Inflammation- induced systemic stress plays an essential role in neoplastic progression. Chronic exposure to chemical carcinogens can induce persistent inflammatory changes which further augment loss in physiological hormesis of an organism thereby favouring carcinogenesis. The present study investigated the role of inflammation and associated systemic stress in the development of cervical carcinoma in a 3-methylcholanthrene (3-MC; a chemical carcinogen) induced in vivo cervical cancer model. When the cervix of 5-6 weeks old virgin female Swiss Albino mice (Mus musculus) was treated with 3-MC (0.6 mg/mL), remarkable alteration in its cervical cytopathology was observed. An increase in duration of 3-MC treatment caused an outburst in the number and variety of infiltrating granulocytes and agranulocytes in mice cervix. Thus, a high leukocyte index was indicative of prevalent cervical inflammatory changes. Elevated activities of SGPT, SGOT, serum alkaline phosphatase enzymes along with the presence of elevated serum creatinine levels suggested liver and renal dysfunctions. These observations were supported by alterations in hepatic histopathology of 3-MC treated mice. Surged activities and expression profiles of inflammatory cytokines (IL-6 and IL-8) in cervix tissue had conclusively established the crucial role played by inflammation- mediated systemic stress in favouring the development of cervical cancer in a carcinogen-induced in vivo model.

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炎症：致癌物诱发的子宫颈癌小鼠发展的主角

炎症诱导的系统性应激在肿瘤进展中起着至关重要的作用。长期暴露于化学致癌物可引起持续的炎症变化，从而进一步增加生物体的生理活力丧失，从而促进致癌作用。本研究调查了炎症和相关的系统性应激在3-甲基胆碱（3-MC；化学致癌物）诱导的体内宫颈癌模型中宫颈癌的发展中的作用。当用3-MC（0.6 mg / mL）处理5-6周龄的原始瑞士白化雌性小鼠（小家鼠）的子宫颈时，观察到子宫颈细胞病理学的显着改变。3-MC治疗时间的延长导致子宫颈浸润性粒细胞和粒细胞的数量和种类爆发。从而，白细胞指数高表明宫颈炎性变化普遍。SGPT，SGOT，血清碱性磷酸酶的活性升高，以及血清肌酐水平升高，提示肝和肾功能异常。这些观察得到3-MC治疗的小鼠肝组织病理学改变的支持。子宫颈组织中炎性细胞因子（IL-6和IL-8）的激增活性和表达谱已最终确定了炎症介导的系统性应激在致癌物诱导的体内模型中促进宫颈癌发展的关键作用。这些观察得到3-MC治疗的小鼠肝组织病理学改变的支持。子宫颈组织中炎性细胞因子（IL-6和IL-8）的激增活性和表达谱已最终确定了炎症介导的系统性应激在致癌物诱导的体内模型中促进宫颈癌发展的关键作用。这些观察得到3-MC治疗的小鼠肝组织病理学改变的支持。子宫颈组织中炎性细胞因子（IL-6和IL-8）的激增活性和表达谱已最终确定了炎症介导的系统性应激在致癌物诱导的体内模型中促进宫颈癌发展的关键作用。