Hyperbaric oxygen therapy attenuates brain radiation-induced cognitive deficits in rats.

IF 3.2 3区医学 Q1 MEDICINE, GENERAL & INTERNAL

International Journal of Medical Sciences Pub Date : 2025-01-01 DOI:10.7150/ijms.104248

Sheng-Yow Ho, Chia-Hui Lin, Chien-Cheng Huang, Cheng-Hsien Lin, Mao-Tsun Lin, Ying-Jan Wang, Jui-Ti Ma, Li-Tsun Shieh, Ching-Ping Chang, Hung-Jung Lin

{"title":"Hyperbaric oxygen therapy attenuates brain radiation-induced cognitive deficits in rats.","authors":"Sheng-Yow Ho, Chia-Hui Lin, Chien-Cheng Huang, Cheng-Hsien Lin, Mao-Tsun Lin, Ying-Jan Wang, Jui-Ti Ma, Li-Tsun Shieh, Ching-Ping Chang, Hung-Jung Lin","doi":"10.7150/ijms.104248","DOIUrl":null,"url":null,"abstract":"<p><p>Effective therapies for cognitive impairments induced by brain irradiation are currently lacking. This study investigated the therapeutic potential of hyperbaric oxygen therapy (HBOT) for radiation-induced brain injury in a randomized controlled experimental model using adult male Wistar rats. Adult male Wistar rats were divided into four experimental groups: 0 Gy whole brain radiotherapy (WBRT) with normal baric air (NBA) treatment, 0 Gy WBRT with HBOT, 10 Gy WBRT with NBA, and 10 Gy WBRT with HBOT. Behavioral tests and histochemical analyses were conducted four weeks post-WBRT to assess cognitive function, hippocampal microgliosis, apoptosis, and lipid peroxidation. Compared with the rats with 0 Gy WBRT on 28 days, the rats with 10 Gy WBRT on 28 days had significantly higher severity of spatial learning and memory dysfunction and hippocampal microgliosis, newborn neuronal apoptosis, and lipid peroxidation. HBOT significantly prevented and reversed WBRT-induced cognitive deficits, hippocampal microgliosis, newborn neuronal apoptosis, and lipid peroxidation. In addition, HBOT prevented and reversed the increased apoptosis among newborn neural stem cells and neuroblasts caused by 10 Gy WBRT on 7 days. The findings suggest that WBRT disrupts neurogenesis and enhance microgliosis, apoptosis of neuronal progenitors, and lipid peroxidation in the dentate gyrus, potentially leading to cognitive deficits and neuronal death. HBOT may offer a protective effect against these cognitive impairments and their underlying mechanisms in adult male rats following WBRT.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"22 2","pages":"283-297"},"PeriodicalIF":3.2000,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11704689/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"International Journal of Medical Sciences","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.7150/ijms.104248","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"MEDICINE, GENERAL & INTERNAL","Score":null,"Total":0}

引用次数: 0

Abstract

Effective therapies for cognitive impairments induced by brain irradiation are currently lacking. This study investigated the therapeutic potential of hyperbaric oxygen therapy (HBOT) for radiation-induced brain injury in a randomized controlled experimental model using adult male Wistar rats. Adult male Wistar rats were divided into four experimental groups: 0 Gy whole brain radiotherapy (WBRT) with normal baric air (NBA) treatment, 0 Gy WBRT with HBOT, 10 Gy WBRT with NBA, and 10 Gy WBRT with HBOT. Behavioral tests and histochemical analyses were conducted four weeks post-WBRT to assess cognitive function, hippocampal microgliosis, apoptosis, and lipid peroxidation. Compared with the rats with 0 Gy WBRT on 28 days, the rats with 10 Gy WBRT on 28 days had significantly higher severity of spatial learning and memory dysfunction and hippocampal microgliosis, newborn neuronal apoptosis, and lipid peroxidation. HBOT significantly prevented and reversed WBRT-induced cognitive deficits, hippocampal microgliosis, newborn neuronal apoptosis, and lipid peroxidation. In addition, HBOT prevented and reversed the increased apoptosis among newborn neural stem cells and neuroblasts caused by 10 Gy WBRT on 7 days. The findings suggest that WBRT disrupts neurogenesis and enhance microgliosis, apoptosis of neuronal progenitors, and lipid peroxidation in the dentate gyrus, potentially leading to cognitive deficits and neuronal death. HBOT may offer a protective effect against these cognitive impairments and their underlying mechanisms in adult male rats following WBRT.

查看原文本刊更多论文

高压氧治疗减轻大鼠脑辐射引起的认知缺陷。

目前对脑辐射引起的认知障碍缺乏有效的治疗方法。本研究以成年雄性Wistar大鼠为实验对象，研究高压氧治疗（HBOT）对辐射性脑损伤的治疗潜力。将成年雄性Wistar大鼠分为4个实验组：0 Gy全脑放疗（WBRT）加正常气压（NBA）治疗、0 Gy全脑放疗加HBOT治疗、10 Gy全脑放疗加NBA治疗、10 Gy全脑放疗加HBOT治疗。wbrt后4周进行行为测试和组织化学分析，以评估认知功能、海马小胶质细胞增生、细胞凋亡和脂质过氧化。与0 Gy WBRT 28天的大鼠相比，10 Gy WBRT 28天的大鼠空间学习记忆功能障碍、海马小胶质细胞增生、新生神经元凋亡和脂质过氧化的严重程度显著提高。HBOT可显著预防和逆转wbrt诱导的认知缺陷、海马小胶质细胞增生、新生神经元凋亡和脂质过氧化。此外，HBOT可在7天内阻止和逆转10 Gy WBRT引起的新生神经干细胞和神经母细胞凋亡的增加。研究结果表明，WBRT破坏神经发生，增强小胶质细胞形成、神经元祖细胞凋亡和齿状回脂质过氧化，可能导致认知缺陷和神经元死亡。在成年雄性大鼠WBRT后，HBOT可能对这些认知障碍及其潜在机制具有保护作用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

International Journal of Medical Sciences MEDICINE, GENERAL & INTERNAL-

CiteScore

7.20

自引率

0.00%

发文量

185

审稿时长

2.7 months

期刊介绍： Original research papers, reviews, and short research communications in any medical related area can be submitted to the Journal on the understanding that the work has not been published previously in whole or part and is not under consideration for publication elsewhere. Manuscripts in basic science and clinical medicine are both considered. There is no restriction on the length of research papers and reviews, although authors are encouraged to be concise. Short research communication is limited to be under 2500 words.