关键词: apoptosis inflammation oxidative stress peroxisome proliferator-activated receptor-α rabbit VX2 hepatic carcinoma transcatheter arterial embolization apoptosis inflammation oxidative stress peroxisome proliferator-activated receptor-α rabbit VX2 hepatic carcinoma transcatheter arterial embolization

来  源:   DOI:10.1515/biol-2022-0068   PDF(Pubmed)

Abstract:
Transcatheter arterial embolization (TAE) is a widely used technique in treating hepatic carcinoma but may cause liver injury in some cases. This study investigated the hepatoprotective effect of the preprocessed peroxisome proliferator-activated receptor-α (PPAR-α) agonist-WY-14643 following TAE. A total of 60 rabbit liver cancer models were developed and divided into a combined treatment (WY-14643 and TAE), TAE, and control groups. After TAE, we examined the histopathological picture and liver functions. Further, the expression of antioxidant enzymes, tumor necrosis factor-α (TNF-α), nuclear factor of κ-light chain of enhancer-activated B cells (NF-κB), PPAR-α, and B-cell lymphoma-2 (Bcl-2) was analyzed. Liver function tests, pathology score, and apoptosis index significantly worsened in the TAE group but were normalized in the combined treatment group. In addition, ELISA results showed that antioxidant enzyme activity significantly increased, while the malondialdehyde content and level of inflammatory cytokines were significantly reduced in the combined treatment group. Furthermore, compared to the TAE group, the expressions of PPAR-α, antioxidant enzymes superoxide dismutase1 (SOD1) and SOD2, and Bcl-2 were significantly elevated, while NF-κB was significantly reduced in the combined treatment group. On the other hand, the expression of NF-κB in tumor tissues was significantly reduced by pretreatment with WY-14643. Therefore, PPAR-α can ameliorate liver injury by exerting its anti-oxidative, anti-inflammatory, and anti-apoptotic functions.
摘要:
经导管动脉栓塞(TAE)是一种广泛用于治疗肝癌的技术,但在某些情况下可能会引起肝损伤。这项研究调查了TAE后预处理的过氧化物酶体增殖物激活受体-α(PPAR-α)激动剂-WY-14643的肝保护作用。共建立了60个兔肝癌模型,并分为联合治疗(WY-14643和TAE),TAE,和对照组。TAE后,我们检查了组织病理学图和肝功能。Further,抗氧化酶的表达,肿瘤坏死因子-α(TNF-α),增强子激活B细胞κ轻链核因子(NF-κB),PPAR-α,分析B细胞淋巴瘤-2(Bcl-2)。肝功能检查,病理学评分,TAE组细胞凋亡指数明显恶化,但联合治疗组细胞凋亡指数恢复正常。此外,ELISA结果显示,抗氧化酶活性显著提高,联合治疗组丙二醛含量和炎性细胞因子水平明显降低。此外,与TAE组相比,PPAR-α的表达式,抗氧化酶超氧化物歧化酶1(SOD1)和SOD2,以及Bcl-2显著升高,联合治疗组NF-κB显著降低。另一方面,WY-14643预处理后,肿瘤组织中NF-κB的表达明显降低。因此,PPAR-α可以通过发挥其抗氧化作用来改善肝损伤,抗炎,和抗凋亡功能。
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