在实验性脑出血中,EGCG的保护作用与HO-1活性和小胶质细胞焦下垂抑制有关。

IF 4.4 3区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Neurochemistry international Pub Date : 2023-11-01 DOI:10.1016/j.neuint.2023.105603
Bing Bao , Xiao-Ping Yin , Xiao-Qing Wen , Yi-Jun Suo , Zhi-Ying Chen , Dong -Ling Li , Qin Lai , Xian-Ming Cao , Qiu-Min Qu
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引用次数: 0

摘要

脑出血(ICH)具有较高的死亡率和致残率,与小胶质细胞焦下垂和神经炎症有关,有效的治疗方法是有限的表没食子儿茶素-3-没食子酸盐(EGCG)已被发现在其他系统性疾病中通过调节对焦下垂的抗炎反应发挥细胞保护作用。然而,EGCG在脑出血后小胶质细胞焦下垂和神经炎症中的作用尚不清楚。在本研究中,我们研究了EGCG预处理对神经炎症介导的神经元焦下垂的影响,以及实验性脑出血中潜在的神经保护机制。EGCG预处理能显著改善小鼠的神经行为能力,减少血肿体积和脑水肿。我们发现EGCG预处理减弱了血红素诱导的炎性细胞因子(IL-1β、IL-18和TNF-α)的释放。EGCG显著上调血红素加氧酶-1(HO-1)的表达,并下调Pyropotic分子和炎性细胞因子的水平,包括Caspase-1、GSDMD、NLRP3、成熟IL-1β和IL-18。EGCG预处理还降低了ICH后Caspase-1阳性小胶质细胞和GSDMD以及NLRP3阳性小胶质胶质细胞的数量。相反,HO-1特异性抑制剂(ZnPP)显著抑制EGCG的抗焦下垂和抗神经炎症作用。因此,EGCG预处理通过上调ICH后HO-1的表达,至少部分通过Caspase1/GSDMD/NLRP3途径减轻了小胶质细胞焦下垂和神经炎症。此外,EGCG预处理促进了ICH后小胶质细胞从M1表型向M2表型的极化。结果表明,EGCG是一种潜在的通过其抗脑出血后焦下垂作用来减轻神经炎症的药物。
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The protective effects of EGCG was associated with HO-1 active and microglia pyroptosis inhibition in experimental intracerebral hemorrhage

Intracerebral hemorrhage (ICH), which has high mortality and disability rate is associated with microglial pyroptosis and neuroinflammation, and the effective treatment methods are limited Epigallocatechin-3-gallate (EGCG) has been found to play a cytoprotective role by regulating the anti-inflammatory response to pyroptosis in other systemic diseases. However, the role of EGCG in microglial pyroptosis and neuroinflammation after ICH remains unclear. In this study, we investigated the effects of EGCG pretreatment on neuroinflammation-mediated neuronal pyroptosis and the underlying neuroprotective mechanisms in experimental ICH. EGCG pretreatment was found to remarkably improved neurobehavioral performance, and decreased the hematoma volume and cerebral edema in mice. We found that EGCG pretreatment attenuated the release of hemin-induced inflammatory cytokines (IL-1β, IL-18, and TNF-α). EGCG significantly upregulated the expression of heme oxygenase-1 (HO-1), and downregulated the levels of pyroptotic molecules and inflammatory cytokines including Caspase-1, GSDMD, NLRP3, mature IL-1β, and IL-18. EGCG pretreatment also decreased the number of Caspase-1-positive microglia and GSDMD along with NLRP3-positive microglia after ICH. Conversely, an HO-1-specific inhibitor (ZnPP), significantly inhibited the anti-pyroptosis and anti-neuroinflammation effects of EGCG. Therefore, EGCG pretreatment alleviated microglial pyroptosis and neuroinflammation, at least in part through the Caspase-1/GSDMD/NLRP3 pathway by upregulating HO-1 expression after ICH. In addition, EGCG pretreatment promoted the polarization of microglia from the M1 phenotype to M2 phenotype after ICH. The results suggest that EGCG is a potential agent to attenuate neuroinflammation via its anti-pyroptosis effect after ICH.

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来源期刊
Neurochemistry international
Neurochemistry international 医学-神经科学
CiteScore
8.40
自引率
2.40%
发文量
128
审稿时长
37 days
期刊介绍: Neurochemistry International is devoted to the rapid publication of outstanding original articles and timely reviews in neurochemistry. Manuscripts on a broad range of topics will be considered, including molecular and cellular neurochemistry, neuropharmacology and genetic aspects of CNS function, neuroimmunology, metabolism as well as the neurochemistry of neurological and psychiatric disorders of the CNS.
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