Microglia, apoptosis and interleukin-1β expression in the effect of Sophora japonica L. on cerebral infarct induced by ischemia-reperfusion in rats

Microglia, apoptosis and interleukin-1β expression in the effect of Sophora japonica L. on cerebral infarct induced by ischemia-reperfusion in rats
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DOI:
10.1142/s0192415x0500303x
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发表时间:
2005-01-01
影响因子:
5.7
通讯作者:
Hsieh, CL
Hsieh, CL
中科院分区:
医学2区
文献类型:
--
作者:
Lao, CJ;Lin, JG;Hsieh, CL

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槐(SJ)是一种传统的中草药,用于凉血止血和治疗痔疮出血。虽然最近的几项研究发现SJ和银杏叶都含有相同的槲皮素和芦丁成分,但只有银杏叶被广泛用于治疗人类脑血管疾病和痴呆症。本实验观察了参简合剂对大鼠脑梗死的影响。共研究了66只Sprague-Dawley(SD)大鼠。通过阻断双侧颈总动脉和右侧大脑中动脉90分钟建立局灶性脑梗死。再灌注24小时后,评价神经功能状态。然后处死大鼠,用氯化2,3,5-三苯基四唑对脑组织进行染色。以神经功能缺损评分和脑梗死面积比为指标,评价参简治疗脑梗死的疗效。另外,在脑梗死区中测量ED 1和白细胞介素-I β免疫染色阳性细胞以及凋亡细胞的数量。结果表明,SJ 100、200 mg/kg预处理和200 mg/kg后处理均能显著降低大鼠神经功能缺损程度和脑梗死面积比。另外,SJ 200 mg/kg预处理还能显著减少缺血再灌注脑梗死大鼠ED 1和IL-1D免疫染色阳性细胞数,并减少凋亡细胞数。本研究表明,SJ可以减少脑缺血再灌注大鼠的脑梗死面积和神经功能缺损,提示其作为治疗人类脑梗死的潜力。SJ的这种作用涉及其对小胶质细胞、白细胞介素-1 β和凋亡的抑制作用。
Sophora Japonica L. (SJ) is a traditional Chinese herb used to cool blood, stop bleeding and to treat hemorrhoids with bleeding. Although several recent studies found that both SJ and Ginkgo biloba have the same components of quercetin and rutin, only Ginkgo biloba has been widely used to treat cerebrovascular disorders and dementia in humans. This study investigated the effect of SJ on cerebral infarct in rats. A total of 66 Sprague-Dawley (SD) rats were studied. Focal cerebral infarct was established by occluding the bilateral common carotid arteries and the right middle cerebral artery for 90 minutes. After 24 hours of reperfusion, the neurological status was evaluated. The rats were then killed, and brain tissue was stained with 2,3,5-triphenyl-tetrazolium chloride. The grading scale of neurological deficit and the ratio of cerebral infarction area were used as an index to evaluate the effect of SJ on cerebral infarct. In addition, the number of ED1 and interleukin-I beta immunostaining positive cells, and apoptotic cells were measured in the cerebral infarction zone. The results indicated that pre-treatment with 100 or 200 mg/kg SJ and post-treatment with 200 mg/kg SJ significantly reduced the grade of neurological deficit and the ratio of cerebral infarction area. In addition, pre-treatment with 200 mg/kg SJ also significantly reduced ED1 and interleukin-ID immunostaining positive cells, and apoptotic cells in ischemia-reperfusion cerebral infarct rats. This study demonstrated that SJ could reduce the cerebral infarction area and neurological deficit induced by ischemia-reperfusion in rats, suggesting its potential as a treatment for cerebral infarct in humans. This effect of SJ involves its suppressive action of microglia, interleukin-1 beta and apoptosis.