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Kirenol regulates the cell proliferative and inflammatory markers in DMBA ‐induced oral squamous cell carcinogenesis in hamster
Environmental Toxicology ( IF 4.5 ) Pub Date : 2020-10-12 , DOI: 10.1002/tox.23039
Yunzhen Deng 1, 2 , Min Ma 1, 2 , Gang Guo 3 , Zhen Tang 4
Affiliation  

This present findings hypothesized the modulatory effects of kirenol on expression pattern of cell proliferative and inflammatory markers during DMBA induced HBP carcinogenesis. The machinery pathways for chemomodulatory effect of kirenol was investigated by analyzing the levels of antioxidants histological changes, lipid peroxidation and molecular expression pathway of PCNA, NF-κB in the DMBA only painted HBPC. Oral cancer was developed in the HBP model by DMBA (0.5%) three times a week for 14th weeks. We analyzed body weight with deregulated molecular expressions pattern of PCNA and NF-κB was noticed in the DMBA induced hamsters compared to control hamsters. Oral administration of kirenol 30 mg/kg bw, to DMBA induced hamster models reverted the activity of the biochemical markers in Group 4. Besides, tumor tissues of hamsters receive antioxidant capability from kirenol exclaimed significant modifications in DMBA induced causes: inhibits cell proliferation (inhibits PCNA expression) and suppresses inflammation (decreased NF-κB expression) of markers. Taken together, the protective effect of that kirenol an augmenting inflammation of the started cells and exhibited antiproliferative, anti-inflammatory, antilipid peroxidative and restores the xenobiotic enzymes levels (phase I and II) system and enhances antioxidant properties in oral carcinoma hamsters, in which turn, is reflected diminished tumor burden, volume, and multiplicity.

中文翻译:

Kirenol 调节 DMBA 诱导的仓鼠口腔鳞状细胞癌变中的细胞增殖和炎症标志物

本研究结果假设在 DMBA 诱导的 HBP 致癌过程中,kirenol 对细胞增殖和炎症标志物的表达模式具有调节作用。通过分析仅涂有HBPC的DMBA中抗氧化剂的组织学变化水平、脂质过氧化水平和PCNA、NF-κB的分子表达途径,研究了kirenol化学调节作用的机制途径。DMBA (0.5%) 每周 3 次,持续第 14 周在 HBP 模型中发展为口腔癌。我们分析了 PCNA 分子表达失调的体重,并且与对照仓鼠相比,在 DMBA 诱导的仓鼠中注意到了 NF-κB。向 DMBA 诱导的仓鼠模型口服 30 毫克/千克体重的 kirenol 恢复了第 4 组中生化标志物的活性。此外,仓鼠的肿瘤组织从 kirenol 获得抗氧化能力惊呼 DMBA 诱导原因的显着改变:抑制细胞增殖(抑制 PCNA 表达)并抑制炎症(降低 NF-κB 表达)标志物。总之,kirenol 的保护作用增强了起始细胞的炎症,并表现出抗增殖、抗炎、抗脂质过氧化和恢复异生素酶水平(I 期和 II 期)系统并增强口腔癌仓鼠的抗氧化特性,其中反过来,反映了肿瘤负荷、体积和多样性的减少。
更新日期:2020-10-12
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