Abstract The effects of quercetin-loaded liposomes (PCL-Q) and their constituents, that is, free quercetin (Q) and ‘empty’ phosphatidylcholine vesicles (PCL), on maxi-K channel activity were studied in single mouse ileal myocytes before and after H2O2-induced oxidative stress. Macroscopic Maxi-K channel currents were recorded using whole-cell patch clamp techniques, while single BKCa channel currents were recorded in the cell-attached configuration. Bath application of PCL-Q (100 μg/ml of lipid and 3 μg/ml of quercetin) increased single Maxi-K channel activity more than threefold, from 0.010 ± 0.003 to 0.034 ± 0.004 (n = 5; p < 0.05), whereas single-channel conductance increased non-significantly from 138 to 146 pS. In the presence of PCL-Q multiple simultaneous channel openings were observed, with up to eight active channels in the membrane patch. Surprisingly, ‘empty’ PCL (100 μg/ml) also produced some channel activation, although it was less potent compared to PCL-Q, that is, these increased NPo from 0.010 ± 0.003 to 0.019 ± 0.003 (n = 5; p < 0.05) and did not affect single-channel conductance (139 pS). Application of PCL-Q restored macroscopic Maxi-K currents suppressed by H2O2-induced oxidative stress in ileal smooth muscle cells. We conclude that PCL-Q can activate Maxi-K channels in ileal myocytes mainly by increasing channel open probability, as well as maintain Maxi-K-mediated whole-cell current under the conditions of oxidative stress. While fusion of the ‘pure’ liposomes with the plasma membrane may indirectly activate Maxi-K channels by altering channel’s phospholipids environment, the additional potentiating action of quercetin may be due to its better bioavailability.

中文翻译：

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脂质体槲皮素增强平滑肌中的 maxi-K 通道开口并在氧化应激后恢复其活性

摘要 在单个小鼠回肠肌细胞中研究了槲皮素负载脂质体 (PCL-Q) 及其成分，即游离槲皮素 (Q) 和“空”磷脂酰胆碱囊泡 (PCL) 对 maxi-K 通道活性的影响。在 H2O2 诱导的氧化应激后。使用全细胞膜片钳技术记录宏观 Maxi-K 通道电流，而在细胞附着配置中记录单个 BKCa 通道电流。PCL-Q（100 μg/ml 脂质和 3 μg/ml 槲皮素）的浴应用使单个 Maxi-K 通道活性增加了三倍以上，从 0.010 ± 0.003 到 0.034 ± 0.004（n = 5；p < 0.05），而单通道电导从 138 pS 非显着增加到 146 pS。在 PCL-Q 存在的情况下，观察到多个同时通道开口，膜贴片中最多有八个活动通道。令人惊讶的是，“空”PCL (100 μg/ml) 也产生了一些通道激活，尽管与 PCL-Q 相比它的效力较低，也就是说，这些将 NPo 从 0.010 ± 0.003 增加到 0.019 ± 0.003（n = 5；p < 0.05) 并且不影响单通道电导 (139 pS)。PCL-Q 的应用恢复了回肠平滑肌细胞中 H2O2 诱导的氧化应激抑制的宏观 Maxi-K 电流。我们得出结论，PCL-Q 主要通过增加通道开放概率来激活回肠肌细胞中的 Maxi-K 通道，并在氧化应激条件下维持 Maxi-K 介导的全细胞电流。虽然“纯”脂质体与质膜的融合可以通过改变通道的磷脂环境间接激活 Maxi-K 通道，