肝硬化患者血清维生素D水平与氧化应激和细胞凋亡标志物的相关性。

Current health sciences journal Pub Date : 2023-01-01 Epub Date: 2023-03-31 DOI:10.12865/CHSJ.49.01.54
Mihnea Marian Pomacu, Diana Maria Trașcă, Vlad Pădureanu, Elena Camelia Stănciulescu, Cristina Jana Busuioc, Cătălina Gabriela Pisoschi, Ana Maria Bugă
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引用次数: 0

摘要

在本研究中,我们研究了根据血清GGT活性分层的肝硬化患者中维生素D与氧化应激和细胞凋亡标志物之间的关系。选择48例不同病因的肝硬化患者,其中58%(n=28)诊断为酒精性肝硬化,42%(n=20)诊断为肝炎病毒感染后的肝硬化。每组根据GGT活性分为三个四分位数。比较25-羟基维生素D[25-(HO)vit D]、氧化应激标志物(过氧化氢酶、超氧化物歧化酶)和细胞凋亡(M30)。GGT水平升高与两组AST、ALT和ALP值升高相关。在比较乙醇诱导的肝硬化患者与对照组的所有四分位数以及病毒诱导的肝硬化的第一个四分位数患者的25-(OH)vit D水平时,观察到统计学上的显著差异。在SOD方面,所有肝硬化亚组与对照组之间存在统计学显著差异。所有肝硬化亚组的CAT值均低于对照组,但仅在Q2.2和Q1.3四分位数之间以及Q2.2和对照组之间存在显著差异。在乙醇诱导的肝硬化患者中,25-(OH)vit D与SOD的相关性产生了具有统计学意义的结果。与对照组和病毒诱导的肝硬化患者相比,酒精性肝硬化患者的M30活性增加,这与GGT活性的程度有关。我们的研究结果强调,维生素D缺乏与肝功能障碍增强有关,而与疾病发作的诱因无关。此外,维生素D缺乏通过促进氧化应激来加重肝损伤,氧化应激影响实质肝细胞的生存机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Correlations of Serum Vitamin D Level with Markers of Oxidative Stress and Apoptosis in Liver Cirrhosis.

Correlations of Serum Vitamin D Level with Markers of Oxidative Stress and Apoptosis in Liver Cirrhosis.

Correlations of Serum Vitamin D Level with Markers of Oxidative Stress and Apoptosis in Liver Cirrhosis.

Correlations of Serum Vitamin D Level with Markers of Oxidative Stress and Apoptosis in Liver Cirrhosis.

In this study we investigated the relationship between vitamin D and markers of oxidative stress and apoptosis in patients with liver cirrhosis stratified according serum GGT activity. Forty-eight patients with liver cirrhosis of various aetiology were selected, among which 58% cases (n=28) diagnosed with alcoholic liver cirrhosis and 42% (n=20) with cirrhosis after hepatitis virus infection. Each group was divided into three quartiles according GGT activity. 25-hydroxyvitamin D [25-(HO) vit D], markers of oxidative stress (catalase, superoxide dismutase) and apoptosis (M30) were compared. Higher levels of GGT were correlated with elevated AST, ALT and ALP values in both groups. A statistically significant difference was observed when comparing 25-(OH) vit D levels of patients suffering from ethanol-induced liver cirrhosis versus control group for all the quartiles as well as for those from the first quartile of viral-induced liver cirrhosis. For SOD, statistically significant differences were noticed between all cirrhosis subgroups and the control group. CAT values in all cirrhosis subgroups were lower than in control, but significant differences were only between Q2.2 and Q1.3 quartiles and Q2.2 and control. Correlation of 25-(OH) vit D versus SOD yields statistically significant results in ethanol-induced cirrhosis patients. M30 activity was increased in patients with alcoholic cirrhosis compared to controls and those with virus-induced cirrhosis, being correlated with the degree of GGT activity. Our results emphasized that vitamin D deficiency is associated with enhanced liver dysfunction regardless of the trigger responsible for disease onset. Furthermore, vitamin D deficiency augments liver injury by promoting oxidative stress which influence the survival mechanisms of parenchymal liver cells.

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