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喷雾干燥K79对血管舒张因子激活及炎症反应的调节作用

Regulatory Effect of Spray-Dried K79 on the Activation of Vasodilatory Factors and Inflammatory Responses.

作者信息

Kim Ki Hwan, Hwang Yongjin, Kang Seok-Seong

机构信息

Department of Food Science and Biotechnology, College of Life Science and Biotechnology, Dongguk University, Goyang 10326, Korea.

Novalacto Co., Ltd., Daejeon 34016, Korea.

出版信息

Food Sci Anim Resour. 2024 Jan;44(1):216-224. doi: 10.5851/kosfa.2023.e78. Epub 2024 Jan 1.

Abstract

The reduction of nitric oxide (NO) bioavailability in the endothelium induces endothelial dysfunction, contributing to the development of hypertension. Although consumption decreases blood pressure, intracellular signaling pathways related to hypertension have not been well elucidated. Thus, this study examined the effect of spray-dried K79 (LpK79) on NO production, intracellular signaling pathways, and inflammatory responses related to vascular function and hypertension. NO production was assessed in human umbilical vein endothelial cells (HUVECs) treated with LpK79. Endothelial NO synthase (eNOS) and intracellular signaling molecules were determined using Western blot analysis. LpK79 dose-dependently increased NO production and activated eNOS via the phosphoinositide 3-kinase/Akt signaling pathway HUVECs. Moreover, LpK79 mitigated the activation of crucial factors pivotal for vascular contraction in smooth muscle cells, such as phospholipase Cγ, myosin phosphatase target subunit 1, and Rho-associated kinase 2. When HUVECs were treated with LpL79 in the presence of lipopolysaccharide (LPS), LpK79 effectively suppressed mRNA and protein expression of pro-inflammatory mediators induced by LPS. These results suggest that LpK79 provided a beneficial effect on the regulation of vascular endothelial function.

摘要

内皮中一氧化氮(NO)生物利用度的降低会导致内皮功能障碍,促进高血压的发展。尽管食用[具体物质未明确,推测是K79相关产品]可降低血压,但与高血压相关的细胞内信号通路尚未得到充分阐明。因此,本研究考察了喷雾干燥的K79(LpK79)对与血管功能和高血压相关的NO生成、细胞内信号通路及炎症反应的影响。在用LpK79处理的人脐静脉内皮细胞(HUVECs)中评估NO生成。使用蛋白质印迹分析测定内皮型一氧化氮合酶(eNOS)和细胞内信号分子。LpK79通过磷脂酰肌醇3激酶/蛋白激酶B(Akt)信号通路剂量依赖性地增加HUVECs中NO的生成并激活eNOS。此外,LpK79减轻了平滑肌细胞中对血管收缩至关重要的关键因子的激活,如磷脂酶Cγ、肌球蛋白磷酸酶靶亚基1和Rho相关激酶2。当在脂多糖(LPS)存在的情况下用LpK79处理HUVECs时,LpK79有效抑制了LPS诱导的促炎介质的mRNA和蛋白表达。这些结果表明,LpK79对血管内皮功能的调节具有有益作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55c1/10789557/eea6de7a3031/kosfa-44-1-216-g1.jpg

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