Yu Shi, Bao-Jun Wang, Chao Chen, Jiang-Xia Pang, Yang Li, Jun Zhang, Mao-Mao Xu
{"title":"[基于激活小胶质细胞的丁苯酞治疗一氧化碳中毒后迟发性脑病的机制]。","authors":"Yu Shi, Bao-Jun Wang, Chao Chen, Jiang-Xia Pang, Yang Li, Jun Zhang, Mao-Mao Xu","doi":"10.3881/j.issn.1000-503X.16017","DOIUrl":null,"url":null,"abstract":"<p><p>Objective To explore the mechanism of butylphthalide (NBP) in regulating microglia activation and inflammatory cytokine expression in the hippocampus of the mouse model of delayed encephalopathy after carbon monoxide poisoning (DEACMP). Methods Wild-type C57 adult mice with normal cognitive function were selected,and DEACMP was modeled by static inhalation of carbon monoxide.The mice were randomized into three groups:DEACMP,control,and NBP.The NBP group was administrated with NBP suspension at 6 mg/kg by gavage for 21 days,and the DEACMP and control groups were administrated with the same amount of vegetable oil by gavage.The hippocampal injury was observed by HE staining.The protein level of ionized calcium-binding adapter molecule 1 (IBA1) was determined by Western blotting,and the levels of downstream inflammatory cytokines were measured by ELISA. Results Compared with the control group,the DEACMP and NBP groups showed prolonged escape latency (<i>P</i>=0.001,<i>P</i>=0.029),reduced nerve cells (<i>P</i>=0.001,<i>P</i>=0.035),up-regulated expression of IBA1 (<i>P</i>=0.001,<i>P</i>=0.042),increased mean fluorescence intensity of IBA1 (<i>P</i>=0.001,<i>P</i>=0.021),and elevated levels of tumor necrosis factor-α (TNF-α) (<i>P</i>=0.002,<i>P</i>=0.024),interleukin (IL)-6 (<i>P</i>=0.001,<i>P</i>=0.015),and IL-1β (<i>P</i>=0.001,<i>P</i>=0.023).Compared with the DEACMP group,the NBP group showed shortened escape latency (<i>P</i>=0.025),increased nerve cells (<i>P</i>=0.039),down-regulated expression of IBA1 (<i>P</i>=0.035),decreased average fluorescence intensity of IBA1 (<i>P</i>=0.031),and lowered levels of TNF-α (<i>P</i>=0.028),IL-6 (<i>P</i>=0.037),and IL-1β (<i>P</i>=0.034). Conclusion NBP can inhibit the activation of microglia and reduce the expression of inflammatory factors,thereby alleviating cognitive dysfunction and brain tissue damage caused by DEACMP.</p>","PeriodicalId":6919,"journal":{"name":"中国医学科学院学报","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"[Mechanism of Butylphthalide in Treating Delayed Encephalopathy After Carbon Monoxide Poisoning Based on Activation of Microglia].\",\"authors\":\"Yu Shi, Bao-Jun Wang, Chao Chen, Jiang-Xia Pang, Yang Li, Jun Zhang, Mao-Mao Xu\",\"doi\":\"10.3881/j.issn.1000-503X.16017\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Objective To explore the mechanism of butylphthalide (NBP) in regulating microglia activation and inflammatory cytokine expression in the hippocampus of the mouse model of delayed encephalopathy after carbon monoxide poisoning (DEACMP). Methods Wild-type C57 adult mice with normal cognitive function were selected,and DEACMP was modeled by static inhalation of carbon monoxide.The mice were randomized into three groups:DEACMP,control,and NBP.The NBP group was administrated with NBP suspension at 6 mg/kg by gavage for 21 days,and the DEACMP and control groups were administrated with the same amount of vegetable oil by gavage.The hippocampal injury was observed by HE staining.The protein level of ionized calcium-binding adapter molecule 1 (IBA1) was determined by Western blotting,and the levels of downstream inflammatory cytokines were measured by ELISA. Results Compared with the control group,the DEACMP and NBP groups showed prolonged escape latency (<i>P</i>=0.001,<i>P</i>=0.029),reduced nerve cells (<i>P</i>=0.001,<i>P</i>=0.035),up-regulated expression of IBA1 (<i>P</i>=0.001,<i>P</i>=0.042),increased mean fluorescence intensity of IBA1 (<i>P</i>=0.001,<i>P</i>=0.021),and elevated levels of tumor necrosis factor-α (TNF-α) (<i>P</i>=0.002,<i>P</i>=0.024),interleukin (IL)-6 (<i>P</i>=0.001,<i>P</i>=0.015),and IL-1β (<i>P</i>=0.001,<i>P</i>=0.023).Compared with the DEACMP group,the NBP group showed shortened escape latency (<i>P</i>=0.025),increased nerve cells (<i>P</i>=0.039),down-regulated expression of IBA1 (<i>P</i>=0.035),decreased average fluorescence intensity of IBA1 (<i>P</i>=0.031),and lowered levels of TNF-α (<i>P</i>=0.028),IL-6 (<i>P</i>=0.037),and IL-1β (<i>P</i>=0.034). Conclusion NBP can inhibit the activation of microglia and reduce the expression of inflammatory factors,thereby alleviating cognitive dysfunction and brain tissue damage caused by DEACMP.</p>\",\"PeriodicalId\":6919,\"journal\":{\"name\":\"中国医学科学院学报\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2024-10-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"中国医学科学院学报\",\"FirstCategoryId\":\"1087\",\"ListUrlMain\":\"https://doi.org/10.3881/j.issn.1000-503X.16017\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"Medicine\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"中国医学科学院学报","FirstCategoryId":"1087","ListUrlMain":"https://doi.org/10.3881/j.issn.1000-503X.16017","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"Medicine","Score":null,"Total":0}
[Mechanism of Butylphthalide in Treating Delayed Encephalopathy After Carbon Monoxide Poisoning Based on Activation of Microglia].
Objective To explore the mechanism of butylphthalide (NBP) in regulating microglia activation and inflammatory cytokine expression in the hippocampus of the mouse model of delayed encephalopathy after carbon monoxide poisoning (DEACMP). Methods Wild-type C57 adult mice with normal cognitive function were selected,and DEACMP was modeled by static inhalation of carbon monoxide.The mice were randomized into three groups:DEACMP,control,and NBP.The NBP group was administrated with NBP suspension at 6 mg/kg by gavage for 21 days,and the DEACMP and control groups were administrated with the same amount of vegetable oil by gavage.The hippocampal injury was observed by HE staining.The protein level of ionized calcium-binding adapter molecule 1 (IBA1) was determined by Western blotting,and the levels of downstream inflammatory cytokines were measured by ELISA. Results Compared with the control group,the DEACMP and NBP groups showed prolonged escape latency (P=0.001,P=0.029),reduced nerve cells (P=0.001,P=0.035),up-regulated expression of IBA1 (P=0.001,P=0.042),increased mean fluorescence intensity of IBA1 (P=0.001,P=0.021),and elevated levels of tumor necrosis factor-α (TNF-α) (P=0.002,P=0.024),interleukin (IL)-6 (P=0.001,P=0.015),and IL-1β (P=0.001,P=0.023).Compared with the DEACMP group,the NBP group showed shortened escape latency (P=0.025),increased nerve cells (P=0.039),down-regulated expression of IBA1 (P=0.035),decreased average fluorescence intensity of IBA1 (P=0.031),and lowered levels of TNF-α (P=0.028),IL-6 (P=0.037),and IL-1β (P=0.034). Conclusion NBP can inhibit the activation of microglia and reduce the expression of inflammatory factors,thereby alleviating cognitive dysfunction and brain tissue damage caused by DEACMP.
期刊介绍：
Acta Academiae Medicinae Sinicae was founded in February 1979. It is a comprehensive medical academic journal published in China and abroad, supervised by the Ministry of Health of the People's Republic of China and sponsored by the Chinese Academy of Medical Sciences and Peking Union Medical College.
The journal mainly reports the latest research results, work progress and dynamics in the fields of basic medicine, clinical medicine, pharmacy, preventive medicine, biomedicine, medical teaching and research, aiming to promote the exchange of medical information and improve the academic level of medicine. At present, the journal has been included in 10 famous foreign retrieval systems and their databases [Medline (PubMed online version), Elsevier, EMBASE, CA, WPRIM, ExtraMED, IC, JST, UPD and EBSCO-ASP]; and has been included in important domestic retrieval systems and databases [China Science Citation Database (Documentation and Information Center of the Chinese Academy of Sciences), China Core Journals Overview (Peking University Library), China Science and Technology Paper Statistical Source Database (China Science and Technology Core Journals) (China Institute of Scientific and Technological Information), China Science and Technology Journal Paper and Citation Database (China Institute of Scientific and Technological Information)].
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