时间标签：数据日期 2026-11-01 · 生成时间 2026-11-01 05:30（Asia/Shanghai）｜ 检索窗口 PubMed edat 2026/10/31–2026/11/01 ｜ 情报发生日期 2026-11-01
研究问题
Specifically, we will incorporate clinical tissue samples and establish standardized, clinically relevant models to further confirm the efficacy of H 2 S in alleviating I/R injury-triggered cellular necroptosis.；Moreover, we will systematically explore the regulatory effects of H 2 S on downstream signaling molecules and transcription factors associated with programmed cell death, aiming to refine and complete the molecular regulatory network…
方法
Additionally, cells were pretreated with 100 mmol/L Nec-1, 400 mmol/L NAC, or different concentrations of hydrogen sulfide, with cells treated with phosphate-buffered saline (PBS) serving as the control.；Subsequently, 100 μL of cells were combined with 5 μL of annexin V-FITC and 10.0 μL of propidium iodide in a 5-mL culture tube, followed by a 15-min incubation at room temperature in the dark.；The SH-SY5Y cells were incubated in a glucose- and fetal bovine serum (FBS)-free medium under an oxygen-free environment (37 °C, 95% N 2 , 5% CO 2 ) for varying durations.
核心结论
These results collectively illustrated the substantial attenuation by NaHS of the cerebral MCAO/R injury induced ultrastructural disturbances in neuronal nuclei, mitochondria, and other organelles.；However, by the third day, the Bederson scores in the sodium hydrosulfide group (2.33 ± 0.52) and the NEC group (2.50 ± 0.54) were significantly reduced compared to the model group (3.33 ± 0.52).；Treatment with NaHS or Nec-1 group significantly reduced brain water content relative to vehicle-treated MCAO animals (*P < 0.05), demonstrating that NaHS and Nec-1 intervention alleviated ischemic brain edema.；These results indicate that pretreatment with hydrogen sulfide at concentrations ranging from 30 to 120 mmol/L for 2–12 h significantly guards against OGD-induced cell death.；Conclusion The findings revealed that I/R injury significantly damages brain cells by inducing RIPK1 mediated necroptosis.
局限
Second, the in vivo data were acquired from preliminary exploratory experiments with a relatively small sample size (n = 3 per group), which may undermine statistical power; follow-up studies with enlarged animal cohorts are therefore…；Furthermore, the efficacy of H 2 S treatment against cerebral ischemia induced by diverse etiologies, including trauma, biochemical insults, and drug-related injury, remains to be systematically validated.
对本项目的价值
干预级证据，可直接进入证据表并校准效应量参照：线粒体是衰老干预的共同下游效应器，可用于跨器官效应的统一读数。 ｜ 价值分 2.7/5（★★★☆☆）
全文来源
PubMed PMC JATS 全文（正文 46,495 字符，已过 DOI 逐字 + 题名指纹双重归属校验）
原文题录
- 英文标题：Exogenous hydrogen sulfide alleviates cerebral ischemia/reperfusion injury via inhibiting RIPK1-mediated neuronal necroptosis and ROS overaccumulation.
- 期刊与标识：Frontiers in molecular biosciences · PMID 42952556 · DOI 10.3389/fmolb.2026.1968646
B 级证据分级：B 级（同行评议临床前研究，主要为动物模型）
本文核心结论来自动物模型或体外细胞学，属临床前证据，不能外推至人体。「延长健康寿命」「改善功能」等表述在小鼠中的意义，与人类临床结局之间仍有距离。
关于本文的文献来源：本站依据 IMA 知识库「五刊监控·深度文献卡片」撰写，依据已获取的期刊全文（方法、样本量与结论已回到原文核对）；未能获取全文的同批条目另行标注「摘要级」，全程未做任何数值推算补全。