Inhibiting oxidative stress and inflammation in acute lung injury using hydrogen: A preclinical systematic review and meta-analysis

Guoshen Zhong, Yanhua Shi, L. Kong, Kaixuan Lv, Lichun Zhang, Mei Yang, Na Tian, Nana Yang
{"title":"Inhibiting oxidative stress and inflammation in acute lung injury using hydrogen: A preclinical systematic review and meta-analysis","authors":"Guoshen Zhong, Yanhua Shi, L. Kong, Kaixuan Lv, Lichun Zhang, Mei Yang, Na Tian, Nana Yang","doi":"10.36922/gtm.0379","DOIUrl":null,"url":null,"abstract":"Acute lung injury (ALI) results from excessive inflammation and disruption of the alveolar-capillary barrier, leading to acute respiratory distress syndrome. Hydrogen, known as a reducing substance, has been commonly used in preclinical trials of ALI. The present paper aims to summarize the effects of hydrogen on animal models of ALI and the possible antioxidant and anti-inflammation mechanisms of hydrogen. We conducted a thorough search of the relevant literature on PubMed, EMBASE, Web of Science, and CNKI. Data retrieved from 20 studies were analyzed to assess the beneficial effects of hydrogen therapy on ALI animal models. To evaluate the effects of hydrogen, commonly assessed outcome indicators include wet-to-dry ratio (W/D), arterial oxygen partial pressure (PaO2), malondialdehyde (MDA), superoxide dismutase (SOD), and tumor necrosis factor-alpha (TNF-α). The results demonstrate that hydrogen reduces pulmonary edema (W/D: 95% CI = −0.98 – −0.85, P < 0.001), mitigates hypoxia (PaO2: 95% CI = 6.08 – 22.30, P < 0.001), represses lipid peroxidation (MDA: 95% CI = −2.12 – −1.06, P < 0.001), scavenges free radicals (SOD: 95% CI = 10.12 – 30.07, P < 0.001), and inhibits inflammatory response (TNF-α: 95% CI = −5.52 – −1.72, P < 0.001). The subgroup analysis showed significant differences between interventions (MDA: P < 0.05; TNF-α: P < 0.05; SOD: P < 0.001). The meta-regression suggests that species may cause heterogeneity (P < 0.05). These results suggest the potential of using hydrogen in clinical trials. Different interventions with hydrogen can affect metabolic transport and distribution in vivo. Further studies should be conducted to validate and confirm these findings.","PeriodicalId":73176,"journal":{"name":"Global translational medicine","volume":"1 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2023-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Global translational medicine","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.36922/gtm.0379","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

Acute lung injury (ALI) results from excessive inflammation and disruption of the alveolar-capillary barrier, leading to acute respiratory distress syndrome. Hydrogen, known as a reducing substance, has been commonly used in preclinical trials of ALI. The present paper aims to summarize the effects of hydrogen on animal models of ALI and the possible antioxidant and anti-inflammation mechanisms of hydrogen. We conducted a thorough search of the relevant literature on PubMed, EMBASE, Web of Science, and CNKI. Data retrieved from 20 studies were analyzed to assess the beneficial effects of hydrogen therapy on ALI animal models. To evaluate the effects of hydrogen, commonly assessed outcome indicators include wet-to-dry ratio (W/D), arterial oxygen partial pressure (PaO2), malondialdehyde (MDA), superoxide dismutase (SOD), and tumor necrosis factor-alpha (TNF-α). The results demonstrate that hydrogen reduces pulmonary edema (W/D: 95% CI = −0.98 – −0.85, P < 0.001), mitigates hypoxia (PaO2: 95% CI = 6.08 – 22.30, P < 0.001), represses lipid peroxidation (MDA: 95% CI = −2.12 – −1.06, P < 0.001), scavenges free radicals (SOD: 95% CI = 10.12 – 30.07, P < 0.001), and inhibits inflammatory response (TNF-α: 95% CI = −5.52 – −1.72, P < 0.001). The subgroup analysis showed significant differences between interventions (MDA: P < 0.05; TNF-α: P < 0.05; SOD: P < 0.001). The meta-regression suggests that species may cause heterogeneity (P < 0.05). These results suggest the potential of using hydrogen in clinical trials. Different interventions with hydrogen can affect metabolic transport and distribution in vivo. Further studies should be conducted to validate and confirm these findings.
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
氢抑制急性肺损伤中的氧化应激和炎症:临床前系统回顾和荟萃分析
急性肺损伤(ALI)是由于过度炎症和肺泡-毛细血管屏障的破坏,导致急性呼吸窘迫综合征。氢是一种还原性物质,常用于急性脑损伤的临床前试验。本文就氢对ALI动物模型的影响及其可能的抗氧化和抗炎机制进行综述。我们在PubMed、EMBASE、Web of Science和CNKI上进行了相关文献的全面检索。我们分析了20项研究的数据,以评估氢疗法对ALI动物模型的有益作用。为了评估氢的影响,通常评估的结局指标包括干湿比(W/D)、动脉氧分压(PaO2)、丙二醛(MDA)、超氧化物歧化酶(SOD)和肿瘤坏死因子-α (TNF-α)。结果表明,氢可以减轻肺水肿(W/D: 95% CI = - 0.98 - - 0.85, P < 0.001),减轻缺氧(PaO2: 95% CI = 6.08 - 22.30, P < 0.001),抑制脂质过氧化(MDA: 95% CI = - 2.12 - - 1.06, P < 0.001),清除自由基(SOD: 95% CI = 10.12 - 30.07, P < 0.001),抑制炎症反应(TNF-α: 95% CI = - 5.52 - - 1.72, P < 0.001)。亚组分析显示干预间差异有统计学意义(MDA: P < 0.05;Tnf -α: p < 0.05;Sod: p < 0.001)。meta回归分析显示物种可能导致异质性(P < 0.05)。这些结果表明在临床试验中使用氢气的潜力。不同的氢干预可以影响体内代谢运输和分布。应该进行进一步的研究来验证和确认这些发现。
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 去求助
来源期刊
自引率
0.00%
发文量
0
期刊最新文献
Cardiac regenerative therapy using induced pluripotent stem cells Hesperetin alleviates pulmonary injury in a blunt chest trauma-induced pulmonary contusion model in rats Recombinant human platelet-derived growth factor-BB-soaked gelatin sponge reduces patient pain in palatal graft donor sites Omicron or no longer omicron: That is the question Targeted detection of Barrett’s neoplasia: A case report
×
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
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 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 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1