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芦丁对糖尿病心肌病(DCM)引起的心肌细胞损伤的影响。

Effect of Tricin on cardiomyocyte damage caused by diabetic cardiomyopathy (DCM).

机构信息

Institution for Drug Clinical Trial, Shanxi Cardiovascular Hospital, Taiyuan, 030024, China.

Department of Pharmacy, Shanxi Cardiovascular Hospital, Taiyuan, 030024, China.

出版信息

BMC Cardiovasc Disord. 2024 Nov 23;24(1):668. doi: 10.1186/s12872-024-04295-y.

DOI:10.1186/s12872-024-04295-y
PMID:39578745
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11585224/
Abstract

OBJECTIVES

Flavonoid compounds exhibit remarkable antioxidant and anti-inflammatory properties in DCM and various other diseases. However, the specific mechanisms by which Tricin, 4',5,7-trihydroxy-3',5'-dimethoxyflavone, exerts its effects in the context of DCM remain to be elucidated.

METHODS

Rat H9C2 cells were cultured and subjected to high glucose conditions to establish a DCM cell model. Tricin was administered in varying concentrations to evaluate its effects on cellular oxidative stress markers, including ROS, LDH, and SOD. Additionally, the levels of inflammatory cytokines TNF-α, IL-1β, and IL-6, as well as the expression of TLR4, MYD88, and p-NF-κB, were assessed through ELISA and Western blotting.

RESULTS

Tricin treatment significantly ameliorated high glucose-induced oxidative stress in H9C2 cells, evidenced by reduced ROS and LDH levels and increased SOD levels in a dose-dependent manner. Furthermore, Tricin effectively suppressed the elevation of pro-inflammatory cytokines TNF-α, IL-1β, and IL-6. Tricin also inhibited the overactivation of the TLR4-MYD88-NF-κB signaling pathway, suggesting its role in modulating key inflammatory processes in DCM.

CONCLUSIONS

Tricin exhibits a protective role against high glucose-induced cardiac damage in a DCM cell model. By reducing oxidative stress and inflammation, and inhibiting the TLR4-MYD88-NF-κB pathway, Tricin shows significant therapeutic potential for DCM treatment. This study underscores the value of Tricin as a novel therapeutic approach for managing diabetic cardiomyopathy, warranting further research and clinical investigation.

CLINICAL TRIAL NUMBER

Not applicable.

摘要

目的

类黄酮化合物在 DCM 和其他各种疾病中表现出显著的抗氧化和抗炎特性。然而,三叶草素(4',5,7-三羟基-3',5'-二甲氧基黄酮)在 DCM 中的作用机制仍有待阐明。

方法

培养大鼠 H9C2 细胞,并使其处于高糖环境中,以建立 DCM 细胞模型。用不同浓度的三叶草素处理细胞,以评估其对细胞氧化应激标志物(ROS、LDH 和 SOD)的影响。此外,通过 ELISA 和 Western blot 评估炎症细胞因子 TNF-α、IL-1β 和 IL-6 的水平,以及 TLR4、MYD88 和 p-NF-κB 的表达。

结果

三叶草素处理显著改善了 H9C2 细胞中高糖诱导的氧化应激,表现为 ROS 和 LDH 水平降低,SOD 水平呈剂量依赖性增加。此外,三叶草素有效地抑制了促炎细胞因子 TNF-α、IL-1β 和 IL-6 的升高。三叶草素还抑制了 TLR4-MYD88-NF-κB 信号通路的过度激活,表明其在调节 DCM 中的关键炎症过程中发挥作用。

结论

三叶草素在 DCM 细胞模型中对高糖诱导的心脏损伤具有保护作用。通过降低氧化应激和炎症,并抑制 TLR4-MYD88-NF-κB 通路,三叶草素显示出对 DCM 治疗的显著治疗潜力。这项研究强调了三叶草素作为一种治疗糖尿病心肌病的新方法的价值,值得进一步研究和临床调查。

临床试验编号

不适用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5d0/11585224/a349befa34ef/12872_2024_4295_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5d0/11585224/2656dcb499cf/12872_2024_4295_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5d0/11585224/9c3054d282a1/12872_2024_4295_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5d0/11585224/f7a1a38ab3db/12872_2024_4295_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5d0/11585224/eaf6503cb990/12872_2024_4295_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5d0/11585224/a349befa34ef/12872_2024_4295_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5d0/11585224/2656dcb499cf/12872_2024_4295_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5d0/11585224/9c3054d282a1/12872_2024_4295_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5d0/11585224/f7a1a38ab3db/12872_2024_4295_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5d0/11585224/eaf6503cb990/12872_2024_4295_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5d0/11585224/a349befa34ef/12872_2024_4295_Fig5_HTML.jpg

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Pharmacol Res. 2023 Oct;196:106874. doi: 10.1016/j.phrs.2023.106874. Epub 2023 Aug 14.
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Tricin attenuates diabetic retinopathy by inhibiting oxidative stress and angiogenesis through regulating Sestrin2/Nrf2 signaling.小麦黄素通过调节Sestrin2/Nrf2信号通路抑制氧化应激和血管生成,从而减轻糖尿病视网膜病变。
Hum Exp Toxicol. 2023 Jan-Dec;42:9603271231171642. doi: 10.1177/09603271231171642.
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