Abstract
This study aimed to characterize an animal model of colorectal cancer (CRC) in the early stages of disease development. Twenty-nine male Wistar rats were divided into two control groups (CTRL1 and CTRL2), receiving EDTA–saline injections and two induced groups (CRC1 and CRC2), receiving 1,2-dimethylhydrazine (DMH) injections for seven consecutive weeks. CRC1 and CTRL1 were euthanized at the 11th week, while CRC2 and CTRL2 were euthanized at the 17th week. DMH treatment decreased microhematocrit values and IL-6, ghrelin, and myostatin serum levels. Histopathological analysis of intestinal sections showed that DMH-treated rats were characterized by moderate to severe epithelial dysplasia. An adenoma was observed in one animal (CRC2 group), and the presence of inflammatory infiltrate at the intestinal level was primarily observed in DMH-treated animals. DMH also induced Ki-67 immunoexpression. The gut microbiota analysis showed a higher abundance of Firmicutes, Clostridia, Clostridiales, Peptostreptococcaceae, Blautia, Romboutsia, and Clostridium sensu stricto in CRC than CTRL rats, whereas Prevotellaceae, Prevotella, Akkermansia, and Lactobacillus levels were more prevalent in CTRL animals. Our results suggest that this model could be helpful to investigate chemoprevention in the early stages of CRC.
Highlights
colorectal cancer (CRC) is the third most common cancer and the second leading cause of cancer death worldwide, with an estimated 935,173 deaths in 2020 [1]
There were no significant variations in body weight, food, or water intake among groups (p > 0.05)
The cecum relative weight of the CRC2 group was considerably higher compared with CTRL groups (p < 0.01)
Summary
CRC is the third most common cancer and the second leading cause of cancer death worldwide, with an estimated 935,173 deaths in 2020 [1]. Most CRC cases are caused by Biomedicines 2022, 10, 409. Biomedicines 2022, 10, 409 random mutations, whereas others are caused by known genetic alterations [2]. The CRC high mortality rate can be linked to a lack of understanding of the potential of animal models available for its research and, their underuse [3]. The available animal models of CRC have been used for more than eight decades to better understand the molecular events involved and evaluate the efficacy of many treatments [4]. An integrative and complementary approach is needed, which will provide a better characterization and understanding of the model, with potentially more conclusive benefits for CRC patients [11,12]
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