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过表达再生肝脏磷酸酶-1(PRL-1)的胎盘来源间充质干细胞通过过氧化物还原酶3增强对硫代乙酰胺损伤大鼠肝脏的抗氧化作用。

Phosphatase of Regenerating Liver-1 (PRL-1)-Overexpressing Placenta-Derived Mesenchymal Stem Cells Enhance Antioxidant Effects via Peroxiredoxin 3 in TAA-Injured Rat Livers.

作者信息

Park Hee Jung, Jun Ji Hye, Kim Jae Yeon, Jang Hye Jung, Lim Ja-Yun, Bae Si Hyun, Kim Gi Jin

机构信息

Department of Bio Convergence Science, CHA University, Seongnam-si 13488, Republic of Korea.

Research Institute of Placenta Science, CHA University, Seongnam-si 13488, Republic of Korea.

出版信息

Antioxidants (Basel). 2022 Dec 26;12(1):46. doi: 10.3390/antiox12010046.

Abstract

DNA damage repair is induced by several factors and is critical for cell survival, and many cellular DNA damage repair mechanisms are closely linked. Antioxidant enzymes that control cytokine-induced peroxide levels, such as peroxiredoxins (Prxs) and catalase (CAT), are involved in DNA repair systems. We previously demonstrated that placenta-derived mesenchymal stem cells (PD-MSCs) that overexpress PRL-1 (PRL-1(+)) promote liver regeneration via antioxidant effects in TAA-injured livers. However, the efficacy of these cells in regeneration and the role of Prxs in their DNA repair system have not been reported. Therefore, our objective was to analyze the Prx-based DNA repair mechanism in naïve or PRL-1(+)-transplanted TAA-injured rat livers. Apoptotic cell numbers were significantly decreased in the PRL-1(+) transplantation group versus the nontransplantation (NTx) group (p < 0.05). The expression of antioxidant markers was significantly increased in PRL-1(+) cells compared to NTx cells (p < 0.05). MitoSOX and Prx3 demonstrated a significant negative correlation coefficient (R2 = −0.8123). Furthermore, DNA damage marker levels were significantly decreased in PRL-1(+) cells compared to NTx cells (p < 0.05). In conclusion, increased Prx3 levels in PRL-1(+) cells result in an effective antioxidant effect in TAA-injured liver disease, and Prx3 is also involved in repairing damaged DNA.

摘要

DNA损伤修复由多种因素诱导,对细胞存活至关重要,并且许多细胞DNA损伤修复机制紧密相连。控制细胞因子诱导的过氧化物水平的抗氧化酶,如过氧化物还原酶(Prxs)和过氧化氢酶(CAT),参与DNA修复系统。我们之前证明,过表达PRL-1(PRL-1(+))的胎盘来源间充质干细胞(PD-MSCs)通过在TAA损伤的肝脏中发挥抗氧化作用来促进肝脏再生。然而,这些细胞在再生中的功效以及Prxs在其DNA修复系统中的作用尚未见报道。因此,我们的目的是分析未处理或PRL-1(+)移植的TAA损伤大鼠肝脏中基于Prx的DNA修复机制。与非移植(NTx)组相比,PRL-1(+)移植组的凋亡细胞数量显著减少(p < 0.05)。与NTx细胞相比,PRL-1(+)细胞中抗氧化标志物的表达显著增加(p < 0.05)。MitoSOX和Prx3表现出显著的负相关系数(R2 = -0.8123)。此外,与NTx细胞相比,PRL-1(+)细胞中的DNA损伤标志物水平显著降低(p < 0.05)。总之,PRL-1(+)细胞中Prx3水平的升高在TAA损伤的肝病中产生有效的抗氧化作用,并且Prx3也参与修复受损的DNA。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e7ca/9855122/4f8b8977df2c/antioxidants-12-00046-g001.jpg

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