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血小板激活因子 (PAF) 强烈增强豚鼠和小鼠膀胱的收缩机械活动。

Platelet-activating factor (PAF) strongly enhances contractile mechanical activities in guinea pig and mouse urinary bladder.

机构信息

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

出版信息

Sci Rep. 2022 Feb 17;12(1):2783. doi: 10.1038/s41598-022-06535-7.

DOI:10.1038/s41598-022-06535-7
PMID:35177680
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8854422/
Abstract

In this study, we investigated the effects of platelet-activating factor (PAF) on the basal tone and spontaneous contractile activities of guinea pig (GP) and mouse urinary bladder (UB) smooth muscle (UBSM) tissues to determine whether PAF could induce UBSM tissue contraction. In addition, we examined the mRNA expression of the PAF receptor, PAF-synthesizing enzyme (lysophosphatidylcholine acyltransferase, LPCAT), and PAF-degrading enzyme (PAF acetylhydrolase, PAF-AH) in GP and mouse UB tissues using RT-qPCR. PAF (10-10 M) strongly enhanced the basal tone and spontaneous contractile activities (amplitude and frequency) of GP and mouse UBSM tissues in a concentration-dependent manner. The enhancing effects of PAF (10 M) on both GP and mouse UBSM contractile activities were strongly suppressed by pretreatment with apafant (a PAF receptor antagonist, GP: 10 M; mouse: 3 × 10 M). The PAF receptor (Ptafr), LPCAT (Lpcat1, Lpcat2), and PAF-AH (Pafah1b3, Pafah2) mRNAs were detected in GP and mouse UB tissues. These findings reveal that PAF strongly enhances the contractile mechanical activities of UBSM tissues through its receptor and suggest that the PAF-synthesizing and -degrading system exists in UBSM tissues. PAF may serve as both an endogenous UBSM constrictor and an endogenous mediator leading to detrusor overactivity.

摘要

在这项研究中，我们研究了血小板激活因子 (PAF) 对豚鼠 (GP) 和小鼠膀胱 (UB) 平滑肌 (UBSM) 组织基础张力和自发性收缩活动的影响，以确定 PAF 是否可以引起 UBSM 组织收缩。此外，我们使用 RT-qPCR 检查了 GP 和小鼠 UB 组织中 PAF 受体、PAF 合成酶 (溶血磷脂酰胆碱酰基转移酶，LPCAT) 和 PAF 降解酶 (PAF 乙酰水解酶，PAF-AH) 的 mRNA 表达。PAF(10-10 M) 以浓度依赖性方式强烈增强 GP 和小鼠 UBSM 组织的基础张力和自发性收缩活动（幅度和频率）。PAF(10 M) 对 GP 和小鼠 UBSM 收缩活性的增强作用均被 apafant（PAF 受体拮抗剂，GP：10 M；小鼠：3×10 M）预处理强烈抑制。PAF 受体 (Ptafr)、LPCAT (Lpcat1、Lpcat2) 和 PAF-AH (Pafah1b3、Pafah2) mRNA 在 GP 和小鼠 UB 组织中均有检测到。这些发现表明，PAF 通过其受体强烈增强 UBSM 组织的收缩机械活性，并表明 PAF 合成和降解系统存在于 UBSM 组织中。PAF 可能既是 UBSM 的内源性收缩剂，也是导致逼尿肌过度活动的内源性介质。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8db0/8854422/9e2be947d61c/41598_2022_6535_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8db0/8854422/5849111d251d/41598_2022_6535_Fig1_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8db0/8854422/fbed2bff6531/41598_2022_6535_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8db0/8854422/d94970a885eb/41598_2022_6535_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8db0/8854422/cf8fd15a324b/41598_2022_6535_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8db0/8854422/9e2be947d61c/41598_2022_6535_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8db0/8854422/5849111d251d/41598_2022_6535_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8db0/8854422/ef778b8d6fc4/41598_2022_6535_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8db0/8854422/529b8bcd7e66/41598_2022_6535_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8db0/8854422/fbed2bff6531/41598_2022_6535_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8db0/8854422/d94970a885eb/41598_2022_6535_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8db0/8854422/cf8fd15a324b/41598_2022_6535_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8db0/8854422/9e2be947d61c/41598_2022_6535_Fig7_HTML.jpg

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