Prevention by acetylsailcylic acid of liver cirrhosis and carcinogenesis as well as generations of 8-hydroxydeoxyguanosine and thiobarbituric acid-reactive substances caused by a choline-deficient, L-amino acid-defined diet in rats |
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Authors: | Denda, Ayumi Tang, Qing Endoh, Takehiro Tsujiuchi, Toshifumi Horiguchi, Kohsuke Noguchi, Osamu Mizumoto, Yasushi Nakae, Dai Konishi, Yoichi |
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Affiliation: | Department of Oncological Pathology, Cancer Center, Nara Medical University 840 Shijo-cho, Kashihara, Nara 634, Japan 1Present address: Department of Pathology, Basic Medical Science Institute Heping-qu, Shenyang, Liaoning, China |
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Abstract: | Effects of acetylsailcylic acid (ASA) (aspirin) on the pathogenesisof fatty liver, cirrhosis and hepatocarcinogenesis caused bya choline-deficient L-amino acid-defined (CDAA) diet were examinedin male Fischer 344 rats fed a CDAA diet supplemented with 0,0.1, 0.2, 0.4 or 0.8% ASA for 30 weeks. ASA at concentrationsof >0.2% prevented the development of both cirrhosis andpreneoplastic and neoplastic nodules, but without any directlyassociated prevention of fatty changes. ASA also prevented hepatocyteproliferation and the generation of thiobarbituric acid-reactivesubstances and 8-hydroxydeoxyguanosine caused by feeding theCDAA diet, analyzed, respectively, after 1, 12 and 12 weeks.The results clearly indicate that the anti-inflammatory drugASA, which is not a lipotropic factor, can prevent the pathogenesisof cirrhosis and hepatocarcinogenesis caused by a CDAA diet,which is possibly partly associated with the prevention of reactiveoxygen species production. |
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