| 曾双,黄永,王开龙.Maresin 1抑制缺血再灌注大鼠脑细胞凋亡及炎症反应[J].安徽医药,2026,30(8):1545-1549. |
| Maresin 1抑制缺血再灌注大鼠脑细胞凋亡及炎症反应 |
| Maresin 1 inhibits ischemia-reperfusion-induced apoptosis and inflammatory responses in rat brain cells |
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| DOI：10.3969/j.issn.1009-6469.2026.08.012 |
| 中文关键词: 巨噬素 1 细胞铁死亡 缺血再灌注 谷胱甘肽过氧化物酶 4 溶质载体家族 7成员 11 |
| 英文关键词: Maresin 1 Ferroptosis Ischemia-reperfusion Glutathione Peroxidase 4 Solute carrier family 7 member 11 |
| 基金项目:国家自然科学基金项目( 82260961、82060902)；广西重点研发计划项目(桂科 AB18126085) |
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| 中文摘要: |
| 目的研究巨噬素 1(Maresin 1)在缺血再灌注脑组织中的作用及机制。方法 2023年 5—12月将 18只雄性 SD大鼠以随机数字表法分为假手术组、缺血再灌注组及缺血再灌注加 Maresin 1干预组(I/R+MaR1组)(每组各 6只)通过构建心肌缺血再灌注模型并予以相应处理，以评估 Maresin 1的心脏保护作用。以大脑中动脉闭塞模型造模缺血再灌注大，鼠作为实验对象并进行 0.9%氯化钠溶液或 Maresin 1注射给药，通过运用改良神经功能缺损评分( mNSS)来评估大鼠的运动功能，脱氧核糖核苷酸末端转移酶介导的缺口末端标记法( TUNEL)检测细胞凋亡情况，实时荧光定量 PCR(q-PCR)检测炎症因子白细胞介素(IL)-1β、肿瘤坏死因子 α(TNF-α)和 IL-6的表达，蛋白质印迹法检测铁死亡通路蛋白谷胱甘肽过氧化物酶 4(GPX4)和溶质载体家族 7成员 11(SLC7A11)的表达水平。结果与假手术组 mNSS相比［(3.67±2.80)分比(14.33±1.37)分］缺血再灌注组大鼠神经功能缺损严重( P<0.001)脑梗死面积增大至( 24.21±4.27)%，神经元凋亡增加至( 12.06±3.96)个 /视野。，而经 Maresin 1干预后， I/R+MaR1组上述损伤均显，著改善: mNSS降至( 9.67±1.03)分，脑梗死面积缩小为( 13.44±2.83)%，神经元凋亡减少至(4.03±1.81)个 /视野(与缺血再灌注组比较，均 P<0.001)。此外，与缺血再灌注组相比， I/R+MaR1组的炎症因子 IL-1β、TNF-α和 IL-6的含量下降(均 P<0.05)，铁死亡通路相关蛋白 GPX4和 SLC7A11的表达量显著升高(均 P<0.05)。结论 Maresin 1能够减轻缺血再灌注大鼠脑组织损伤，减轻凋亡及炎症反应，并且有可能通过调控铁死亡通路实现。 |
| 英文摘要: |
| Objective To investigate the role and mechanism of Maresin 1 in ischemia-reperfusion brain tissue. Methods From May to December 2023, 18 male SD rats were randomly divided into sham group, ischemia-reperfusion group, and ischemia-reperfusionplus Maresin 1 intervention group (I/R+MaR1 group) (6 rats in each group) using a random number table method. A myocardial isch-emia-reperfusion model was constructed and treated accordingly to evaluate the cardioprotective effect of Maresin 1. Using a model ofmiddle cerebral artery occlusion, we examined ischemia-reperfusion rats as subjects and administered 0.9% Sodium chloride solutionor Maresin 1 injections. We assessed motor function using the modified neurological severity score (mNSS). We measured apoptosis us-ing terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL). We assessed the expression of inflammatory fac-tors Interleukin-1 beta (IL-1β), Tumor Necrosis Factor-alpha (TNF-α), and Interleukin-6 (IL-6) via Quantitative Polymerase Chain Re-action (q-PCR). The expression levels of ferroptosis pathway protein glutathione peroxidase 4 (GPX4) and solute carrier family 7 mem-ber 11 (SLC7A11) were detected by western blotting. Results Compared with the mNSS of the sham group [(3.67±2.80) points vs. (14.33±1.37) points], the ischemia-reperfusion group showed severe neurological deficits (P<0.001), increased cerebral infarction areato (24.21±4.27)%, and increased neuronal apoptosis to (12.06±3.96) per field of view. After intervention with Maresin 1, the above-men-tioned injuries were significantly improved in the I/R+MaR1 group: mNSS decreased to (9.67±1.03) points, the infarct area decreasedto (13.44±2.83)%, and neuronal apoptosis decreased to (4.03±1.81) per field of view (compared with the ischemia-reperfusion group, all P<0.001). Moreover, compared with the ischemia-reperfusion group, the levels of inflammatory cytokines (IL-1β, TNF-α, and IL.6) were down-regulated (all P< 0.05), while the expression of ferroptosis-related proteins (GPX4 and SLC7A11) was significantly up-regu-lated (all P < 0.05) in the I/R+MaR1 group.Conclusion Maresin 1 mitigates brain tissue damage in ischemia-reperfusion in rats. It re-duces apoptosis and inflammatory responses, potentially through the regulation of the ferroptosis pathway. |
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