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丁苯酞对急性脑梗死大鼠神经损伤的保护作用

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目的 探究丁苯酞通过调节Toll样受体4(TLR4)/核转录因子-κB(NF-κB)通路对急性脑梗死(ACI)大鼠神经损伤的保护作用.方法 SD大鼠随机分为假手术组、模型组、低、中、高剂量实验组,除假手术组外均建立ACI体内模型.造模2d后,低、中、高剂量实验组灌胃给予20、40和80 mg·kg-1 丁苯酞,qd,假手术组、模型组灌胃等量0.9%NaCl,均灌胃7d.统计各组大鼠神经功能评分、双侧贴纸去除时间、平衡木过杆评分、脑含水量和脑梗死体积,酶联免疫吸附试验法(ELISA)检测血清和海马组织轴突生长抑制因子A(Nogo-A)、血清炎性因子表达,用蛋白质印迹法检测TLR4/NF-κB通路蛋白表达.结果 假手术组、模型组和低、中、高剂量实验组的神经功能评分分别为0、(3.55±0.52)、(2.55±0.52)、(1.82±0.60)和(0.91±0.30)分,海马组织Nogo-A 表达量分别为(0.93±0.23)、(6.32±0.53)、(5.10±0.55)、(3.54±0.57)和(1.58±0.30)ng·L-1,血清 Nogo-A 表达量分别为(0.49±0.12)、(5.09±0.82)、(3.83±0.54)、(2.23±0.64)和(1.13±0.25)ng·L-1,TLR4 蛋白相对表达水平分别 为 0.44±0.05、1.23±0.14、0.93±0.07、0.75±0.06 和0.55±0.07,p-p65 NF-κB蛋白相对表达水平分别为0.32±0.05、0.82±0.06、0.68±0.08、0.57±0.07 和 0.44±0.05.假手术组的上述指标与模型组比较,在统计学上差异均有统计学意义(均P<0.05);模型组的上述指标与低、中、高剂量实验组比较,在统计学上差异均有统计学意义(均P<0.05).结论 丁苯酞可通过调节TLR4/NF-κB通路改善ACI大鼠神经功能,并减轻炎症损伤,从而发挥神经保护作用.
Protective effects of butylphthalein on nerve injury in rats with acute cerebral infarction
Objective To investigate the protective effect of butyrolphthalein on nerve injury in rats with acute cerebral infarction(ACI)by regulating Toll-like receptor 4(TLR4)/nuclear transcription factor-κB(NF-κB)pathway.Methods SD rats were randomly divided into model group and experimental-L,-M,-H groups;ACI models were established in vivo except sham operation group.The experimental-L,-M,-H groups were given 20,40,80 mg·kg-1 butylphthalide,qd,for 7 days;the sham operation group and the model group were given the same amount of 0.9%NaCl,for 7 days.Neural function score,bilateral sticker removal time,balance beam crossing score,cerebral water content and cerebral infarction volume of rats in each group were measured.The expression of axonal growth inhibitory factor A(Nogo-A)and serum inflammatory factor in hippocampus were detected by enzyme-linked immunosorbent assay(ELISA).The expression of TLR4/NF-κB pathway related proteins was detected by Western blot.Results The neural function scores of sham operation group,model group,and experimental-L,-M,-H groups were 0,3.55±0.52,2.55±0.52,1.82±0.60,0.91±0.30,respectively;the Nogo-A in hippocampus were(0.93±0.23),(6.32±0.53),(5.10±0.55),(3.54±0.57),(1.58±0.30)ng·L-1,respectively;serum Nogo-A were(0.49±0.12),(5.09±0.82),(3.83±0.54),(2.23±0.64),(1.13±0.25)ng·L-1,respectively;TLR4 protein expression were 0.44±0.05,1.23±0.14,0.93±0.07,0.75±0.06,0.55±0.07,respectively;the expressions of p-p65 NF-κB protein were 0.32±0.05,0.82±0.06,0.68±0.08,0.57±0.07,0.44±0.05,respectively.There were statistically significant differences between sham operation group and model group(all P<0.05).There were significant differences in the above indexes between the model group and the experimental-L,-M,-H groups(P<0.05).Conclusion Butylphthalein can play a neuroprotective role in ACI rats by regulating TLR4/NF-κB pathway to improve nerve function and reduce inflammatory damage.

butylphthaleinacute cerebral infarctionnerve injuryToll-like receptor 4/nuclear transcription factor-κB pathwayprotection

周丽、张玲、李伟海、梁鹏、闫贵国、郭百海

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酒泉市人民医院药剂科,甘肃酒泉 735000

酒泉市人民医院神经内科,甘肃酒泉 735000

丁苯酞 急性脑梗死 神经损伤 Toll样受体4/核转录因子-κB通路 保护

2024

中国临床药理学杂志
中国药学会

中国临床药理学杂志

CSTPCD北大核心
影响因子:1.91
ISSN:1001-6821
年,卷(期):2024.40(10)
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