Tongqiao Yizhi granule repress the nuclear factor kappa-b/nucleotide oligomerization domain-like receptors 3/caspase-1 pyroptosis pathway in the hippocampus to counter vascular dementia in rats.

L I Yanjiao, Hao Linyao, L I Shuangyang, Luo Yanqi, Wang Juan, Wang Raoqiong, Bai Xue
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Abstract

Objective: To explore the mechanism by which Tongqiao Yizhi granule (, TQYZKL) intervenes pyroptosis to treat vascular dementia (VaD) in a rat model.

Methods: The rat model of VaD was established by two-vessel occlusion (2VO). The rats were randomly divided into Sham group, Model group, Nimodipine group, TQYZKL (6.2 g?kg-1?d-1), TQYZKL (12.4 g?kg-1?d-1), TQYZKL (24.8 g?kg-1?d-1). The Morris water maze (MWM) test was carried out to test the learning and memory function; Hematoxylin-eosin staining and transmission electron microscopy (TEM) to observe the pathological damage in the hippocampus; Tunel fluorescence staining to detect neuronal pyroptosis in the hippocampus. The expression levels of pyroptosis-related proteins, namely Golgi peripheral membrane protein p65 (P65), nucleotide oligomerization domain-like receptors 3 (NLRP3), caspase-1 and Gasdermin D (GSDMD), were detected using Western blotting and reverse transcription polymerase chain reaction. Moreover, the serum levels of interleukin-1β (IL-1β) and interleukin-18 (IL-18) were determined through the enzyme-linked immunosorbent assay.

Results: The study revealed that TQYZKL effectively improved the ability of VaD ratsto learn and memorize, relieved the pathological damage in the hippocampus, restored neuronal morphology, and reduced the expression of pyroptosis-related proteins P65, NLRP3, caspase-1, GSDMD-N, IL-18 and IL-1β (P < 0.05).

Conclusion: TQYZKL inhibits neuronal pyroptosis in the hippocampus of VaD rats by regulating nuclear factor kappa-B/NLRP3/caspase-1 signaling pathway, thus exerting a therapeutic effect on VaD in the rats.

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通窍益智颗粒抑制海马核因子卡巴-b/核苷酸寡聚化结构域样受体3/caspase-1热解通路,对抗大鼠血管性痴呆。
目的在大鼠模型中探讨通窍益智颗粒(TQYZKL)干预血管性痴呆(VaD)的机制:方法:通过双血管闭塞(2VO)建立大鼠血管性痴呆模型。大鼠随机分为 Sham 组、模型组、尼莫地平组、TQYZKL(6.2 g?kg-1?d-1)组、TQYZKL(12.4 g?kg-1?d-1)组、TQYZKL(24.8 g?kg-1?d-1)组。进行Morris水迷宫(MWM)测试以检测学习和记忆功能;血栓素-伊红染色和透射电子显微镜(TEM)观察海马的病理损伤;Tunel荧光染色检测海马神经元的脓毒症。利用Western印迹和反转录聚合酶链反应检测了与热蛋白沉积相关的蛋白,即高尔基外周膜蛋白p65(P65)、核苷酸寡聚化结构域样受体3(NLRP3)、caspase-1和Gasdermin D(GSDMD)的表达水平。此外,还通过酶联免疫吸附试验测定了血清中白细胞介素-1β(IL-1β)和白细胞介素-18(IL-18)的水平:研究发现,TQYZKL能有效提高VaD大鼠的学习和记忆能力,缓解海马的病理损伤,恢复神经元形态,降低热蛋白相关蛋白P65、NLRP3、caspase-1、GSDMD-N、IL-18和IL-1β的表达(P<0.05):TQYZKL通过调节核因子卡巴-B/NLRP3/caspase-1信号通路,抑制VaD大鼠海马神经元的脓毒症,从而对VaD大鼠产生治疗作用。
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