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二十二碳六烯酸对胃底平滑肌引起的乙酰胆碱、血管紧张素 II 和缓激肽收缩的抑制机制。

Inhibitory mechanisms of docosahexaenoic acid on carbachol-, angiotensin II-, and bradykinin-induced contractions in guinea pig gastric fundus smooth muscle.

机构信息

Department of Chemical Pharmacology, Faculty of Pharmaceutical Sciences, Toho University, Miyama 2-2-1, Funabashi-City, Chiba, 274-8510, Japan.

Department of Organic Chemistry, Faculty of Pharmaceutical Sciences, Toho University, Miyama 2-2-1, Funabashi-City, Chiba, 274-8510, Japan.

出版信息

Sci Rep. 2024 May 22;14(1):11720. doi: 10.1038/s41598-024-62578-y.

DOI:10.1038/s41598-024-62578-y
PMID:38778154
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11111694/
Abstract

We studied the inhibitory actions of docosahexaenoic acid (DHA) on the contractions induced by carbachol (CCh), angiotensin II (Ang II), and bradykinin (BK) in guinea pig (GP) gastric fundus smooth muscle (GFSM), particularly focusing on the possible inhibition of store-operated Ca channels (SOCCs). DHA significantly suppressed the contractions induced by CCh, Ang II, and BK; the inhibition of BK-induced contractions was the strongest. Although all contractions were greatly dependent on external Ca, more than 80% of BK-induced contractions remained even in the presence of verapamil, a voltage-dependent Ca channel inhibitor. BK-induced contractions in the presence of verapamil were not suppressed by LOE-908 (a receptor-operated Ca channel (ROCC) inhibitor) but were suppressed by SKF-96365 (an SOCC and ROCC inhibitor). BK-induced contractions in the presence of verapamil plus LOE-908 were strongly inhibited by DHA. Furthermore, DHA inhibited GFSM contractions induced by cyclopiazonic acid (CPA) in the presence of verapamil plus LOE-908 and inhibited the intracellular Ca increase due to Ca addition in CPA-treated 293T cells. These findings indicate that Ca influx through SOCCs plays a crucial role in BK-induced contraction in GP GFSM and that this inhibition by DHA is a new mechanism by which this fatty acid inhibits GFSM contractions.

摘要

我们研究了二十二碳六烯酸（DHA）对胃底平滑肌（GFSM）中由乙酰胆碱（CCh）、血管紧张素 II（Ang II）和缓激肽（BK）诱导的收缩的抑制作用，特别关注其对钙库操纵性钙通道（SOCCs）的可能抑制作用。DHA 显著抑制了由 CCh、Ang II 和 BK 诱导的收缩；对 BK 诱导的收缩的抑制作用最强。尽管所有的收缩都严重依赖于外部钙，但即使在电压依赖性钙通道抑制剂维拉帕米存在的情况下，仍有超过 80%的 BK 诱导的收缩仍然存在。维拉帕米存在下的 BK 诱导的收缩不受 LOE-908（受体操纵性钙通道（ROCC）抑制剂）的抑制，但受 SKF-96365（SOCC 和 ROCC 抑制剂）的抑制。维拉帕米加 LOE-908 存在下的 BK 诱导的收缩被 DHA 强烈抑制。此外，DHA 抑制了维拉帕米加 LOE-908 存在下由环匹阿尼酸（CPA）诱导的 GFSM 收缩，并抑制了 CPA 处理的 293T 细胞中由于 Ca 加入而导致的细胞内 Ca 增加。这些发现表明，通过 SOCC 流入的 Ca 在 GP GFSM 中的 BK 诱导收缩中起着至关重要的作用，并且 DHA 的这种抑制作用是该脂肪酸抑制 GFSM 收缩的一种新机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb27/11111694/55314dbbde36/41598_2024_62578_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb27/11111694/a576b6e130a4/41598_2024_62578_Fig1_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb27/11111694/308edc887f4f/41598_2024_62578_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb27/11111694/3f3ba425be4c/41598_2024_62578_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb27/11111694/55314dbbde36/41598_2024_62578_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb27/11111694/a576b6e130a4/41598_2024_62578_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb27/11111694/b21bd13d5ff5/41598_2024_62578_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb27/11111694/565e47c791a0/41598_2024_62578_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb27/11111694/c1c0031a2ba2/41598_2024_62578_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb27/11111694/f937c3e2b2f2/41598_2024_62578_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb27/11111694/308edc887f4f/41598_2024_62578_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb27/11111694/3f3ba425be4c/41598_2024_62578_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb27/11111694/55314dbbde36/41598_2024_62578_Fig8_HTML.jpg

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