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

Guoshen Zhong, Yanhua Shi, L. Kong, Kaixuan Lv, Lichun Zhang, Mei Yang, Na Tian, Nana Yang
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摘要

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