DOC

Ginkgo biloba extract on focal cerebral ischemia in rats_31

By Leroy Stevens,2014-10-30 18:39
10 views 0
Ginkgo biloba extract on focal cerebral ischemia in rats_31

Ginkgo biloba extract on focal cerebral ischemia in rats

     Abstract Objective To observe the Ginkgo biloba extract (GBE) on focal cerebral ischemia in rats, and to explore its mechanism. Methods suture middle cerebral artery occlusion in

    rat focal cerebral ischemia model building to observe the GBE on the symptoms of nerve injury rat model, cerebral infarction area and serum SOD activity, MDA content of impact. Results GBE could significantly improve the neurological symptoms of focal cerebral ischemia in rats, reducing the scope of cerebral infarction and serum MDA, serum SOD activity increased. Conclusion GBE on focal cerebral ischemia has a protective effect, the mechanism may be related to antioxidant effects.

     Key Words Ginkgo biloba extract; rats; focal cerebral ischemia; infarct size; lipid peroxidation

     Effect of Ginkgo biloba Extract on Cerebral Ischemia-

    reperfusion Injury in Rats

     WANG Guang ming

     Guangdong Chemical and Pharmaceutical Professional

    College, Guangzhou 510520, China

     Abstract: ObjectiveTo observe the effect of Ginkgo biloba extract (GBE) on cerebral ischemia injury in rats and explore its mechanism.MethodsRat cerebral ischemia injury model was induced by middle cerebral artery occlusion, the nerve injury

    symptoms were evaluated, the infarction area and the level of SOD and MDA in serum wrer determined.ResultsGBE could improve

    the nerve injury symptoms, reduce the infraction area of brain and the level of MDA, increase the activity of

    SOD.ConclusionGBE has protective effect on cerebral ischemia injury in rats and its mechanism may be associated with antioxidant activity.

     Key words: Ginkgo biloba; Rats; Cerebral ischemia injury; Infarction area; Lipid preoxidation

     Division of Ginkgo biloba Ginkgo biloba Ginkgo biloba Ginkgo biloba leaf plants, sexual bitter, astringent, flat, the main function of promoting blood circulation Huayu, Tung network rolling. At present, the extract (Ginkgo biloba extract, GBE) is widely used to treat cardiovascular and

    cerebrovascular disease and its sequela. Studies have shown that, GBE's main active ingredients of flavonoid glycosides and terpene lactones [1]. In this study, suture middle cerebral artery occlusion in rat focal cerebral ischemia model

    building to observe the GBE on focal cerebral ischemia in rats and to explore its mechanism, in order to provide clinical cerebrovascular disease prevention and treatment reference.

     1 Materials

     1.1 Animals Male SD rats weighing (200 ? 20) g, by the

    Guangdong Medical Science Institute. Adaptive feeding 1 week before the experiment.

     1.2 Drugs and reagents of Ginkgo biloba extract (trade name: Tian Bao Ning films), Zhejiang CONBA Group Pharmaceutical Co., Ltd., Spec 40 mg (which contains Ginkgo

    flavone glycosides 9.8 mg), lot number 030,124. Nimodipine, Tianjin Central Pharmaceutical Co., Ltd. production, batch number 031.22 thousand. 2,3,5 - triphenyl tetrazolium chloride

    (TTC), AR, Shanghai Pharmaceutical Group, Shanghai Chemical

    Reagent Company. SOD, MDA kit, Nanjing Jiancheng Bio-

    engineering Institute, lot number, respectively 20040128,20040120.

     1.3 Instruments Electronic Analytical Balance, Shanghai Jing Section analytical instrument factory. LXJ-IIB low-speed

    large-capacity centrifuge, Shanghai Anting Scientific Instrument Factory. 754 UV-Vis spectrophotometer, Shanghai

    Analysis Instrument Factory.

     2 Methods

     2.1 Animal grouping and drug delivery to take 60 rats were randomly divided into six groups, namely, GBE high,

    medium and low-dose group (dose of 48,24,12 mg / kg),

    nimodipine group (dose of 2 mg / kg), model control group and sham operation group, n = 10. Modeling in each group, respectively, before the administration, a time / d, were administered four times, delivery volume were 10 ml / kg. Model control group and sham-operated group to the same volume

    of saline.

     2.2 The modeling approach after the last administration 1 h, the light of literature method [2,3], with 10% chloral hydrate (350 mg / kg) intraperitoneal injection of

    anesthetized rats, supine fixed, regular disinfection of the skin, the middle neck incision , blunt separation of the right common carotid artery, external carotid artery and internal carotid artery. Downward along the internal carotid artery

    pterygopalatine artery was isolated, and coagulation. Artery clip with carotid artery occlusion in internal carotid artery near the carotid artery down the wing artery was isolated, and coagulation. Artery clip with carotid artery occlusion in

    internal carotid artery near bifurcation of common carotid artery cut all the ports, will be a fishing line (diameter 0.30 mm) along the internal carotid artery to the brain slowly into the mouth of the resistance was somewhat stop, insert a length of about (18.0 ? 0.5) mm, ligation of a fixed fishing line. Ligation of internal carotid artery proximal end of the clip removed artery to restore blood flow in the external carotid artery. Sham-operated group except non-inserted

    fishing line the middle cerebral artery occlusion, the other operations with the surgical group.

     2.3 OUTCOME MEASURES

     2.3.1 neurological symptom score reference to literature method [4,5], according to extent of the damage developing neurological symptoms rating scale. No symptoms of nerve

    injury grade ?; not fully extend the left forepaw of ?

    level; not fully extend the left forepaw, turning in circles to the left of ? level; not fully extend the left forepaw, to the left of the dumping of grade ? ; not spontaneously walk,

loss of consciousness for the grade ?. According to the above

    criteria, in modeling after 24 h, single-blind method on rats

    in each group to conduct neurological symptom score.

     2.3.2 of serum SOD activity and MDA content determination after model 24 h, chloral hydrate anesthetized rats, abdominal aortic blood, centrifugal separation of serum, according to kit methods of operation, colorimetric determination of serum SOD activity and MDA content.

     2.3.3 Determination of the scope of decapitated cerebral

    infarction, remove odor, cerebellum, saline wash, filter paper exhaust moisture, the brain along the coronal plane slice thickness of 5 mm slices, and placing 1% TTC phosphate buffer solution at 37 ? in dark incubation temperature 10 min, wash Staining, and then 10% neutral formaldehyde solution, fixed 24

    h, remove the dye, said the total weight, and infarct area were cut weighed to calculate infarct size. Infarct size = infarct weight × 100% / total Someshige.

     2.4 Statistical analysis using ? s, said more than a few

    between the two groups were compared using single factor analysis of variance, data statistics using SPSS13.0FOR Windows software processing. Statistical tests used Ridit level. Reposted elsewhere in the paper for free download http://

     3 Results

     3.1 the impact of symptoms of nerve injury from the Table 1 we can see that after administration 24 h, GBE high-dose

    symptoms of nerve injury in rats significantly improved compared with the model control group, there was significant difference (P <0.05).

     Table 1 on the impact of symptoms of nerve injury (abbreviated)

     3.2 the impact of infarct size from Table 2 we can see, GBE high and middle dose rats significantly reduced cerebral weight, compared with the model control group, significant differences. GBE range of high-dose rats with cerebral

    infarction is also significantly reduced compared with the model control group, significant differences. GBE, the low-

    dose range in rats with cerebral infarction there was a downward trend, but with the model control group showed no

    significant difference (P> 0.05). Table 2 Infarct weight and infarct size of the results (omitted)

     3.3 Serum SOD activity and MDA content in 3 we can see from the table, GBE high dose of serum SOD activity was significantly increased, and the model group were

    significantly different (P <0.05). GBE high and middle dose of serum MDA levels decreased significantly, compared with the model control group, there was significant difference (P <0.05). Table 3 on Serum SOD Activity and MDA Content

    (abbreviated)

     4 Discussion

     Ischemic cerebrovascular disease with its high incidence, high morbidity and high mortality rates and serious threat to people's health. Cerebral ischemia can cause serious delayed neuronal damage, which affects the prognosis and functional

    recovery. Most seen in clinical cerebral ischemia middle cerebral artery and its blood supply region of brain tissue due to ischemia and hypoxia, the depletion of energy metabolism caused by avascular necrosis, the corresponding

    control zone in the motor, sensory and language barriers, learning and memory impaired. Middle cerebral artery model of cerebral ischemia in the intraluminal suture method is simple, without craniotomy, preparation area is relatively constant, differences in the scope of small cerebral infarction has been widely used to study the cerebral protective effect of drugs [6]. Therefore, the present study, middle cerebral artery thread occlusion model of GBE observed protective effect against cerebral ischemia.

     Normal vivo free radical generation and removal of biological homeostasis, cerebral ischemia, a large number of free radicals, so that the enhanced role of the brain lipid peroxidation, leading to barrier cells and cell damage, neuronal necrosis or apoptosis, causes or exacerbates ischemic brain edema. For the antioxidant enzymes SOD, is the main body of the free radical scavenger, superoxide radicals can catalyze disproportionation reaction to produce hydrogen and oxygen peroxide, and superoxide free radicals produced by

    other free radical production and proliferation of key steps,

    SOD activity can indirectly reflect the body's free radical scavenging ability. MDA is a lipid peroxidation end product, reflecting the organization of free radicals and cell content

    of the extent of injury [7]. Therefore, the determination of the activity or concentration of these substances change could reflect the effects of drugs against cerebral ischemic injury strength.

     Experimental results show that, GBE could significantly

    improve the neurological symptoms of focal cerebral ischemia in rats to reduce brain infarct size and serum MDA, serum SOD activity to enhance and improve the ischemic brain tissue pathological changes of the focal cerebral ischemic injury has

    a protective effect.

     References

     [1] Kressmann S, Muller WE, Blume HH, et

    al.Pharmaceutical quality of different Ginkgo biloba brands [J]. Pharm pharmacol, 2002,54 (5): 661.

     [2] Longa EZ, Weinstein PR, Carison S, et al.Reversible

    middle cer ebral artery occlusion without craniectomy in rats [J]. Stroke, 1989,20 (1): 84.

     [3] TSUI Shuk Wan, BIAN Ru-Lian, CHEN Xiu.

    Pharmacological experiments methodology, 3rd edition [M]. Beijing: People's Health Publishing House, 2002:1066.

     [4] Lundy EF, Solik BS, Frank RS, et al.Morphometric evalu tion of brain infarcts in rats and gerbils [J]. Pharmacol methods, 1986,16 (3): 201.

     [5] Bederson JB, Pitts LH, Germano SM, et al.Evaluation

    of 2,3,5 triphenyltetrazolium chloride as a stain for detection and quantification of experimental cerebral infarction in rats [J]. Stoke, 1986,17:1304.

     [6] Luo Yong, Dong-wei. Wistar rats were plug-line method

    of focal cerebral ischemia / reperfusion model in experimental

    study [J]. Chongqing Medical University, 2002,27 (1): 1.

     [7] Yu Zhi Ling, Zhang GQ, Zhao red flag. Pueraria lobata flavone protective effect against cerebral ischemia [J]. China Pharmaceutical University, 1997,28 (1): 310. Reposted

    elsewhere in the paper for free download http: / /

Report this document

For any questions or suggestions please email
cust-service@docsford.com