Liang Hai, Yang Miao, Zeng Cheng, Wu Wei, Zhao Liying, Wang Yu
Department of Pharmacy, The People's Hospital of Bozhou, Bozhou, Anhui Province, China.
Department of Neurology, The People's Hospital of Bozhou, Bozhou, Anhui Province, China.
PeerJ. 2021 Jan 8;9:e10644. doi: 10.7717/peerj.10644. eCollection 2021.
Perfluorooctane sulfonate (PFOS), a type of perfluorinated compounds (PFCs), can induce various organ toxicity, including hepatomegaly, immunotoxicity, and gut microbiota disorder. PFCs have been associated with inflammatory bowel disease (IBD). Yet, whether PFOS exposure causes IBD-like disorder and the underlying mechanism remains undefined. Here, we investigated the influence of PFOS exposure on the development of IBD-like disorder in rats.
Sprague-Dawley rats were intraperitoneally injected with PFOS (1 or 10 mg/kg) or normal saline (NS) every other day for 15 days. Body weight, serum concentrations of serum amyloid A (SAA) and high sensitivity C reactive protein (hsCRP) were measured. Pathological assessments of villi height and crypt depth in the proximal duodenum and jejunum were performed using H&E staining. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining was used to assay cell apoptosis in the jejunum. The infiltration of inflammatory cells and cytokines in the jejunum were detected by immunohistochemistry analysis.
PFOS (10 mg/kg) significantly increased the body weight, SAA and hsCRP, whereas no significant differences were observed in PFOS 1 mg/kg group of rats. The villi height and crypt depth in the proximal duodenum and jejunum were significantly reduced upon PFOS exposure. PFOS induced higher histopathological score in intestinal tissues compared to NS. Notably, TUNEL-positive cells were significantly higher in the jejunum upon PFOS exposure. Further, neutrophil and macrophage accumulated, and inflammatory cytokines infiltration were also remarkably increased in rats exposed to PFOS.
PFOS induces IBD-like phenotypes in rats, with associated inflammatory infiltration to intestinal.
全氟辛烷磺酸（PFOS）是一种全氟化合物（PFCs），可诱发多种器官毒性，包括肝肿大、免疫毒性和肠道微生物群紊乱。PFCs与炎症性肠病（IBD）有关。然而，PFOS暴露是否会导致类似IBD的疾病及其潜在机制仍不明确。在此，我们研究了PFOS暴露对大鼠类似IBD疾病发展的影响。
将Sprague-Dawley大鼠每隔一天腹腔注射PFOS（1或10mg/kg）或生理盐水（NS），共15天。测量体重、血清淀粉样蛋白A（SAA）和高敏C反应蛋白（hsCRP）的血清浓度。使用苏木精-伊红（H&E）染色对十二指肠近端和空肠的绒毛高度和隐窝深度进行病理评估。采用末端脱氧核苷酸转移酶dUTP缺口末端标记（TUNEL）染色法检测空肠细胞凋亡。通过免疫组织化学分析检测空肠中炎症细胞和细胞因子的浸润情况。
PFOS（10mg/kg）显著增加了体重、SAA和hsCRP，而在PFOS 1mg/kg组大鼠中未观察到显著差异。PFOS暴露后，十二指肠近端和空肠的绒毛高度和隐窝深度显著降低。与NS相比，PFOS诱导肠道组织的组织病理学评分更高。值得注意的是，PFOS暴露后空肠中TUNEL阳性细胞显著增多。此外，暴露于PFOS的大鼠中性粒细胞和巨噬细胞积聚，炎症细胞因子浸润也显著增加。
PFOS在大鼠中诱导出类似IBD的表型，并伴有肠道炎症浸润。
