Xiang Yao , Junlong Kang , Yufei Li , Haoran Zhang , Zhibin Yang , E. Chen
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The effect of MEL on neuronal cell apoptosis was observed by flow cytometry.</p></div><div><h3>Results</h3><p>Compared with the saline group, MEL treatment significantly increased the density of neurons in the cerebral cortical and reduced the cerebral infarct size after MCAO (33.9 ± 8.8% vs. 15.8 ± 3.9%, <em>P</em> < 0.05). Meanwhile, the time for MEL-treated rats to complete the water maze task on the 11th day after MCAO was significantly shorter than that of rats in the saline group (<em>P</em> < 0.05). MEL treatment also prolonged the rotarod retention time on day 14 after MCAO. Immunohistochemistry analysis showed that MEL inhibited the activation of microglia and suppressed the expression of TNF-α, IL-6, and IL-1β in the brain after ischemia. MEL treatment resulted in a significant decrease in TLR4, MyD88, and NF-κB p65 levels in extracts from the ischemic cerebral cortex. Finally, MEL reduced neuronal apoptosis induced by ischemic stroke (<em>P</em> < 0.05).</p></div><div><h3>Conclusion</h3><p>MEL treatment promotes neurological function recovery after cerebral ischemia in rats. These effects are potentially mediated through anti-inflammatory and anti-apoptotic mechanisms.</p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"107 ","pages":"Article 102462"},"PeriodicalIF":2.5000,"publicationDate":"2024-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Melittin protects against neural cell damage in rats following ischemic stroke\",\"authors\":\"Xiang Yao , Junlong Kang , Yufei Li , Haoran Zhang , Zhibin Yang , E. 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引用次数: 0
摘要
方法大鼠大脑中动脉闭塞(MCAO)60分钟,随机分为对照组、生理盐水组和MEL组。各组大鼠在MCAO前一天腹腔注射MEL,直至死亡。采用莫里斯水迷宫和旋转测试评估大鼠的运动功能和认知能力。用9.4特斯拉核磁共振成像扫描和评估大鼠大脑的梗死体积。免疫组织化学用于检测MEL对小胶质细胞的作用部位。Western blot 和 ELISA 用于测量 MEL 对促炎细胞因子产生的影响。结果与生理盐水组相比,MEL能显著增加MCAO后大脑皮层神经元的密度,缩小脑梗死面积(33.9±8.8% vs. 15.8±3.9%,P <0.05)。同时,MEL治疗大鼠在MCAO后第11天完成水迷宫任务的时间明显短于生理盐水组大鼠(P < 0.05)。MEL治疗还延长了MCAO后第14天大鼠的旋转木马保持时间。免疫组化分析表明,MEL抑制了小胶质细胞的活化,并抑制了缺血后脑中TNF-α、IL-6和IL-1β的表达。MEL 处理可显著降低缺血大脑皮层提取物中 TLR4、MyD88 和 NF-κB p65 的水平。结论 MEL 治疗可促进大鼠脑缺血后神经功能的恢复。这些作用可能是通过抗炎和抗凋亡机制介导的。
Melittin protects against neural cell damage in rats following ischemic stroke
Objective
In this study, we explored the neuroprotective effect of melittin (MEL) after brain ischemia using a rat model.
Methods
The rats underwent middle cerebral artery occlusion (MCAO) for 60 min and were randomly divided into the control group, saline group, and MEL group. Rats in each group were injected intraperitoneally with MEL one day before MCAO until sacrificed. Morris water maze and rotation test were used to assess locomotor function and cognitive ability. The 9.4 Tesla MRI was used to scan and assess the infarct volume of the rat brains. Immunohistochemistry was used to detect the sites of action of MEL on microglia. Western blot and ELISA were used to measure the effect of MEL on the production of pro-inflammatory cytokines. The effect of MEL on neuronal cell apoptosis was observed by flow cytometry.
Results
Compared with the saline group, MEL treatment significantly increased the density of neurons in the cerebral cortical and reduced the cerebral infarct size after MCAO (33.9 ± 8.8% vs. 15.8 ± 3.9%, P < 0.05). Meanwhile, the time for MEL-treated rats to complete the water maze task on the 11th day after MCAO was significantly shorter than that of rats in the saline group (P < 0.05). MEL treatment also prolonged the rotarod retention time on day 14 after MCAO. Immunohistochemistry analysis showed that MEL inhibited the activation of microglia and suppressed the expression of TNF-α, IL-6, and IL-1β in the brain after ischemia. MEL treatment resulted in a significant decrease in TLR4, MyD88, and NF-κB p65 levels in extracts from the ischemic cerebral cortex. Finally, MEL reduced neuronal apoptosis induced by ischemic stroke (P < 0.05).
Conclusion
MEL treatment promotes neurological function recovery after cerebral ischemia in rats. These effects are potentially mediated through anti-inflammatory and anti-apoptotic mechanisms.
期刊介绍:
The aim of Neuropeptides is the rapid publication of original research and review articles, dealing with the structure, distribution, actions and functions of peptides in the central and peripheral nervous systems. The explosion of research activity in this field has led to the identification of numerous naturally occurring endogenous peptides which act as neurotransmitters, neuromodulators, or trophic factors, to mediate nervous system functions. Increasing numbers of non-peptide ligands of neuropeptide receptors have been developed, which act as agonists or antagonists in peptidergic systems.
The journal provides a unique opportunity of integrating the many disciplines involved in all neuropeptide research. The journal publishes articles on all aspects of the neuropeptide field, with particular emphasis on gene regulation of peptide expression, peptide receptor subtypes, transgenic and knockout mice with mutations in genes for neuropeptides and peptide receptors, neuroanatomy, physiology, behaviour, neurotrophic factors, preclinical drug evaluation, clinical studies, and clinical trials.