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Coenzyme Q10 attenuates rat hepatocarcinogenesis via the reduction of CD59 expression and phospholipase D activity.
Cell Biochemistry and Function ( IF 2.8 ) Pub Date : 2020-01-27 , DOI: 10.1002/cbf.3487
Mahmoud Abdel-Latif 1 , Suzan Saidan 2 , Basant M Morsy 2
Affiliation  

The current study aimed to test the profile of serum lipids, phospholipase D (PLD) activity, and CD59 expression pattern in rat hepatocellular carcinoma (HCC) after therapeutic treatment with Coenzyme Q10 (CoQ10). Three rat groups were allocated as normal control, untreated HCC, and treated HCC (HCC + CoQ10). The levels of serum α‐fetoprotein (AFP) and tumour necrosis factor (TNF)‐α were assessed using enzyme‐linked immunosorbent assay (ELISA), while proliferating cell nuclear antigen (PCNA) was detected using immunohistochemistry (IHC). Serum lipids, classical (CH50), and alternative (APH50) pathways of complement activation, the liver cell HMG‐CoA reductase (HMGCR), and PLD activities were assayed colorimetrically. The protein expression of CD59, scavenger receptor class B type 1 (SRB1), B cell lymphoma‐2 (Bcl2), and cleaved Caspase‐3 (Casp‐3) were detected using western blotting, while the level of serum CD59 (sCD59) was assessed using dot‐blot. CoQ10 reduced the cell proliferation, histological alterations, and the levels of AFP and TNF‐α but increased lipids, CH50, and sCD59 in serum. In the liver cell, CoQ10 decreased and increased PLD and HMGCR enzyme activities, respectively. In addition, reduction of liver CD59, Bcl2, and SRB1 vs increased cleaved Casp‐3 expressions was observed. Statistical correlation indicated an inverse relationship between CH50 and each of CD59 expression and PLD activity after treatment with CoQ10. In conclusion, CoQ10 could protect against rat HCC through increased lipids and the reduction of CD59 expression and PLD activity.

中文翻译:

辅酶Q10通过降低CD59表达和磷脂酶D活性来减轻大鼠肝癌的发生。

目前的研究旨在测试用辅酶Q10(CoQ10)治疗后大鼠肝细胞癌(HCC)中的血脂,磷脂酶D(PLD)活性和CD59表达模式。将三组大鼠分为正常对照组,未治疗的HCC和已治疗的HCC(HCC + CoQ10)。使用酶联免疫吸附测定(ELISA)评估血清甲胎蛋白(AFP)和肿瘤坏死因子(TNF)-α的水平,同时使用免疫组织化学(IHC)检测增殖的细胞核抗原(PCNA)。用比色法测定血清脂质,补体激活的经典(CH50)和替代(APH50)途径,肝细胞HMG-CoA还原酶(HMGCR)和PLD活性。CD59,B类清道夫受体(SRB1),B细胞淋巴瘤2(Bcl2),并使用Western印迹检测了裂解的Caspase-3(Casp-3),而血清CD59(sCD59)的水平采用点印迹法评估。CoQ10减少了细胞增殖,组织学改变以及AFP和TNF-α的水平,但增加了血清中的脂质,CH50和sCD59。在肝细胞中,辅酶Q10分别降低和增加了PLD和HMGCR酶的活性。此外,观察到肝脏CD59,Bcl2和SRB1的减少与Casp-3裂解表达的增加有关。统计相关性表明,用CoQ10处理后,CH50与CD59的表达和PLD活性之间呈反比关系。总之,辅酶Q10可以通过增加脂质和减少CD59表达和PLD活性来预防大鼠肝癌。CoQ10减少了细胞增殖,组织学改变以及AFP和TNF-α的水平,但增加了血清中的脂质,CH50和sCD59。在肝细胞中,辅酶Q10分别降低和增加了PLD和HMGCR酶的活性。此外,观察到肝脏CD59,Bcl2和SRB1的减少与Casp-3裂解表达的增加有关。统计相关性表明,用CoQ10处理后,CH50与CD59的表达和PLD活性之间呈反比关系。总之,辅酶Q10可以通过增加脂质,降低CD59表达和PLD活性来预防大鼠肝癌。CoQ10减少了细胞增殖,组织学改变以及AFP和TNF-α的水平,但增加了血清中的脂质,CH50和sCD59。在肝细胞中,辅酶Q10分别降低和增加了PLD和HMGCR酶的活性。此外,观察到肝脏CD59,Bcl2和SRB1的减少与Casp-3裂解表达的增加有关。统计相关性表明,用CoQ10处理后,CH50与CD59表达和PLD活性之间呈反比关系。总之,辅酶Q10可以通过增加脂质,降低CD59表达和PLD活性来预防大鼠肝癌。分别。此外,观察到肝脏CD59,Bcl2和SRB1的减少与Casp-3裂解表达的增加有关。统计相关性表明,用CoQ10处理后,CH50与CD59表达和PLD活性之间呈反比关系。总之,辅酶Q10可以通过增加脂质,降低CD59表达和PLD活性来预防大鼠肝癌。分别。此外,观察到肝脏CD59,Bcl2和SRB1的减少与Casp-3裂解表达的增加有关。统计相关性表明,用CoQ10处理后,CH50与CD59表达和PLD活性之间呈反比关系。总之,辅酶Q10可以通过增加脂质,降低CD59表达和PLD活性来预防大鼠肝癌。
更新日期:2020-01-27
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