A; traumatic brain injury; ATPase; SOD; t-PA; MMP-9; ISCHEMIA-REPERFUSION INJURY; OXIDATIVE STRESS; MITOCHONDRIAL DAMAGE; MECHANISMS; PROTECTS; HEART;
D O I
10.1080/10286020903510636
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
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.
引用
收藏
页码:239 / 247
页数:9
相关论文
共 25 条
[1]  
Anup R, 1999, INDIAN J BIOCHEM BIO, V36, P266
[2]  
Biros M H, 2001, Curr Opin Crit Care, V7, P444, DOI 10.1097/00075198-200112000-00012
[3]  
Blaustein M. P., 1977, AM J PHYSIOL, V1, P165
[4]   Changes in rat cerebral mitochondrial succinate dehydrogenase activity after brain trauma [J].
Borges, N ;
Cerejo, A ;
Santos, A ;
Sarmento, A ;
Azevedo, I .
INTERNATIONAL JOURNAL OF NEUROSCIENCE, 2004, 114 (02) :217-227
[5]   Management of severe head injury: Institutional variations in care and effect on outcome [J].
Bulger, EM ;
Nathens, AB ;
Rivara, FP ;
Moore, M ;
MacKenzie, EJ ;
Jurkovich, GJ .
CRITICAL CARE MEDICINE, 2002, 30 (08) :1870-1876
[6]   ESTIMATION OF THE EXTENT OF LIPID-PEROXIDATION IN THE ISCHEMIC AND REPERFUSED HEART BY MONITORING LIPID METABOLIC PRODUCTS WITH THE AID OF HIGH-PERFORMANCE LIQUID-CHROMATOGRAPHY [J].
CORDIS, GA ;
MAULIK, N ;
BAGCHI, D ;
ENGELMAN, RM ;
DAS, DK .
JOURNAL OF CHROMATOGRAPHY, 1993, 632 (1-2) :97-103
[7]   EFFECTS OF TOLUENE AND N-HEXANE ON RAT SYNAPTOSOMAL MEMBRANE FLUIDITY AND INTEGRAL ENZYME-ACTIVITIES [J].
ENGELKE, M ;
DIEHL, H ;
TAHTI, H .
PHARMACOLOGY & TOXICOLOGY, 1992, 71 (05) :343-347
[8]   Protective effect of boldine on oxidative mitochondrial damage in streptozotocin-induced diabetic rats [J].
Jang, YY ;
Song, JH ;
Shin, YK ;
Han, ES ;
Lee, CS .
PHARMACOLOGICAL RESEARCH, 2000, 42 (04) :361-371
[9]   Mechanisms of disease: Plasminogen-activator inhibitor type 1 and coronary artery disease. [J].
Kohler, HP ;
Grant, PJ .
NEW ENGLAND JOURNAL OF MEDICINE, 2000, 342 (24) :1792-1801
[10]   Mitochondrial damage induced by conditions of oxidative stress [J].
Kowaltowski, AJ ;
Vercesi, AE .
FREE RADICAL BIOLOGY AND MEDICINE, 1999, 26 (3-4) :463-471