Department of Biotechnology, Karunya Institute of Technology and Sciences, Coimbatore 641 114, Tamil Nadu, India.
School of Science, Arts, Media and Management, Karunya Institute of Technology and Sciences, Coimbatore 641 114, Tamil Nadu, India.
Life Sci. 2021 Nov 15;285:119967. doi: 10.1016/j.lfs.2021.119967. Epub 2021 Sep 17.
Inflammation provides favourable microenvironment for cancer development. An enhanced COX-2 gene expression is a key inflammatory mediator of cancers and the drug that inhibits it, helps to manage cancer effectively and increases survival rate. The objective is to analyse the inflammatory changes and COX-2 gene expression in benzo (a) pyrene induced mice and to evaluate the regulatory effect of all trans retinoic acid.
The body and organ weights were recorded in B(a)P induced mice. The haematological parameters and serum inflammatory markers of carcinogenesis were tested. The H & E stained liver and lung tissues were examined for histopathologic changes. The COX-2 gene expression was analysed by RT-PCR and qPCR in lung and liver.
The decreased body weight, increased organ weights and the damages in liver and lung were observed in B(a)P induced mice and were prevented significantly upon ATRA treatment. The lowered Hb, RBC and lymphocytes and an enhanced WBC, monocytes and neutrophils observed in B(a)P group were significantly reversed in treated group. A drastic increase in cancer associated inflammatory markers observed in B(a)P induced mice were significantly (P ≤ 0.001) reduced in treated mice. The RT-PCR product density of COX-2 gene was very high in B(a)P group (lung-0.43 ± 0.06; liver-0.39 ± 0.04) significantly lower in treated group (lung-0.12 ± 0.03; liver-0.08 ± 0.03) with a significant difference in RQ values (B(a)P lung-18.46 ± 0.04, liver-12.46 ± 0.08; treated lung-5.93 ± 0.07, liver-2.92 ± 0.10).
The ATRA has decreased the inflammatory condition with downregulation of COX-2 gene expression and thereby prevented carcinogenesis during early stage of B(a)P induced cancer development.
炎症为癌症的发展提供了有利的微环境。COX-2 基因表达增强是癌症的关键炎症介质，而抑制其表达的药物有助于有效管理癌症并提高存活率。本研究旨在分析苯并（a）芘诱导的小鼠的炎症变化和 COX-2 基因表达，并评估全反式维甲酸的调节作用。
记录苯并（a）芘诱导的小鼠的体重和器官重量。检测致癌过程中的血液学参数和血清炎症标志物。用 H&E 染色检查肝和肺组织的组织病理学变化。通过 RT-PCR 和 qPCR 分析肺和肝组织中的 COX-2 基因表达。
在苯并（a）芘诱导的小鼠中观察到体重减轻、器官重量增加以及肝和肺损伤，而 ATRA 治疗可显著预防这些损伤。在苯并（a）芘组中观察到的 Hb、RBC 和淋巴细胞降低以及 WBC、单核细胞和中性粒细胞升高在治疗组中得到显著逆转。在苯并（a）芘诱导的小鼠中观察到的与癌症相关的炎症标志物显著（P≤0.001）降低在治疗组中。COX-2 基因的 RT-PCR 产物密度在苯并（a）芘组中非常高（肺 0.43±0.06；肝 0.39±0.04），在治疗组中显著降低（肺 0.12±0.03；肝 0.08±0.03），RQ 值有显著差异（苯并（a）芘肺 18.46±0.04，肝 12.46±0.08；治疗肺 5.93±0.07，肝 2.92±0.10）。
ATRA 降低了炎症状态，下调了 COX-2 基因表达，从而在苯并（a）芘诱导的癌症发展早期预防了癌症发生。
