Gharieb Katia, Doumandji Nezli, Bensalem Wafa, Bellon Rachel Paul, Inoubli Lilia, Siddeek Bénazir, Traverse-Glehen Alexandra, Decaussin-Petrucci Myriam, Trabucchi Michele, Benahmed Mohamed, Mauduit Claire
Institut National de la Santé et de la Recherche Médicale, Unité 1065, Centre Méditerranéen de Médecine Moléculaire (C3M), Team 10, Nice F-06204, France; Université de Nice Sophia-Antipolis, Unité de Formation et de Recherche (UFR) Médecine, Nice F-06000, France.
Université Lyon 1, UFR Médecine Lyon Sud, Lyon F-69921, France; Hospices Civils de Lyon, Hopital Lyon Sud, Laboratoire d'Anatomie et de Cytologie Pathologiques, Pierre-Bénite F-69495, France.
Toxicol Lett. 2024 Dec;402:1-14. doi: 10.1016/j.toxlet.2024.10.001. Epub 2024 Oct 3.
Increasing number of studies suggested that environmental deleterious impacts (such as estrogen-like endocrine disruptors, EDCs, unhealthy diet) during early human development affect the risk of developing non-communicable diseases including prostate cancer (PCa) later in life. To test if the combination of EDCs and unhealthy induces adult prostate lesions, we developed an experimental model of adult male Sprague Dawley rats exposed during gestation (from day 7) to weaning to high fat diet (HFD 60 % fat), or to a xenoestrogen (estradiol benzoate, EB, 2.5 µg/d) from post-natal days 1-5, or to a combination of both. EB and EB+HFD exposures induced decreased prostate weight in adult rats along with inflammatory status. A white blood cell infiltrate was observed after EB exposure and more dramatic lesions were observed with the combined exposure, along with a gland destruction. The lesions, following EB or EB+HFD exposure, are associated with elevated mRNA levels for TNFa, IL6 and CCL2/MCP1 pro-inflammatory cytokines while the levels of the anti-inflammatory IL10 cytokine remained unchanged. This activation of NLRP3 and elevated levels of CASP1 were observed following EB or EB+HFD exposures associated with elevated mRNA levels for IL1b, substrates for the NLRP3 complex. HFD exposure alone has mild if not pro-inflammatory effects in adult prostate. In conclusion, we showed that developmental combined exposure to EB and HFD programmed prostate inflammatory lesions in adult prostate. Since proliferative inflammatory atrophy and chronic inflammation of prostate may drive cell to become cancer cells, our model might be useful for study onset of PCa.
越来越多的研究表明,人类早期发育过程中的环境有害影响(如雌激素样内分泌干扰物、内分泌干扰化学物质、不健康饮食)会影响日后患包括前列腺癌(PCa)在内的非传染性疾病的风险。为了测试内分泌干扰化学物质和不健康因素的组合是否会诱发成年前列腺病变,我们建立了一个成年雄性斯普拉格-道利大鼠的实验模型,使其在妊娠期(从第7天开始)到断奶期间暴露于高脂肪饮食(60%脂肪的HFD),或在出生后第1 - 5天暴露于一种外源性雌激素(苯甲酸雌二醇,EB,2.5μg/d),或同时暴露于两者。EB和EB + HFD暴露导致成年大鼠前列腺重量减轻以及炎症状态。EB暴露后观察到白细胞浸润,联合暴露时观察到更严重的病变,同时伴有腺体破坏。EB或EB + HFD暴露后的病变与促炎细胞因子TNFa、IL6和CCL2/MCP1的mRNA水平升高有关,而抗炎细胞因子IL10的水平保持不变。在与IL1b(NLRP3复合物的底物)的mRNA水平升高相关的EB或EB + HFD暴露后,观察到NLRP3的这种激活和CASP1水平升高。单独的HFD暴露对成年前列腺即使没有促炎作用也有轻微影响。总之,我们表明发育过程中联合暴露于EB和HFD会使成年前列腺发生前列腺炎性病变。由于前列腺的增殖性炎性萎缩和慢性炎症可能会促使细胞变成癌细胞,我们的模型可能有助于研究前列腺癌的发病机制。