{"title":"罗格列酮在 ICH 大鼠模型中通过激活 PPARγ 和 CD36 促进小胶质细胞分布","authors":"Qiong Mu, Qian He, Hailong Zhou, Yingning Xu, Guofeng Wu","doi":"","DOIUrl":null,"url":null,"abstract":"<p><strong>Objectives: </strong>Intracerebral hemorrhage (ICH) is a serious public health problem with high mortality and morbidity. The current study aims to investigate the effects of rosiglitazone on the microglial distribution and the expression of PPARγ and CD36 in the ICH rat model.</p><p><strong>Methods new: </strong>Sprague-Dawley male rats (n=116) were randomly divided into four groups: control, ICH, rosiglitazone, and PPARγ antagonist (GW9662). Hematoxylin-eosin staining was used to observe the brain edema in the ICH rat model. The effect of rosiglitazone on the expression of OX-42, a microglial marker, was evaluated by immunohistochemistry. Immunohistochemistry, quantitative real-time PCR, and western blot were utilized to assess the role of rosiglitazone in the expression of PPARγ and CD36.</p><p><strong>Results: </strong>ICH rats exhibited a remarkable brain edema at 72 h. OX-42 expression was significantly increased in brain tissues of ICH rats. Rosiglitazone remarkably promoted the OX-42 expression in ICH rats, whereas GW9662 suppressed OX-42 expression. In addition, immunohistochemistry analysis showed that rosiglitazone markedly enhanced the expression of PPARγ and CD36 in brain tissues around the hematoma in ICH rats, while GW9662 inhibited their expression in ICH rats. Moreover, rosiglitazone significantly promoted the mRNA and protein expression of PPARγ and CD36 in the brain tissues of ICH rats, while GW9662 showed the opposite trend.</p><p><strong>Conclusion: </strong>Rosiglitazone may improve microglial distribution via promoting the expression of PPARγ and CD36 around the hematoma in the ICH rat model, which may provide effective therapeutic targets for the treatment of ICH.</p>","PeriodicalId":94154,"journal":{"name":"Neuro endocrinology letters","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2024-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Rosiglitazone Promotes Microglial Distribution via Activation of PPARγ and CD36 in the ICH Rat Model.\",\"authors\":\"Qiong Mu, Qian He, Hailong Zhou, Yingning Xu, Guofeng Wu\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objectives: </strong>Intracerebral hemorrhage (ICH) is a serious public health problem with high mortality and morbidity. The current study aims to investigate the effects of rosiglitazone on the microglial distribution and the expression of PPARγ and CD36 in the ICH rat model.</p><p><strong>Methods new: </strong>Sprague-Dawley male rats (n=116) were randomly divided into four groups: control, ICH, rosiglitazone, and PPARγ antagonist (GW9662). Hematoxylin-eosin staining was used to observe the brain edema in the ICH rat model. The effect of rosiglitazone on the expression of OX-42, a microglial marker, was evaluated by immunohistochemistry. Immunohistochemistry, quantitative real-time PCR, and western blot were utilized to assess the role of rosiglitazone in the expression of PPARγ and CD36.</p><p><strong>Results: </strong>ICH rats exhibited a remarkable brain edema at 72 h. OX-42 expression was significantly increased in brain tissues of ICH rats. Rosiglitazone remarkably promoted the OX-42 expression in ICH rats, whereas GW9662 suppressed OX-42 expression. In addition, immunohistochemistry analysis showed that rosiglitazone markedly enhanced the expression of PPARγ and CD36 in brain tissues around the hematoma in ICH rats, while GW9662 inhibited their expression in ICH rats. Moreover, rosiglitazone significantly promoted the mRNA and protein expression of PPARγ and CD36 in the brain tissues of ICH rats, while GW9662 showed the opposite trend.</p><p><strong>Conclusion: </strong>Rosiglitazone may improve microglial distribution via promoting the expression of PPARγ and CD36 around the hematoma in the ICH rat model, which may provide effective therapeutic targets for the treatment of ICH.</p>\",\"PeriodicalId\":94154,\"journal\":{\"name\":\"Neuro endocrinology letters\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2024-04-07\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Neuro endocrinology letters\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neuro endocrinology letters","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
摘要
目的：脑出血（ICH）是一个严重的公共卫生问题，死亡率和发病率都很高。新方法：将 Sprague-Dawley 雄性大鼠（n=116）随机分为四组：对照组、ICH 组、罗格列酮组和 PPARγ 拮抗剂组（GW9662）。采用苏木精-伊红染色法观察 ICH 大鼠脑水肿情况。免疫组化法评估了罗格列酮对小胶质细胞标记物 OX-42 表达的影响。免疫组化、实时定量 PCR 和 Western 印迹技术用于评估罗格列酮在 PPARγ 和 CD36 表达中的作用：ICH 大鼠在 72 h 后出现明显的脑水肿，OX-42 在 ICH 大鼠脑组织中的表达显著增加。罗格列酮明显促进 ICH 大鼠 OX-42 的表达，而 GW9662 则抑制 OX-42 的表达。此外，免疫组化分析表明，罗格列酮显著增强了 ICH 大鼠血肿周围脑组织中 PPARγ 和 CD36 的表达，而 GW9662 则抑制了它们在 ICH 大鼠中的表达。此外，罗格列酮能显著促进 ICH 大鼠脑组织中 PPARγ 和 CD36 的 mRNA 和蛋白表达，而 GW9662 则表现出相反的趋势：结论：罗格列酮可通过促进血肿周围 PPARγ 和 CD36 的表达来改善 ICH 大鼠模型中微小胶质细胞的分布，从而为治疗 ICH 提供有效的治疗靶点。
Rosiglitazone Promotes Microglial Distribution via Activation of PPARγ and CD36 in the ICH Rat Model.
Objectives: Intracerebral hemorrhage (ICH) is a serious public health problem with high mortality and morbidity. The current study aims to investigate the effects of rosiglitazone on the microglial distribution and the expression of PPARγ and CD36 in the ICH rat model.
Methods new: Sprague-Dawley male rats (n=116) were randomly divided into four groups: control, ICH, rosiglitazone, and PPARγ antagonist (GW9662). Hematoxylin-eosin staining was used to observe the brain edema in the ICH rat model. The effect of rosiglitazone on the expression of OX-42, a microglial marker, was evaluated by immunohistochemistry. Immunohistochemistry, quantitative real-time PCR, and western blot were utilized to assess the role of rosiglitazone in the expression of PPARγ and CD36.
Results: ICH rats exhibited a remarkable brain edema at 72 h. OX-42 expression was significantly increased in brain tissues of ICH rats. Rosiglitazone remarkably promoted the OX-42 expression in ICH rats, whereas GW9662 suppressed OX-42 expression. In addition, immunohistochemistry analysis showed that rosiglitazone markedly enhanced the expression of PPARγ and CD36 in brain tissues around the hematoma in ICH rats, while GW9662 inhibited their expression in ICH rats. Moreover, rosiglitazone significantly promoted the mRNA and protein expression of PPARγ and CD36 in the brain tissues of ICH rats, while GW9662 showed the opposite trend.
Conclusion: Rosiglitazone may improve microglial distribution via promoting the expression of PPARγ and CD36 around the hematoma in the ICH rat model, which may provide effective therapeutic targets for the treatment of ICH.
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