首页|熊果苷调节Gas6/Axl信号通路对缺氧缺血性脑损伤新生大鼠的神经保护作用

熊果苷调节Gas6/Axl信号通路对缺氧缺血性脑损伤新生大鼠的神经保护作用

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目的 研究熊果苷通过调节Gas6/Axl信号通路对缺氧缺血性脑损伤(HIBD)新生大鼠神经保护的作用.方法 采用Rice-Vannucci法构建HIBD新生大鼠模型,并将造模成功的48只新生大鼠随机分为Model组、低剂量熊果苷组(50mg/kg)、高剂量熊果苷组(100mg/kg)、高剂量熊果苷+Anticancer agent 109组(100mg/kg+3.00mg/kgGas6/Axl抑制剂);再选12只新生大鼠作为NC组.平衡木法对各组大鼠进行行为学评估;苏木精-伊红(H-E)染色检测大鼠脑组织病理损伤;TTC染色法检测脑梗死面积;ELISA法检测大鼠血清中白细胞介素6(IL-6)、超氧化物歧化酶(SOD)、丙二醛(MDA)、脑源性神经营养因子(BDNF)的表达;Western blot检测大鼠海马组织中Gas6、磷酸化Axl(p-Axl)、Axl蛋白表达.结果 与Model组比较,低剂量熊果苷组和高剂量熊果苷组大鼠行为学评分降低,脑组织结构较正常,大鼠脑梗死面积减少,血清中IL-6、MDA表达减少,SOD、BDNF表达增加,Gas6、Axl蛋白表达增多,p-Axl蛋白表达减少(P<0.05).高剂量熊果苷+Anticanceragent 109组与高剂量熊果苷组比较,结果相反,HIBD大鼠神经损伤加重(P<0.05).结论 熊果苷可能通过激活Gas6/Axl信号通路对缺氧缺血性脑损伤新生大鼠发挥神经保护作用.
Neuroprotective effect of arbutin on neonatal rats with hypoxic ischemic brain damage by regulating the Gas6/Axl signaling pathway
Objective To investigate the neuroprotective effect of arbutin on neonatal rats with hypoxic ischemic brain damage(HIBD)by regulating the Gas6/Axl signaling pathway.Methods The Rice-Vannucci method was applied to construct a neonatal rat model of HIBD,48 newly born rats that were successfully modeled were randomly separated into a Model group,a low-dose arbutin group(50 mg/kg),a high-dose arbutin group(100 mg/kg),and a high-dose arbu-tin+Anticancer agent 109 group(100 mg/kg+3.00 mg/kg Gas6/Axl inhibitor),another 12 newborn rats were regarded as the NC group.The balance beam method was used to evaluate the behavior of each group of rats.Hematoxylin eosin(H-E)stain-ing was used to detect pathological damage in brain tissue.TTC staining method was used to detect the area of cerebral in-farction.ELISA was used to detect the expression of interleukin-6(IL-6),superoxide dismutase(SOD),malondialdehyde(MDA),and brain derived neurotrophic factor(BDNF)in serum.Western blot was used to detect the expression of Gas6,phosphorylated Axl(p-Axl),and Axl proteins in hippocampal tissue.Results Compared with the Model group,the behavioral scores of rats in the low-dose and high-dose arbutin groups decreased,and the brain tissue structure was more normal,the area of cerebral infarction in rats reduced,the expression of IL-6 and MDA in serum decreased,the expression of SOD and BDNF increased,the expression of Gas6 and Axl proteins increased,the expression of p-Axl protein decreased(P<0.05).The results of the high-dose arbutin+Anticancer agent 109 group were opposite to those of the high-dose arbutin group,and the nerve damage in HIBD rats worsened(P<0.05).Conclusion Arbutin may exert neuroprotective effects on neonatal rats with hypoxic ischemic brain damage by activating the Gas6/Axl signaling pathway.

arbutinGas6/Axl signaling pathwayhypoxic ischemic brain damageneuroprotection

王晓静、敖雪、张宏燕、马兵

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承德市妇幼保健院新生儿科,河北承德 067000

熊果苷 Gas6/Axl信号通路 缺氧缺血性脑损伤 神经保护

承德市科技计划自筹经费项目(2023)

202301A004

2024

中国优生与遗传杂志
中国优生科学协会

中国优生与遗传杂志

CSTPCD
影响因子:0.527
ISSN:1006-9534
年,卷(期):2024.32(2)
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