The Role of Thymoquinone in Mitigating Carbon Tetrachloride-Induced Hepatocellular Carcinoma in Rats: Targeting the CHOP-1/JNK/P38 MAPK, NFκB/TNF-α/IL-10, and Bax/Bcl-2/Caspase-3 Signalling Pathways

IF 0.8 4区生物学 Q4 BIOLOGY

Folia Biologica-Krakow Pub Date : 2021-03-31 DOI:10.3409/FB_69-1.01

R. Hussein, L. Rashed, B. Aboulhoda, Ghada Mahmoud Abdelaziz, E. Abdelhady, S. M. A. El-Aal, A. Shamseldeen, M. M. Khalifa, H. Morsi

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引用次数: 1

Abstract

The present study was conducted to evaluate the effect of thymoquinone (TQ) on hepatocellular carcinoma (HCC) in rats. Our study has reported that TQ treatment of experimentally-induced HCC results in the up-regulation of the Jun-N-terminal kinase and p38 mitogen activated protein kinase pathway (JNK/p38 MAPK) and the enhancement of anti-inflammatory, anti-oxidant, and pro-apoptotic machineries. TQ resulted in a significant decrease in the levels of nuclear factor kappa-light-chain-enhancer of activated B-cells (NFκB), tumor necrosis factor-α (TNF-α), and a significant increase in the anti-inflammatory interleukin-10 (IL-10). The pro-apoptotic effect of TQ was demonstrated through stimulating the apoptotic Bcl-2-associated X (Bax) gene and inhibiting the anti-apoptotic B-cell lymphoma 2 (Bcl-2) gene together with increasing the level of caspase 3 and up-regulating the C/EBP homologous protein (CHOP-1) gene expression. TQ treatment also enhanced the activity of the ROS scavenger, superoxide dismutase (SOD), and decreased the level of the lipid peroxidation product malondialdehyde (MDA). TQ-dependent suppression of HCC was associated with the up-regulation of JNK/p38 MAPK, enhanced CHOP-1 expression, and subsequently increased Bax gene expression.

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胸腺醌在减轻四氯化碳诱导的大鼠肝癌中的作用：靶向CHOP-1/JNK/P38MAPK、NFκB/TNF-α/IL-10和Bax/Bcl-2/Caspase-3信号通路

本研究旨在评价胸腺醌（TQ）对大鼠肝细胞癌（HCC）的影响。我们的研究报道，TQ治疗实验诱导的HCC导致Jun-N-末端激酶和p38丝裂原活化蛋白激酶途径（JNK/p38 MAPK）的上调，以及抗炎、抗氧化和促凋亡机制的增强。TQ导致活化B细胞的核因子-κ轻链增强子（NFκB）、肿瘤坏死因子-α（TNF-α）水平显著降低，抗炎白细胞介素-10（IL-10）水平显著增加。TQ通过刺激凋亡的Bcl-2相关X（Bax）基因、抑制抗凋亡的B细胞淋巴瘤2（Bcl-2）基因、增加胱天蛋白酶3水平和上调C/EBP同源蛋白（CHOP-1）基因表达来证明其促凋亡作用。TQ处理还提高了ROS清除剂、超氧化物歧化酶（SOD）的活性，降低了脂质过氧化产物丙二醛（MDA）的水平。TQ依赖性抑制HCC与JNK/p38 MAPK上调、CHOP-1表达增强以及随后Bax基因表达增加有关。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Folia Biologica-Krakow 医学-生物学

CiteScore

1.10

自引率

14.30%

发文量

审稿时长

>12 weeks

期刊介绍： Folia Biologica (Kraków) is an international online open access journal accepting original scientific articles on various aspects of zoology: phylogeny, genetics, chromosomal studies, ecology, biogeography, experimental zoology and ultrastructural studies. The language of publication is English, articles are assembled in four issues per year.