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                    "value": "p- Methoxycinnamic acid (p-MCA), an active phenolic compound derived from the rice bran, turmeric and Kaempferia galangal, is known to exhibit numerous pharmacological properties. We investigated that chemopreventive effect of p-MCA against N-nitrosodiethylamine (NDEA) induced hepatocarcinogenesis in male wistar rats. Rats were subjectively divided into five groups. Group 1 served as control and was fed modified pellet diet and water. Group 2 received the reference drug (Sorafenib [11.4 mg/kg b.w]). Group 3, 4 and 5 rats received the hepatocarcinogen (NDEA) intraperitoneally in addition to 2-acetylaminofluorene (AAF) as promotor. In addition group 4 rats received p-MCA at the dose of 80 mg/kg b.w. and group 5 rats received sorafenib at the dose of 11.4 mg/kg b.w throughout the experimental period. Our results established that supplementation with p-MCA and the reference drug (sorafenib) to NDEA induced rats significantly decreased the incidence of cancer in the liver, besides altering the phase I and phase II xenobiotic enzymes. Furthermore the increased expressions of collagen, lipid and glycogen accumulation observed in NDEA alone-induced rats were comparable with those of the control rats, p-MCA and sorafenib alone treated rats. Our results proved that p-MCA was equally effective that of the reference drug sorafenib (which is used currently for the treatment of hepatocellular carcinoma against NDEA induced hepatocarcinogenesis",
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                    "value": "p- Methoxycinnamic acid (p-MCA), an active phenolic compound derived from the rice bran, turmeric and Kaempferia galangal, is known to exhibit numerous pharmacological properties. We investigated that chemopreventive effect of p-MCA against N-nitrosodiethylamine (NDEA) induced hepatocarcinogenesis in male wistar rats. Rats were subjectively divided into five groups. Group 1 served as control and was fed modified pellet diet and water. Group 2 received the reference drug (Sorafenib [11.4 mg/kg b.w]). Group 3, 4 and 5 rats received the hepatocarcinogen (NDEA) intraperitoneally in addition to 2-acetylaminofluorene (AAF) as promotor. In addition group 4 rats received p-MCA at the dose of 80 mg/kg b.w. and group 5 rats received sorafenib at the dose of 11.4 mg/kg b.w throughout the experimental period. Our results established that supplementation with p-MCA and the reference drug (sorafenib) to NDEA induced rats significantly decreased the incidence of cancer in the liver, besides altering the phase I and phase II xenobiotic enzymes. Furthermore the increased expressions of collagen, lipid and glycogen accumulation observed in NDEA alone-induced rats were comparable with those of the control rats, p-MCA and sorafenib alone treated rats. Our results proved that p-MCA was equally effective that of the reference drug sorafenib (which is used currently for the treatment of hepatocellular carcinoma against NDEA induced hepatocarcinogenesis",
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