Experimental design
40 rats were randomly divided into 4 groups: Control (untreated with carcinogen or MRN-100); MRN-100 treated (MRN-100-treated only), MNNG treated (carcinogen-treated only), and MNNG plus MRN-100 treated (MRN-100 and carcinogen-treated). In order to induce gastric/esophageal cancer, rats were given carcinogen MNNG at dose 200 mg/kg body weight once daily by oral gavage for 2 weeks, followed by oral administration of NaCl (1ml/rat) once every 3 days for 4 weeks. Concomitantly with chemical induction, the rats were given MRN-100-free water (groups 1 and 3) or MRN-100 water (groups 2 and 4) for a total of 33 weeks. All animals were weighed at different time intervals. At the end of experimental period (33 weeks), animals were killed and examined for the following: histopathological changes in the esophageal and gastric tissues, changes in the weight of livers and spleens, and redox status in the blood and stomach tissues.
Experimental design
40 rats were randomly divided into 4 groups: Control (untreated with carcinogen or MRN-100); MRN-100 treated (MRN-100-treated only), MNNG treated (carcinogen-treated only), and MNNG plus MRN-100 treated (MRN-100 and carcinogen-treated). In order to induce gastric/esophageal cancer, rats were given carcinogen MNNG at dose 200 mg/kg body weight once daily by oral gavage for 2 weeks, followed by oral administration of NaCl (1ml/rat) once every 3 days for 4 weeks. Concomitantly with chemical induction, the rats were given MRN-100-free water (groups 1 and 3) or MRN-100 water (groups 2 and 4) for a total of 33 weeks. All animals were weighed at different time intervals. At the end of experimental period (33 weeks), animals were killed and examined for the following: histopathological changes in the esophageal and gastric tissues, changes in the weight of livers and spleens, and redox status in the blood and stomach tissues.
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