1.北京中医药大学东直门医院 北京 100700
2.北京中医药大学东方医院
李中康,男,在读博士生
# 杨惠民,男,硕士,教授、主任医师,博士生导师,E-mail:yanghuimin012005@163.com
纸质出版日期:2021-07-30,
收稿日期:2021-01-09,
移动端阅览
李中康, 杨惠民, 刘重琪, 等. 调脂通脉解毒方对脑梗死大鼠Toll样受体4、核因子κB p65影响的实验研究[J]. 现代中医临床, 2021,28(4):46-51.
Zhongkang Li, Huimin Yang, Zhongqi Liu, et al. Effect of Tiaozhi Tongmai Jiedu Formula on Toll-like receptor 4 and nuclear factor κB p65 in rats with cerebral infarction[J]. Modern Chinese Clinical Medicine, 2021,28(4):46-51.
李中康, 杨惠民, 刘重琪, 等. 调脂通脉解毒方对脑梗死大鼠Toll样受体4、核因子κB p65影响的实验研究[J]. 现代中医临床, 2021,28(4):46-51. DOI: 10.3969/j.issn.2095-6606.2021.04.010.
Zhongkang Li, Huimin Yang, Zhongqi Liu, et al. Effect of Tiaozhi Tongmai Jiedu Formula on Toll-like receptor 4 and nuclear factor κB p65 in rats with cerebral infarction[J]. Modern Chinese Clinical Medicine, 2021,28(4):46-51. DOI: 10.3969/j.issn.2095-6606.2021.04.010.
目的
2
观察调脂通脉解毒方对脑梗死损伤大鼠神经功能缺损、脑梗死体积、Toll样受体4(TLR4)、核因子κB p65(NF-κB p65)表达水平的影响,探讨其治疗脑梗死的可能机制。
方法
2
将60只SPF级雄性大鼠随机分为假手术组、模型组、调脂通脉解毒方低剂量组(简称低剂量组)、调脂通脉解毒方中剂量组(简称中剂量组)、调脂通脉解毒方高剂量组(简称高剂量组),每组12只。除假手术组外,其余各组均用线栓法致大鼠左侧大脑中动脉闭塞(MCAO)建立脑梗死损伤模型。给药组分别给予相应剂量的调脂通脉解毒方灌胃,假手术组和模型组给予生理盐水灌胃。分别记录各组大鼠的神经功能缺损状况。灌胃2周后测定脑梗死体积百分比,并取缺血侧大脑皮层组织,检测TLR4和NF-κB p65蛋白的表达情况。
结果
2
各组大鼠神经功能缺损评分比较,与模型组比较,调脂通脉解毒方低剂量组、中剂量组、高剂量组均降低(
P
<
0.05),与低剂量组比较,中剂量组和高剂量组均降低(
P
<
0.05),与中剂量组比较,高剂量组降低(
P
<
0.05)。各组大鼠脑梗死体积百分比比较,与模型组比较,低剂量组、中剂量组和高剂量组均减少(
P
<
0.05)。与低剂量组、中剂量组比较,高剂量组均减少(
P
<
0.05)。各组大鼠TLR4,NF-κB p65蛋白表达水平比较,与假手术组比较,模型组、低剂量组、中剂量组TLR4蛋白表达水平均升高(
P
<
0.05),高剂量组与假手术组比较,TLR4蛋白表达水平差异无统计学意义(
P
>
0.05)。与假手术组比较,模型组、低剂量组、中剂量组、高剂量组NF-κB p65蛋白表达水平均升高(
P
<
0.05)。与模型组比较,低剂量组、中剂量组、高剂量组TLR4和NF-κB p65蛋白表达水平均降低(
P
<
0.05)。与低剂量组比较,高剂量组TLR4蛋白水平降低(
P
<
0.05),中剂量组、高剂量组NF-κB p65蛋白水平均降低(
P
<
0.05)。与中剂量组比较,高剂量组TLR4和NF-κB p65蛋白水平均降低(
P
<
0.05)。
结论
2
调脂通脉解毒方可以改善脑梗死后神经功能缺损情况,并可以减少脑梗死体积,降低脑梗死大鼠脑组织中的TLR4和NF-κB p65蛋白的表达,减轻炎症性损伤,提示其可能通过抑制NF-κB通路炎症因子表达对脑梗死后神经功能损伤发挥保护作用。
Objective
2
To observe the effects of Tiaozhi Tongmai Jiedu Formula on the neurological deficit
the infarction volume and the expression levels of Toll-like receptor 4(TLR4) and nuclear factor κB p65(NF-κB p65)in rats with cerebral infarction
and to explore the possible mechanism underlying it.
Methods
2
Sixty male SPF rats were randomly assigned to the sham operation group
model group
low-
medium- and high-dose Tiaozhi Tongmai Jiedu Formula groups(
n
=12 in each group). Except the sham operation group
left middle cerebral artery occlusion (MCAO)was used to establish the model of cerebral infarction in all the other groups. The administration groups were given Tiaozhi Tongmai Jiedu Formula with corresponding doses by intragastric gavage. The sham operation group and model group were gavaged with normal saline. The neurological deficits of rats in each group were recorded. The cerebral infarction volume was measured 2 weeks after intragastric gavage and the expression levels of TLR4 and NF-κB p65 in cortical tissue of the ischemic side were determined.
Results
2
As compared with the model group
the neurological deficit scores were all decreased in the low-
medium- and high-dose Tiaozhi Tongmai Jiedu Formula groups (
P
<
0.05). As compared with the low-dose group
neurological deficit scores were all decreased in the medium- and high-dose groups (
P
<
0.05). The neurological deficit scores were lower in the high- dose group than in the medium-dose group(
P
<
0.05). As compared with the model group
the percentage of cerebral infarction volume in the low-
medium- and high-dose groups were all decreased(
P
<
0.05). As compared with low- and medium-dose groups
the percentage of cerebral infarction volume was decreased in the high-dose group(
P
<
0.05). As compared with the sham operation group
the expression levels of TLR4 and NF-κB p65 were all increased in the model
low- and medium-dose groups (
P
<
0.05). There was no significant difference in TLR4 expression level between the high-dose group and the sham operation group(
P
<
0.05). As compared with the sham operation group
the expression levels of NF-κB p65 in the model group
low-
medium- and high-dose groups were increased(
P
<
0.05). As compared with the model group
the expression levels of TLR4 and NF-κB p65 in the low-
medium- and high-dose groups were decreased(
P
<
0.05). As compared with low-dose group
TLR4 expression level was decreased in the high-dose group(
P
<
0.05) and the expression levels of NF-κB p65 were decreased in the medium- and high- dose groups(
P
<
0.05). As compared with medium-dose group
the expression levels of TLR4 and NF-κB p65 were decreased in the high-dose group(
P
<
0.05).
Conclusions
2
Tiaozhi Tongmai Jiedu Formula can improve the neurological deficit after cerebral infarction
reduce the volume of cerebral infarction and reduce the expression levels of TLR4 and NF-κB p65 in brain tissues of cerebral infarction in rats and alleviate inflammatory injury
which suggests that it may play a protective role in the neurological injury after cerebral infarction by inhibiting inflammatory factors in NF-κB pathways.
调脂通脉解毒方脑梗死神经功能缺损脑梗死体积Toll样受体4核因子κB p65大鼠
Tiaozhi Tongmai Jiedu Formulacerebral infarctionneurological deficitcerebral infarction volumeToll-like receptor 4(TLR4)nuclear factor κB p65(NF-κB p65)rats
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