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朝藿定通过抑制 PI3K/AKT 信号通路减轻阿霉素诱导的肾病中的炎症和细胞凋亡。

Epimedium sagittatum Maxim ameliorates adriamycin-induced nephropathy by restraining inflammation and apoptosis via the PI3K/AKT signaling pathway.

机构信息

School of Pharmacy, Henan University of Chinese Medicine, Zhengzhou, China.

The Engineering and Technology Center for Chinese Medicine Development of Henan Province, Zhengzhou, China.

出版信息

Immun Inflamm Dis. 2023 Jun;11(6):e904. doi: 10.1002/iid3.904.

DOI:10.1002/iid3.904
PMID:37382268
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10266158/
Abstract

BACKGROUND

Modern pharmacological studies show that Epimedium sagittatum Maxim (EPI) has antioxidant, antiapoptotic, anti-inflammatory effects. However, the effects of EPI on adriamycin-induced nephropathy are unclear.

AIM

The main purpose of this study is to investigate the effects of EPI on adriamycin-induced nephropathy in rats.

METHODS

The chemical composition of EPI was detected by high performance liquid chromatography. Network pharmacology was used to collect the effects of EPI on adriamycin nephropathy; renal histological changes, podocyte injury, inflammatory factors, oxidative stress levels, apoptosis levels, and the PI3K/AKT signaling pathway were examined. Moreover, analyze the effects of icariin (the representative component of EPI) on adriamycin-induced apoptosis and PI3K/AKT signaling pathway of NRK-52e cells.

RESULTS

Network pharmacological results suggested that EPI may ameliorate adriamycin-induced nephropathy by inhibiting inflammatory response and regulating the PI3K/AKT signaling pathway. The experimental results showed that EPI could improve pathological injury, renal function, podocyte injury, and inhibit inflammation, oxidative stress, apoptosis in adriamycin-induced nephropathy rats through the PI3K/AKT signaling pathway. Furthermore, icariin inhibited adriamycin-induced mitochondrial apoptosis in NRK-52e cells.

CONCLUSION

This study suggested that EPI ameliorates adriamycin-induced nephropathy by reducing inflammation and apoptosis through the PI3K/AKT signaling pathway, icariin may be the pharmacodynamic substance basis for this effect.

摘要

背景

现代药理学研究表明，淫羊藿（EPI）具有抗氧化、抗凋亡、抗炎作用。然而，EPI 对阿霉素肾病的作用尚不清楚。

目的

本研究主要目的是探讨 EPI 对阿霉素肾病大鼠的作用。

方法

采用高效液相色谱法检测 EPI 的化学成分。网络药理学收集 EPI 对阿霉素肾病的作用；观察肾脏组织学变化、足细胞损伤、炎症因子、氧化应激水平、细胞凋亡水平及 PI3K/AKT 信号通路。此外，分析淫羊藿苷（EPI 的代表性成分）对阿霉素诱导的 NRK-52e 细胞凋亡及 PI3K/AKT 信号通路的影响。

结果

网络药理学结果表明，EPI 可能通过抑制炎症反应和调节 PI3K/AKT 信号通路改善阿霉素肾病。实验结果表明，EPI 可通过 PI3K/AKT 信号通路改善阿霉素肾病大鼠的病理损伤、肾功能、足细胞损伤，抑制炎症、氧化应激和细胞凋亡。此外，淫羊藿苷抑制阿霉素诱导的 NRK-52e 细胞线粒体凋亡。

结论

本研究表明，EPI 通过减少炎症和凋亡，改善阿霉素肾病，PI3K/AKT 信号通路可能是其作用的药效物质基础，淫羊藿苷可能是其作用的药效物质基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5c7/10266158/68975776487b/IID3-11-e904-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5c7/10266158/df4f861c2445/IID3-11-e904-g005.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5c7/10266158/46c0efe9a5a0/IID3-11-e904-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5c7/10266158/3d02174930d9/IID3-11-e904-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5c7/10266158/a036a737a754/IID3-11-e904-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5c7/10266158/ea58d9f2324d/IID3-11-e904-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5c7/10266158/4146ea33d6b5/IID3-11-e904-g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5c7/10266158/aaa0a9e576c5/IID3-11-e904-g003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5c7/10266158/68975776487b/IID3-11-e904-g008.jpg

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