Aim

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.

Materials and methods

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.

Key findings

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).

Significance

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.

中文翻译：

---

全反式视黄酸（ATRA）对苯并（a）芘诱导小鼠肺癌发生的炎症和COX-2基因表达的调节

目的

炎症为癌症的发展提供了有利的微环境。增强的 COX-2 基因表达是癌症的关键炎症介质和抑制它的药物，有助于有效控制癌症并提高存活率。目的是分析苯并 (a) 芘诱导小鼠的炎症变化和 COX-2 基因表达，并评估全反式维甲酸的调节作用。

材料和方法

在 B( a )P 诱导的小鼠中记录体重和器官重量。测试了血液学参数和致癌作用的血清炎症标志物。检查H&E染色的肝和肺组织的组织病理学变化。通过 RT-PCR 和 qPCR 在肺和肝脏中分析 COX-2 基因表达。

主要发现

在 B( a )P 诱导的小鼠中观察到体重下降、器官重量增加以及肝和肺损伤，并且在 ATRA 治疗后显着防止。在 B( a )P 组中观察到的 Hb、RBC 和淋巴细胞的降低以及 WBC、单核细胞和中性粒细胞的增加在治疗组中显着逆转。在 B( a )P 诱导的小鼠中观察到的癌症相关炎症标志物的急剧增加在治疗的小鼠中显着降低（P ≤ 0.001）。B( a )P组COX-2基因的RT-PCR产物密度非常高（肺-0.43±0.06；肝-0.39±0.04），治疗组（肺-0.12±0.03；肝-0.08±0.04）显着降低0.03) 与 RQ 值显着差异 (B( a)P 肺-18.46 ± 0.04，肝-12.46 ± 0.08；治疗肺 - 5.93 ± 0.07，肝 - 2.92 ± 0.10）。

意义

ATRA 通过下调 COX-2 基因表达降低了炎症状况，从而在 B( a )P 诱导的癌症发展的早期防止了致癌作用。