Abstract
Colorectal cancer is a very prevalent diagnosed cancer. The current study was performed in order to examine the role of BRAE (Basella rubra aqueous extract) in regulating aberrant crypt foci (ACF) formation, cell proliferation and inhibition of apoptosis in a colon carcinogenesis model in male Wistar rats. Rats were randomly allocated into six groups. Group I served as control, and group II acted as a drug control administered BRAE (250mg/kg b.w.) orally for 30 weeks. Rats in group III-VI were given subcutaneous injections of DMH (25mg/kg b.w. weekly) for 15 weeks to initiate colon carcinogenesis. Those in group IV and VI were administered BRAE along with DMH injections. Rats in group V were administered with BRAE after cessation of DMH injection. After 30 weeks of experimental period colons were obtained from experimental groups and analyzed for ACF incidence, argyrophilic nucleolar organizing region- associated proteins (AgNOR) count, histopathological and immunohistochemical changes. Only in DMH exposed groups were ACF and AgNOR numbers increased. Administration of BRAE appreciably decreased the numbers of ACF and AgNOR in BRAE treated groups. Histopathological findings revealed a high level of dysplastic changes with decreased number of goblet cells found only in only DMH injected rats. Administration of BRAE in treated group rats reversed these changes. Expression markers for cell proliferation (PCNA and Ki67) were elevated in DMH treated rats, but reduced with BRAE treatement. This expression was reversed with apoptosis markers (p53 and Caspase-3). Thus the results results of the present study were found to be significant and confirmed the potential efficacy of BRAE against colon carcinogenesis.
Highlights
Colorectal cancer is the third most diagnosed cancer and it is a prime cause of morbidity and mortality in worldwide (Gellad et al, 2010; American Cancer Society, 2014)
The current study was performed in order to examine the role of BRAE (Basella rubra aqueous extract) in regulating aberrant crypt foci (ACF) formation, cell proliferation and inhibition of apoptosis in a colon carcinogenesis model in male Wistar rats
Humans exposed to hydrazine derivatives through environmental pollution and food contamination in day to day life (Ratasark et al, 2014). 1, 2-dimethylhydrazine (DMH) is an environment pollutant and eminent experimental model to study the pathogenesis of colon cancer in rodents
Summary
Colorectal cancer is the third most diagnosed cancer and it is a prime cause of morbidity and mortality in worldwide (Gellad et al, 2010; American Cancer Society, 2014). 1, 2-dimethylhydrazine (DMH) is an environment pollutant and eminent experimental model to study the pathogenesis of colon cancer in rodents. This animal model resembles the way of human exposure to environment carcinogen. Dimethylhydrazine is a cancer causing substance that has ability to induce the colon cancer It is a procarcinogen, metabolically activated in liver by a step wise reactions through intermediates like azoxymethane (AOM) and methylazoxy methane (MAM) and into carcinogenic metabolite methyldiazonium ion. Metabolically activated in liver by a step wise reactions through intermediates like azoxymethane (AOM) and methylazoxy methane (MAM) and into carcinogenic metabolite methyldiazonium ion This active carcinogen is transported to the colon via bile and blood. The formation of methyldiazonium ion in the body of rats induces DNA damage and mutations (Perse et al, 2011; Hamiza et al, 2012)
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