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氯吡格雷对多微生物脓毒症的肺保护作用。

LUNG PROTECTIVE EFFECTS OF CLOPIDOGREL IN POLYMICROBIAL SEPSIS.

机构信息

DEPARTMENT OF PHARMACOLOGY & THERAPEUTICS, FACULTY OF MEDICINE, UNIVERSITY OF KUFA, KUFA, IRAQ.

出版信息

Pol Merkur Lekarski. 2023;51(4):321-329. doi: 10.36740/Merkur202304104.

Abstract

OBJECTIVE

Aim: The goal of this experiment was to examine if Clopidogrel might protect the lungs during sepsis by modulating the inflammatory and oxidative stress markers.

PATIENTS AND METHODS

Materials and Methods: Twenty-four adult male Swiss-albino mice aged 8-12 weeks, with a weighing of 20-30 g, were randomized into 4 equal groups (n=6): sham (Laparotomy without cecal ligation and puncture [CLP]), CLP (laparotomy plus CLP), vehicle (DMSO 1 hour prior to CLP), Clopidogrel (50 mg/g IP 1 hour before to CLP). ELISA was used to assess Lung tissue levels of pro-inflammatory and oxidative stress markers.

RESULTS

Results: F2 isoprostane levels were significantly higher in the sepsis group (p<0.05) in comparison with sham group, while Clopidogrel was considerably lower (p<0.05) in the inflammatory and oxidative stress markers in comparison to sepsis group. Histologically, all mice in the sepsis group had considerable (p=0.05) lung tissue damage, but Clopidogrel considerably decreased lung tissue injury (p=0.05).

CONCLUSION

Conclusion: Clopidogrel was found to reduce lung tissue cytokine concentrations (IL-1, TNF a, IL-6, F2 isoprostane, GPR 17, MIF) in male mice during CLP-induced polymicrobial sepsis by modulation of pro-inflammatory and oxidative stress cascade signaling pathways, to the best of our abilities, no study has looked at the effect of Clopidogrel on MIF levels.

摘要

目的

本实验旨在研究氯吡格雷是否通过调节炎症和氧化应激标志物来保护脓毒症患者的肺部。

患者和方法

24 只成年雄性瑞士白化病小鼠,年龄 8-12 周,体重 20-30g,随机分为 4 组(n=6):假手术组(仅行剖腹术,不行盲肠结扎穿孔术[CLP])、CLP 组(剖腹术加 CLP)、载体组(CLP 前 1 小时给予 DMSO)、氯吡格雷组(CLP 前 1 小时给予 50mg/g IP)。采用 ELISA 法检测肺组织中促炎和氧化应激标志物的水平。

结果

与假手术组相比,脓毒症组 F2 异前列烷水平显著升高(p<0.05),而氯吡格雷组在炎症和氧化应激标志物方面明显降低(p<0.05)。组织学检查显示,所有脓毒症组小鼠的肺组织损伤均显著(p=0.05),但氯吡格雷组的肺组织损伤明显减少(p=0.05)。

结论

氯吡格雷可通过调节促炎和氧化应激级联信号通路,降低 CLP 诱导的多微生物脓毒症雄性小鼠肺组织细胞因子浓度(IL-1、TNF-α、IL-6、F2 异前列烷、GPR17、MIF),据我们所知,尚无研究观察氯吡格雷对 MIF 水平的影响。

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