CST3 alleviates bilirubin-induced neurocytes' damage by promoting autophagy.

IF 1.8 4区 医学 Q4 NEUROSCIENCES
Translational Neuroscience Pub Date : 2023-10-16 eCollection Date: 2023-01-01 DOI:10.1515/tnsci-2022-0314
Zhenkun Li, Yating Du
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引用次数: 0

Abstract

High concentrations of unconjugated bilirubin (UCB) have toxic effects. The aim of our study was to find a way to elevate UCB tolerance or inhibit its toxicity in neurocytes. It has been reported that cystatin C (CST3) concentrations have a significant positive correlation with total bilirubin (TB) levels and a negative correlation with albumin levels. In addition, CST3 can directly bind UCB, decrease human umbilical vein endothelial cells' permeability, improve blood-brain barrier integrity after ischemic brain injury in mice, and induce autophagy. We hypothesized that CST3 could increase the solubility of UCB, decrease permeability of neurocytes, induce autophagy of neurocytes, and alleviate bilirubin-induced damage. To verify our hypothesis, we measured TB and conjugated bilirubin levels, and the permeability and autophagy of neurocytes treated with UCB and CST3. Our findings suggest that CST3 can protect against UCB-induced damage in neurocytes and that autophagy played an important role in this process.

Abstract Image

Abstract Image

Abstract Image

CST3通过促进自噬减轻胆红素诱导的神经细胞损伤。
高浓度的非结合胆红素(UCB)具有毒性作用。我们研究的目的是找到一种提高UCB耐受性或抑制其对神经细胞毒性的方法。据报道,胱抑素C(CST3)浓度与总胆红素(TB)水平呈显著正相关,与白蛋白水平呈负相关。此外,CST3可以直接结合UCB,降低人脐静脉内皮细胞的通透性,改善小鼠缺血性脑损伤后血脑屏障的完整性,并诱导自噬。我们假设CST3可以增加UCB的溶解度,降低神经细胞的通透性,诱导神经细胞自噬,减轻胆红素诱导的损伤。为了验证我们的假设,我们测量了TB和结合胆红素水平,以及用UCB和CST3治疗的神经细胞的通透性和自噬。我们的研究结果表明,CST3可以预防UCB诱导的神经细胞损伤,自噬在这一过程中发挥了重要作用。
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来源期刊
CiteScore
3.00
自引率
4.80%
发文量
45
审稿时长
>12 weeks
期刊介绍: Translational Neuroscience provides a closer interaction between basic and clinical neuroscientists to expand understanding of brain structure, function and disease, and translate this knowledge into clinical applications and novel therapies of nervous system disorders.
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