10%二氧化碳改善大鼠蛛网膜下腔出血后的认知功能:通过PI3K/AKT信号通路抑制神经元凋亡。

IF 3 Q2 MEDICINE, RESEARCH & EXPERIMENTAL
Medical Gas Research Pub Date : 2025-09-01 Epub Date: 2025-03-12 DOI:10.4103/mgr.MEDGASRES-D-24-00116
Liuyang Tang, Daochen Wen, Zichao Huang, Xingwei Lei, Xiaoguo Li, Yajun Zhu, Su Hai, Zongduo Guo
{"title":"10%二氧化碳改善大鼠蛛网膜下腔出血后的认知功能:通过PI3K/AKT信号通路抑制神经元凋亡。","authors":"Liuyang Tang, Daochen Wen, Zichao Huang, Xingwei Lei, Xiaoguo Li, Yajun Zhu, Su Hai, Zongduo Guo","doi":"10.4103/mgr.MEDGASRES-D-24-00116","DOIUrl":null,"url":null,"abstract":"<p><p>Many patients experience long-term cognitive dysfunction after subarachnoid hemorrhage (SAH), and effective treatments are currently lacking. Carbon dioxide (CO 2 ), an inexpensive and easily produced gas, forms carbonic acid when dissolved in water. Studies have suggested that hypercapnia may have neuroprotective effects. However, the optimal concentration of CO 2 for therapeutic inhalation is still unclear. This study aimed to investigate the effects of various CO 2 concentrations on cognitive function in SAH rats and to explore the potential molecular mechanisms involved. In this study, we established a rat model of SAH by endovascular perforation of the internal carotid artery. The rat models inhaled CO 2 at concentrations of 10%, 20%, or 30%, for 1 hour after modeling. The results showed that inhalation of 10% CO 2 improved cortical blood flow following SAH, while higher concentrations of CO 2 (20% and 30%) worsened cortical hypoperfusion. The partial pressure of CO 2 did not change 1 hour after SAH, but it significantly increased with the inhalation of 10% CO 2 . Additionally, 10% CO 2 effectively inhibited neuronal apoptosis, enhanced locomotor activity, and improved memory and learning abilities in SAH rats. Moreover, 10% CO 2 upregulated the phosphorylation of phosphatidylinositol 3 kinase) and protein kinase B, increased the expression of Bcl-2, and decreased the expression of Bax. In conclusion, inhaling 10% CO 2 restores cerebral perfusion, inhibits neuronal apoptosis, and improves cognitive function in SAH rats. In contrast, higher concentrations of CO 2 led to worsened hypoperfusion. The neuroprotective effect of 10% CO 2 may occur through the activation of the phosphatidylinositol 3-kinase/protein kinase B signaling pathway.</p>","PeriodicalId":18559,"journal":{"name":"Medical Gas Research","volume":" ","pages":"391-397"},"PeriodicalIF":3.0000,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12054663/pdf/","citationCount":"0","resultStr":"{\"title\":\"10% carbon dioxide improves cognitive function after subarachnoid hemorrhage in rats: inhibiting neuronal apoptosis through the PI3K/AKT signaling pathway.\",\"authors\":\"Liuyang Tang, Daochen Wen, Zichao Huang, Xingwei Lei, Xiaoguo Li, Yajun Zhu, Su Hai, Zongduo Guo\",\"doi\":\"10.4103/mgr.MEDGASRES-D-24-00116\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Many patients experience long-term cognitive dysfunction after subarachnoid hemorrhage (SAH), and effective treatments are currently lacking. Carbon dioxide (CO 2 ), an inexpensive and easily produced gas, forms carbonic acid when dissolved in water. Studies have suggested that hypercapnia may have neuroprotective effects. However, the optimal concentration of CO 2 for therapeutic inhalation is still unclear. This study aimed to investigate the effects of various CO 2 concentrations on cognitive function in SAH rats and to explore the potential molecular mechanisms involved. In this study, we established a rat model of SAH by endovascular perforation of the internal carotid artery. The rat models inhaled CO 2 at concentrations of 10%, 20%, or 30%, for 1 hour after modeling. The results showed that inhalation of 10% CO 2 improved cortical blood flow following SAH, while higher concentrations of CO 2 (20% and 30%) worsened cortical hypoperfusion. The partial pressure of CO 2 did not change 1 hour after SAH, but it significantly increased with the inhalation of 10% CO 2 . Additionally, 10% CO 2 effectively inhibited neuronal apoptosis, enhanced locomotor activity, and improved memory and learning abilities in SAH rats. Moreover, 10% CO 2 upregulated the phosphorylation of phosphatidylinositol 3 kinase) and protein kinase B, increased the expression of Bcl-2, and decreased the expression of Bax. In conclusion, inhaling 10% CO 2 restores cerebral perfusion, inhibits neuronal apoptosis, and improves cognitive function in SAH rats. In contrast, higher concentrations of CO 2 led to worsened hypoperfusion. The neuroprotective effect of 10% CO 2 may occur through the activation of the phosphatidylinositol 3-kinase/protein kinase B signaling pathway.</p>\",\"PeriodicalId\":18559,\"journal\":{\"name\":\"Medical Gas Research\",\"volume\":\" \",\"pages\":\"391-397\"},\"PeriodicalIF\":3.0000,\"publicationDate\":\"2025-09-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12054663/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Medical Gas Research\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.4103/mgr.MEDGASRES-D-24-00116\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/3/12 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q2\",\"JCRName\":\"MEDICINE, RESEARCH & EXPERIMENTAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Medical Gas Research","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.4103/mgr.MEDGASRES-D-24-00116","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/3/12 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
引用次数: 0

摘要

许多患者在蛛网膜下腔出血(SAH)后出现长期认知功能障碍,目前缺乏有效的治疗方法。二氧化碳(CO2)是一种廉价且容易产生的气体,当它溶解在水中时会形成碳酸。研究表明,高碳酸血症可能具有神经保护作用。然而,治疗性吸入二氧化碳的最佳浓度仍不清楚。本研究旨在探讨不同CO2浓度对SAH大鼠认知功能的影响,并探讨其可能的分子机制。在这项研究中,我们建立了大鼠内颈动脉血管内穿孔的SAH模型。造模后大鼠分别吸入浓度为10%、20%或30%的CO2 1小时。结果表明,吸入10%的CO2可改善SAH后皮质血流量,而较高浓度的CO2(20%和30%)则加重了皮质灌注不足。SAH后1小时CO2分压没有变化,但随着吸入10% CO2, CO2分压明显升高。此外,10% CO2有效抑制SAH大鼠神经元凋亡,增强运动活动,改善记忆和学习能力。此外,10% CO2上调了磷脂酰肌醇3激酶和蛋白激酶B的磷酸化,增加了Bcl-2的表达,降低了Bax的表达。综上所述,吸入10% CO2可恢复SAH大鼠脑灌注,抑制神经元凋亡,改善认知功能。相反,较高浓度的二氧化碳导致灌注不足恶化。10% CO2的神经保护作用可能是通过激活磷脂酰肌醇3-激酶/蛋白激酶B信号通路来实现的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
10% carbon dioxide improves cognitive function after subarachnoid hemorrhage in rats: inhibiting neuronal apoptosis through the PI3K/AKT signaling pathway.

Many patients experience long-term cognitive dysfunction after subarachnoid hemorrhage (SAH), and effective treatments are currently lacking. Carbon dioxide (CO 2 ), an inexpensive and easily produced gas, forms carbonic acid when dissolved in water. Studies have suggested that hypercapnia may have neuroprotective effects. However, the optimal concentration of CO 2 for therapeutic inhalation is still unclear. This study aimed to investigate the effects of various CO 2 concentrations on cognitive function in SAH rats and to explore the potential molecular mechanisms involved. In this study, we established a rat model of SAH by endovascular perforation of the internal carotid artery. The rat models inhaled CO 2 at concentrations of 10%, 20%, or 30%, for 1 hour after modeling. The results showed that inhalation of 10% CO 2 improved cortical blood flow following SAH, while higher concentrations of CO 2 (20% and 30%) worsened cortical hypoperfusion. The partial pressure of CO 2 did not change 1 hour after SAH, but it significantly increased with the inhalation of 10% CO 2 . Additionally, 10% CO 2 effectively inhibited neuronal apoptosis, enhanced locomotor activity, and improved memory and learning abilities in SAH rats. Moreover, 10% CO 2 upregulated the phosphorylation of phosphatidylinositol 3 kinase) and protein kinase B, increased the expression of Bcl-2, and decreased the expression of Bax. In conclusion, inhaling 10% CO 2 restores cerebral perfusion, inhibits neuronal apoptosis, and improves cognitive function in SAH rats. In contrast, higher concentrations of CO 2 led to worsened hypoperfusion. The neuroprotective effect of 10% CO 2 may occur through the activation of the phosphatidylinositol 3-kinase/protein kinase B signaling pathway.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Medical Gas Research
Medical Gas Research MEDICINE, RESEARCH & EXPERIMENTAL-
CiteScore
5.10
自引率
13.80%
发文量
35
期刊介绍: Medical Gas Research is an open access journal which publishes basic, translational, and clinical research focusing on the neurobiology as well as multidisciplinary aspects of medical gas research and their applications to related disorders. The journal covers all areas of medical gas research, but also has several special sections. Authors can submit directly to these sections, whose peer-review process is overseen by our distinguished Section Editors: Inert gases - Edited by Xuejun Sun and Mark Coburn, Gasotransmitters - Edited by Atsunori Nakao and John Calvert, Oxygen and diving medicine - Edited by Daniel Rossignol and Ke Jian Liu, Anesthetic gases - Edited by Richard Applegate and Zhongcong Xie, Medical gas in other fields of biology - Edited by John Zhang. Medical gas is a large family including oxygen, hydrogen, carbon monoxide, carbon dioxide, nitrogen, xenon, hydrogen sulfide, nitrous oxide, carbon disulfide, argon, helium and other noble gases. These medical gases are used in multiple fields of clinical practice and basic science research including anesthesiology, hyperbaric oxygen medicine, diving medicine, internal medicine, emergency medicine, surgery, and many basic sciences disciplines such as physiology, pharmacology, biochemistry, microbiology and neurosciences. Due to the unique nature of medical gas practice, Medical Gas Research will serve as an information platform for educational and technological advances in the field of medical gas.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信