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首页> 外文期刊>Cellular Physiology and Biochemistry >Exogenous Hydrogen Sulfide Ameliorates Diabetes-Associated Cognitive Decline by Regulating the Mitochondria-Mediated Apoptotic Pathway and IL-23/IL-17 Expression in db/db Mice
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Exogenous Hydrogen Sulfide Ameliorates Diabetes-Associated Cognitive Decline by Regulating the Mitochondria-Mediated Apoptotic Pathway and IL-23/IL-17 Expression in db/db Mice

机译：外源性硫化氢通过调节线粒体介导的细胞凋亡途径和db / db小鼠中IL-23 / IL-17的表达来缓解糖尿病相关的认知功能下降。

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>Background: Diabetes-associated cognitive decline (DACD) is one of the complications of diabetes and leads to cognitive impairment and an increased risk of dementia. However, the exact mechanism of DACD has not been fully characterized, and a successful therapy for this issue has not been established. This study aimed to detect the anti-apoptotic and anti-inflammatory effects of hydrogen sulfide (H2S) on DACD. Methods: We used a behavioural scoring method, Western blot, TUNEL staining and immunofluorescence staining to investigate the expression of the mitochondrial apoptotic pathway and the IL-23/IL-17 axis in db/db mice with or without sodium hydrosulfide (NaHS) administration. Results: NaHS administration mice exhibited reduced time to find the platform and a shorter swimming distance (P<0.05), while the time spent in the target quadrant was increased compared to that of the db/db group (P<0.05). Pro-apoptotic proteins, including cleaved Caspase-3, cleaved Caspase-9, Bax and cytochrome C, were elevated in the db/db group (P<0.01) but were downregulated in the db/db+NaHS group (P<0.05). Exogenous H2S decreased the numbers of TUNEL-positive cells in the db/db mice (P<0.05). The Western blot analysis showed that the expression levels of IL-23/IL-17 were lower in the NaHS administration group than in the db/db group (P<0.05). Conclusion: We demonstrated that H2S improved the spatial learning and memory abilities of the db/db mice by modulating the mitochondrial apoptotic pathway and the IL-23/IL-17 axis, which were found to be associated with DACD. H2S treatment may help prevent the progression of apoptotic hippocampal neurons in db/db mice and inform the development of a new therapeutic target.
机译：> 背景： 糖尿病相关的认知功能减退（DACD）是糖尿病的并发症之一，并导致认知障碍和痴呆症风险增加。但是，DACD的确切机制尚未完全阐明，并且尚未建立针对该问题的成功疗法。本研究旨在检测硫化氢（H 2 S）对DACD的抗凋亡和抗炎作用。 方法： 我们使用行为评分方法，蛋白质印迹，TUNEL染色和免疫荧光染色来研究线粒体凋亡途径和IL-23 / IL-17轴的表达在有或没有氢硫化钠（NaHS）给药的db / db小鼠中使用。 结果： NaHS给药小鼠的平台发现时间减少，游泳距离更短（P <0.05），而与之相比，在目标象限中花费的时间增加了db / db组的数据（P <0.05）。 db / db组的促凋亡蛋白（包括裂解的Caspase-3，裂解的Caspase-9，Bax和细胞色素C）升高（P <0.01），而在db / db + NaHS组降低（P <0.05）。 。外源H 2 S减少了db / db小鼠的TUNEL阳性细胞数量（P <0.05）。 Western印迹分析表明，NaHS给药组中IL-23 / IL-17的表达水平低于db / db组（P <0.05）。 结论： 我们证明了H 2 S通过调节线粒体凋亡途径和线粒体细胞凋亡途径改善了db / db小鼠的空间学习和记忆能力。发现IL-23 / IL-17轴与DACD相关。 H 2 S处理可能有助于阻止db / db小鼠凋亡的海马神经元的进展，并为新的治疗靶标的开发提供信息。

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