SAC and Berberine Mediated Repression of Reactive Species and Hepatoprotection After DEN + CCl4 Exposure
Oxidative stress is proposed to play a pivotal role in the development of hepatocellular carcinoma. With an accelerated metabolism cancer cells demand high reactive species accumulation to maintain their indiscriminate cell growth and proliferation. Here we wanted to see the status of reactive speci...
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Published in | Proceedings of the Zoological Society Vol. 70; no. 1; pp. 28 - 41 |
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Main Authors | , , , , , , , , , |
Format | Journal Article Conference Proceeding |
Language | English |
Published |
New Delhi
Springer India
01.06.2017
Springer Nature B.V |
Subjects | |
Online Access | Get full text |
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Summary: | Oxidative stress is proposed to play a pivotal role in the development of hepatocellular carcinoma. With an accelerated metabolism cancer cells demand high reactive species accumulation to maintain their indiscriminate cell growth and proliferation. Here we wanted to see the status of reactive species in the chemically induced liver cancer. For this purpose swiss albino mice were exposed to DEN and CCl
4
to develop an in vivo model of hepatocarcinoma. Depletion of cellular antioxidants regulated accretion of reactive species during the development of DEN + CCl
4
induced tumor formation in hepatocytes. Currently available therapeutics for heptatocellular carcinoma is costly and coupled with certain bystander effects to the surrounding control cells. Therefore considering the antioxidant properties of SAC and berberine we treated DEN + CCl
4
exposed mice after the development of liver tumor. Results effectively pointed out the usefulness of the alternative treatment with SAC and berberine in hepatoprotection. Replenishment of both enzymatic and non enzymatic antioxidant efficiently reduced accumulation of reactive species and that eventually closely associated with effective reduction in tumor number and size after drug treatment in DEN + CCl
4
exposed mice. |
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Bibliography: | ObjectType-Article-1 ObjectType-Feature-2 SourceType-Conference Papers & Proceedings-1 content type line 22 |
ISSN: | 0373-5893 0974-6919 |
DOI: | 10.1007/s12595-015-0156-5 |