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柴胡皂苷 D 可减轻脂多糖诱导的肺上皮细胞的炎症反应和细胞凋亡。

Saikosaponin D attenuates inflammatory response and cell apoptosis of lipopolysaccharide-induced lung epithelial cells.

机构信息

Department of Emergency medical, The First Affiliated Hospital of Bengbu Medical College, Bengbu, China.

出版信息

Clin Respir J. 2023 Oct;17(10):1017-1024. doi: 10.1111/crj.13688. Epub 2023 Aug 24.

DOI:10.1111/crj.13688
PMID:37619985
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10542997/
Abstract

BACKGROUND

Acute lung injury (ALI) is a prevalent complication of sepsis with high mortality rate. Saikosaponin D (SSD) is a triterpenoid saponin that has been reported to alleviate sepsis-triggered renal injury in mice. Nonetheless, the therapeutic effect of SSD on sepsis-evoked ALI is unclarified.

METHODS

Lipopolysaccharide (LPS) from Escherichia coli 055:B5 was utilized to stimulate lung epithelial cell line MLE-12. A mouse model of sepsis was established. CCK-8 assay was employed for determining cytotoxicity. ELISA was utilized for determining proinflammatory cytokine production. Flow cytometry and western blotting were implemented for evaluating cell apoptosis. Hematoxylin-eosin staining was conducted for histologic analysis of murine lung tissues.

RESULTS

SSD alleviated LPS-triggered inflammation and cell apoptosis of MLE-12 cells. SSD treatment ameliorated the pathological damages, inflammatory response, and cell apoptosis in the lungs of septic mice.

CONCLUSION

SSD protects against sepsis-triggered ALI by inhibiting inflammation and cell apoptosis in MLE-12 cells and septic mouse mice.

摘要

背景

急性肺损伤(ALI)是脓毒症的一种常见并发症,死亡率很高。柴胡皂苷 D(SSD)是一种三萜皂苷,据报道可减轻小鼠脓毒症引起的肾损伤。然而,SSD 对脓毒症引起的 ALI 的治疗效果尚不清楚。

方法

采用大肠杆菌 055:B5 的脂多糖(LPS)刺激肺上皮细胞系 MLE-12。建立脓毒症小鼠模型。用 CCK-8 法测定细胞毒性。ELISA 法测定促炎细胞因子的产生。流式细胞术和 Western blot 法评估细胞凋亡。苏木精-伊红(H&E)染色法进行小鼠肺组织的组织学分析。

结果

SSD 减轻了 LPS 诱导的 MLE-12 细胞炎症和细胞凋亡。SSD 治疗改善了脓毒症小鼠肺部的病理损伤、炎症反应和细胞凋亡。

结论

SSD 通过抑制 MLE-12 细胞和脓毒症小鼠的炎症和细胞凋亡来保护 LPS 诱导的 ALI。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c195/10542997/19a99f16e023/CRJ-17-1017-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c195/10542997/26f7e86e1da0/CRJ-17-1017-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c195/10542997/14bf6893108e/CRJ-17-1017-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c195/10542997/551055ceaa5e/CRJ-17-1017-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c195/10542997/19a99f16e023/CRJ-17-1017-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c195/10542997/26f7e86e1da0/CRJ-17-1017-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c195/10542997/14bf6893108e/CRJ-17-1017-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c195/10542997/551055ceaa5e/CRJ-17-1017-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c195/10542997/19a99f16e023/CRJ-17-1017-g001.jpg

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J Inflamm Res. 2024 May 13;17:2927-2938. doi: 10.2147/JIR.S454777. eCollection 2024.
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