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红花多糖调节Gas6/Axl信号通路对大鼠缺血性脑卒中的影响
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陈彩凤 ,陆韵薇 ,李建宇 (1.解放军总医院第五医学中心中医科,北京 100039;2.深圳市中医院脑病与
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心理病科,广东 深圳 518000)
中图分类号 R965 文献标志码 A 文章编号 1001-0408(2026)08-1015-06
DOI 10.6039/j.issn.1001-0408.2026.08.08
摘 要 目的 探讨红花多糖(SPS)调节生长停滞特异性蛋白6(Gas6)/Axl受体酪氨酸激酶(简称为“Axl”)信号通路对大鼠缺血
性脑卒中(IS)的影响。方法 采用改良线栓法构建大脑中动脉闭塞IS模型大鼠,再随机分为模型(Model)组,SPS低、高剂量(SPS-
L、SPS-H,50、100 mg/kg)组、中西药结合(SPS-H+Nim,SPS 100 mg/kg+ Nim 15 mg/kg)组,每组10只。另取10只大鼠作为假手术
(Sham)组。各组大鼠灌胃相应剂量的药物或等体积生理盐水,连续干预14 d。给药结束后24 h,评估各组大鼠的神经功能;观察
海马组织形态学变化,检测血清中白细胞介素6(IL-6)、IL-1β、肿瘤坏死因子α(TNF-α)含量,脑梗死面积百分比,神经元凋亡率和
海马组织中丙二醛(MDA)、超氧化物歧化酶(SOD)、脑源性神经营养因子(BDNF)含量以及Gas6、磷酸化Axl(p-Axl)、Axl、B细胞
淋巴瘤2(Bcl-2)、Bcl-2相关X蛋白(Bax)的蛋白相对表达量。结果 与Model组比较,SPS-L组、SPS-H组和SPS-H+Nim组大鼠神
经功能显著改善;血清中IL-6、TNF-α、IL-1β含量和脑梗死面积百分比、神经元凋亡率以及海马组织中MDA含量、p-Axl及Bax蛋
白相对表达量均显著降低(P<0.05 或 P<0.01),海马组织中 SOD、BDNF 含量,Gas6、Axl 及 Bcl-2 蛋白相对表达量均显著升高
(P<0.05或P<0.01);海马组织缺血性损伤均有不同程度改善。结论 SPS可能通过激活Gas6/Axl信号通路,降低IS大鼠神经炎
症、氧化应激和神经元凋亡,减轻神经损伤,改善神经功能。
关键词 缺血性脑卒中;红花多糖;Gas6/Axl信号通路;神经炎症;神经元凋亡
Effects of safflower polysaccharide on ischemic stroke in rats by regulating the Gas6/Axl signaling pathway
CHEN Caifeng ,LU Yunwei ,LI Jianyu(1. Dept. of Traditional Chinese Medicine, Fifth Medical Center of the
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General Hospital of the Chinese People’s Liberation Army, Beijing 100039, China;2. Dept. of Neurology and
Psychiatry, Shenzhen Traditional Chinese Medicine Hospital, Guangdong Shenzhen 518000, China)
ABSTRACT OBJECTIVE To investigate the effects of safflower polysaccharide (SPS) on ischemic stroke (IS) in rats by
regulating the growth arrest-specific protein 6 (Gas6)/Axl receptor tyrosine kinase (Axl) signaling pathway. METHODS The
modified suture-occluded method was employed to establish a rat model of middle cerebral artery occlusion (MCAO) for IS. The
rats were then randomly divided into the model (Model) group, SPS low- and high-dose (SPS-L, SPS-H, 50 and 100 mg/kg)
groups, and integrated traditional Chinese and Western medicine (SPS-H+Nim, SPS 100 mg/kg+Nim 15 mg/kg) group, with 10
rats in each group. Another 10 rats were selected as the sham operation (Sham) group. Rats in each group were administered
corresponding doses of medication or an equal volume of normal saline intragastrically, with continuous intervention for 14 days.
The neurological function of rats in each group was evaluated 24 hours after drug administration. The morphological changes in
hippocampal tissue were observed. The contents of interleukin-6 (IL-6), IL-1β, and tumor necrosis factor-α (TNF-α) in serum,
the percentage of cerebral infarction area, the neuronal apoptosis rate, as well as the contents of malondialdehyde (MDA),
superoxide dismutase (SOD), and brain-derived neurotrophic factor (BDNF) in hippocampal tissue, and the relative protein
expression levels of Gas6, phosphorylated Axl (p-Axl), Axl, B-cell lymphoma-2 (Bcl-2), and Bcl-2 associated X protein (Bax)
were measured. RESULTS Compared with Model group, the neurological function of rats in SPS-L group, SPS-H group and SPS-
H+Nim group improved significantly, while serum contents of IL-6, TNF-α, and IL-1β, the percentage of cerebral infarction area,
the apoptotic rate of neurons as well as MDA content and relative protein expression of p-Axl and Bax were decreased significantly
(P<0.05 or P<0.01). The contents of SOD and BDNF, as well as the relative protein expression of Gas6, Axl, and Bcl-2 in
hippocampal tissue, were significantly increased (P<0.05 or P<0.01), and the ischemic injury in hippocampal tissue improved to
varying degrees. CONCLUSIONS SPS can reduce neuroinflammation, oxidative stress, and neuronal apoptosis in IS rats, alleviate
nerve injury, and improve neurological function, which may
Δ 基金项目 北京市自然科学基金-首都医学创新联合基金项目
be achieved by activating the Gas6/Axl signaling pathway.
(No.L2510007);深圳市科技计划项目(No.JCYJ20230807094817035) KEYWORDS
*第一作者 主治医师,硕士。研究方向:中医内科、脑血管疾病。 ischemic stroke; safflower polysaccharide;
E-mail:drcindy79_2025@163.com Gas6/Axl signaling pathway; neuroinflammation; neuronal
# 通信作者 副主任医师,硕士。研究方向:中医内科、针灸镇痛。 apoptosis
E-mail:lijiananjing@sina.com
中国药房 2026年第37卷第8期 China Pharmacy 2026 Vol. 37 No. 8 · 1015 ·

