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12. Curcumin prevents alcohol-induced liver disease in rats by inhibiting the expression of NF-[kappa]B-dependent genes

Author

Nanji, Amin A., Jokelainen, Kalle, Tipoe, George L., Rahemtulla, Amir, Thomas, Peter, and Dannenberg, Andrew J.

Subjects
Cytochemistry -- Research, Drinking age -- Physiological aspects, Liver cirrhosis -- Care and treatment, Liver cirrhosis -- Genetic aspects, Antioxidants -- Usage, Cyclooxygenases -- Physiological aspects, Nitric oxide -- Physiological aspects, Liver diseases -- Genetic aspects, Liver diseases -- Physiological aspects, Liver diseases -- Prevention, Endotoxins -- Physiological aspects, Turmeric -- Physiological aspects, Biological sciences
Abstract

Induction of NF-[kappa]B-mediated gene expression has been implicated in the pathogenesis of alcoholic liver disease (ALD). Curcumin, a phenolic antioxidant, inhibits the activation of NF-[kappa]B. We determined whether treatment with curcumin would prevent experimental ALD and elucidated the underlying mechanism. Four groups of rats (6 rats/group) were treated by intragastric infusion for 4 wk. One group received fish oil plus ethanol (FE); a second group received fish oil plus dextrose (FD). The third and fourth groups received FE or FD supplemented with 75 mg. [kg.sup.-]*[day.sup.-] of curcumin. Liver samples were analyzed for histopathology, lipid peroxidation, NF-[kappa]B binding, TNF-[alpha], IL-12, monocyte chemotactic protein-I, macrophage inflammatory protein-2, cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and nitrotyrosine. Rats fed FE developed fatty liver, necrosis, and inflammation, which was accompanied by activation of NF-[kappa]B and the induction of cytokines, chemokines, COX-2, iNOS, and nitrotyrosine formation. Treatment with curcumin prevented both the pathological and biochemical changes induced by alcohol. Because endotoxin and the Kupffer cell are implicated in the pathogenesis of ALD, we investigated whether curcumin suppressed the stimulatory effects of endotoxin in isolated Kupffer cells. Curcumin blocked endotoxin-mediated activation of NF-[kappa]B and suppressed the expression of cytokines, chemokines, COX-2, and iNOS in Kupffer cells. Thus curcumin prevents experimental ALD, in part by suppressing induction of NF-[kappa]B-dependent genes. antioxidants; cyclooxygenase; nitric oxide

Published
2003

17. Increased severity of alcoholic liver injury in female rats: role of oxidative stress, endotoxin, and chemokines

Author

Nanji, Amin A., Jokelainen, Kalle, Fotouhinia, Maryam, Rahemtulla, Amir, Thomas, Peter, Tipoe, George L., Su, Grace L., and Dannenberg, Andrew J.

Subjects
Oxidation, Physiological -- Research, Endotoxins -- Physiological aspects, Cytokines -- Physiological aspects, Liver -- Necrosis, Liver diseases -- Physiological aspects, Biological sciences
Abstract

Nanji, Amin A., Kalle Jokelainen, Maryam Fotouhinia, Amir Rahemtulla, Peter Thomas, George L. Tipoe, Grace L. Su, and Andrew J. Dannenberg. Increased severity of alcoholic liver injury in female rats: role of oxidatire stress, endotoxin, and chemokines. Am J Physiol Gastrointest Liver Physiol 281: G1348-G1356, 2002.--Alcoholic liver injury is more severe and rapidly developing in women than men. To evaluate the reason(s) for these gender-related differences, we determined whether pathogenic mechanisms important in alcoholic liver injury in male rats were further upregulated in female rats. Male and age-matched female rats (7/group) were fed ethanol and a diet containing fish oil for 4 wk by intragastric infusion. Dextrose isocalorically replaced ethanol in control rats. We analyzed liver histopathology, lipid peroxidation, cytochrome P-450 (CYP)2E1 activity, nonheme iron, endotoxin, nuclear factor-KB (NF-[kappa]B) activation, and mRNA levels of cyclooxygenase-1 (COX-1) and COX-2, tumor necrosis factor-[alpha] (TNF-[alpha]), monocyte chemotactic protein-1 (MCP-1), and macrophage inflammatory protein-2 (MIP-2). Alcohol-induced liver injury was more severe in female vs. male rats. Female rats had higher endotoxin, lipid peroxidation, and nonheme iron levels and increased NF-[kappa]B activation and upregulation of the chemokines MCP-1 and MIP-2. CYP2E1 activity and TNF-[alpha] and COX-2 levels were similar in male and female rats. Remarkably, female rats fed fish oil and dextrose also showed necrosis and inflammation. Our findings in ethanol-fed rats suggest that increased endotoxemia and lipid peroxidation in females stimulate NF-[kappa]B activation and chemokine production, enhancing liver injury. TNF-[alpha] and COX-2 upregulation are probably important in causing liver injury but do not explain gender-related differences. cytokines; cyclooxygenase-2; tumor necrosis factor-[alpha]

Published
2001

21. CONTRIBUTORS

Author

Abel, Ernest, primary, Acquaah-Mensah, George, additional, Adachi, Junko, additional, Addolorato, Giovanni Gasbarrini, additional, Aertgeerts, Bert, additional, Ahlgren, Sara, additional, Albano, Emanuele, additional, Albertsen, Katrine, additional, Albrecht, Jan, additional, Allen, Jeffrey W., additional, Allison, Paul, additional, Ammendola, Angelo, additional, Ancona, Carlo, additional, Arteel, Gavin E., additional, Arun, C.P., additional, Aschner, Michael, additional, Avogaro, Angelo, additional, Badawy, A.A.-B., additional, Bailey, Shannon M., additional, Barak, A.J., additional, Barefoot, John, additional, Barnett, Nancy P., additional, Batey, R.G., additional, Bautista, Abraham P., additional, Beauvieux, M.C., additional, Becker, Ulrik, additional, Beilin, Lawerence J., additional, Bell, Richard L., additional, Berry, K., additional, Bertelli, A.A.E., additional, Blondell, Richard D., additional, Bonthius, Daniel J., additional, Borges, Adrian, additional, Bosco, Cleofina, additional, Boughton, Robert, additional, Braulio, Valeria Bender, additional, Bravaccio, Francesco, additional, Braun, Jan, additional, Brecher, Arthur S., additional, Breese, George R., additional, Brooks, P.J., additional, Bu, Eli Torild Hellandsjo, additional, Bunout, Daniel, additional, Campbell, Stewart, additional, Campillo, Bernard, additional, Cao, Q., additional, Capristo, Esmeralda, additional, Carey, K.B., additional, Casey, Carol A., additional, Castellon, Steven A., additional, Castro, Jose A., additional, Castro, Gerardo, additional, Çelik, Y., additional, Chambers, Christina D., additional, Chambers, Geoff K., additional, Chandra, Dev, additional, Cheever, Laura W., additional, Cherpitel, C.J., additional, Cheung, Connie, additional, Clark, Duncan B., additional, Clark, Colleen, additional, Clemens, Dahn L., additional, Conigliaro, Joseph, additional, Conigrave, Katherine M., additional, Constantinescu, Anastasia, additional, Cook, Jocelyn L., additional, Cornier, M-A., additional, Couch, David B., additional, Covas, María Isabel, additional, Crampton, James A., additional, Criswell, H.E., additional, Dammann, Gerhard, additional, Davidge, S.T., additional, Day, Darren, additional, de Gaetano, G., additional, De la Maza, María Pía, additional, Di Castelnuovo, A., additional, Dierkes, Jutta, additional, Donohue, Terrence M., additional, Douglas, Tania, additional, Dudley, Robert, additional, Duggal, M., additional, Dulli, D.A., additional, Egerer, Gerlinde, additional, Ellingson, John S., additional, Enomoto, Nobuyuki, additional, Estruch, Romon, additional, Fabbri, Andrea, additional, Farrés, Jaume, additional, Fernández-Solà, Joaquim, additional, Federico, Alessandro, additional, Fiellin, David A., additional, Fink, A., additional, Freeman, W.M., additional, French, Samuel W., additional, Frost, Robert A., additional, Gallis, J.L., additional, Gao, B., additional, Gasbarrini, Giovanni, additional, Geraghty, Madeleine C., additional, Gibson, Chris L., additional, Gonzàlez-Reimers, Emilio, additional, Gooch, R.S., additional, Gordon, Adam J., additional, Grau, Joseph-Maria, additional, Gray, M.O., additional, Grobbee, Diederick E, additional, Grønbæk, Morten, additional, Grubwieser, Petra, additional, Haas, Michael J., additional, Haas, Stefan L., additional, Haber, P.S., additional, Hasin, Deborah, additional, Hendriks, Henk F.J., additional, von Heymann, Christian, additional, Higgins, Elisabeth, additional, Hinkin, Charles H., additional, Hirsch, Sandra, additional, Homanics, Gregg E., additional, Hunter, Ross J., additional, Hustad, John T.P., additional, Kahrberg, Ana M. Hutton, additional, Ikejima, Kenichi, additional, Izevbigie, Ernest B., additional, Jain, Hitender, additional, Kalant, Harold, additional, Kesmodel, Ulrik, additional, Kharbanda, Kusum K., additional, Kitamura, Tsuneo, additional, Klapp, Burghard F., additional, Kox, Wolfgang, additional, Kresina, T.F., additional, Kroke, Anja, additional, Ladero, José María, additional, Lambert, Jason C., additional, Lang, Charles H., additional, Laposata, M., additional, Lebeau-Craven, Rebecca, additional, Levine, Andrew J., additional, Lieber, Charles S., additional, Loguercio, Carmela, additional, Lunetta, Philippe, additional, Marchesini, Giulio, additional, Marshall, Stephen J., additional, Martin, Colin R., additional, Martìnez, Susana E., additional, McBride, William J., additional, McKim, Ross A., additional, McVicker, Benita L., additional, Meintjes, Ernesta M., additional, Meurman, Jukka H., additional, Mezzani, Laura, additional, Miller, J. Mitchell, additional, Miñana, Juan Bautista, additional, Mitton, Kenneth P., additional, Mühlbauer, Eckhard, additional, Murata, M., additional, Murphy, James, additional, Murphy, James M., additional, Nakahara, Tatsuo, additional, Nanji, Amin A., additional, Nath, Raghu G., additional, Nemtsov, A.V., additional, Nicolás, Josep–María, additional, Nushida, Hideyuki, additional, Ogurtsov, P.P., additional, Okamura, Tomonori, additional, Pallardo, Federico V., additional, Pantazis, Nicholas J., additional, Parés, Xavier, additional, Parlesak, Alexandr, additional, Patussi, Valentino, additional, Pavlic, Marion, additional, Pease, Camilla K., additional, Peng, Giia-Sheun, additional, Piquero, Alex R., additional, Poikolainen, Kari, additional, Porte, Sergio, additional, Preedy, Victor, additional, Puddey, Ian B., additional, Reilly, Matthew E., additional, Rich, Alexander R., additional, Rivera, Gonzalo, additional, Rodd, Z.A., additional, Rodrigo, Ramón, additional, Rommelspacher, H., additional, Rotondo, S., additional, Sacanella, Emilio, additional, Salem, Raneem O., additional, Sander, Michael, additional, Santolaria-Fernandez, Francisco, additional, Sastre, Juan, additional, Sato, Nobuhiro, additional, Scafato, Emanuele, additional, Schiaffonati, Luisa, additional, Schneider, Alexander, additional, Schwartz, Marlene B., additional, Seitz, Helmut, additional, Shourie, S., additional, Sierksma, Aafje, additional, Sindeler, Holly, additional, Singer, H.C. Manfred V., additional, Sinha, Rajita, additional, Smith, Gordon S., additional, Soldin, Offie P., additional, Spies, Claudia, additional, Mørch, Lina Steinrud, additional, Stickel, Felix, additional, Suwa, Y., additional, Suuronen, Riitta, additional, Takei, Yoshiyuki, additional, Thatcher, Dawn L., additional, Theruvathu, Jacob A., additional, Thiele, Geoffrey M., additional, Tiengo, Antonio, additional, Timms, Peter M., additional, Trevithick, John R., additional, Tuma, Dean J., additional, Ueno, Yasuhiro, additional, Urbano-Márquez, Alvaro, additional, Vaglenova, Julia, additional, Vandelli, Alberto, additional, Veis, Judith H., additional, Ventura, Holly E., additional, Vidali, Matteo, additional, Viña, José, additional, Vrana, K.E., additional, Walter, Marc, additional, Wang, Jianhua, additional, Waxman, Rachel, additional, Werner, David F., additional, Westin, J., additional, Worrall, Simon, additional, Worst, T.J., additional, Yamashina, Shunhei, additional, Yin, S.J., additional, Zielinska, Magdalena, additional, and Zilkens, Renate R., additional

Published
2005
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29. Apoptosis and necrosis: two types of cell death in alcoholic liver disease

Author

Nanji, Amin A. and Hiller-Sturmhofel, Susanne

Subjects
Alcohol -- Physiological aspects -- Health aspects -- Research, Alcoholism -- Health aspects -- Research, Cell death -- Research -- Health aspects -- Physiological aspects, Alcohol, Denatured -- Physiological aspects -- Health aspects -- Research, Liver diseases -- Research, Necrosis -- Research, Health, Psychology and mental health, Sociology and social work, Physiological aspects, Research, Health aspects
Abstract

Many people who drink heavily over extended periods of time (i.e., several years) develop increasingly severe liver damage, including fatty liver, alcoholic hepatitis, and alcoholic cirrhosis. Fatty liver is caused [...]

Published
1997

42. Downregulation of nuclear sex steroid receptor activity correlates with severity of alcoholic liver injury

Author

EAGON, PATRICIA K., ELM, MARY S., TADIC, STASA D., and NANJI, AMIN A.

Subjects
Ingestion -- Physiological aspects, Hormones, Sex -- Physiological aspects, Androgens -- Physiological aspects, Liver -- Wounds and injuries, Biological sciences
Abstract

Chronic ethanol ingestion in rats and humans results in significant alterations in sex steroid levels and expression of sex hormone-dependent phenotype. In this study, we used the intragastric feeding model in male rats to determine hepatic sex hormone receptor activity under circumstances of chronic ethanol exposure and differing degrees of liver injury induced by type of dietary fat. Pathological analysis and quantitation of hepatic androgen receptor (AR) and estrogen receptor (ER) activity, serum sex hormones, and sex hormone-responsive protein and mRNA expression were performed. The activity of the physiologically relevant nuclear form of both AR and ER was significantly decreased with ethanol and correlated inversely with the severity of liver injury. Serum testosterone levels, as well as expression of an androgen-dependent hepatic mRNA, were decreased by ethanol and progressive liver injury. Serum estradiol increased with liver injury. We postulate that these changes in receptor activity may be due to the oxidative stress, reduced cellular energy, and/or altered cytokine milieu known to occur in this model. ethanol; estrogen; androgen

Published
2001

44. Hepatic response to chronic hypoxia in experimental rat model through HIF-1 alpha, activator protein-1 and NF-kappa B

Author

Lau, Thomas Y.H., Xiao, Jia, Liong, Emily C., Liao, Linchuan, Leung, Tung-Ming, Nanji, Amin A., Fung, Man Lung, and Tipoe, George L.

Subjects
6 - Ciencias aplicadas::61 - Medicina [CDU], 5 - Ciencias puras y naturales::57 - Biología::576 - Biología celular y subcelular. Citología [CDU], Nitric oxide, Hypoxia
Abstract

Chronic liver diseases are commonly associated with tissue hypoxia that may cause inflammation, oxidative stress, liver cell injury and increased nuclear transcriptional regulation. The hepatic response to chronic hypoxia at the molecular level has not yet been clearly understood until now. The aim of this study is to investigate whether nuclear transcription factors [hypoxia-inducible factor-1 (HIF-1α), activator protein-1 (AP-1), nuclear factor-kappa B (NF-κB)] exhibit activity changes during hepatic response to chronic hypoxia. Blood and liver samples were collected from adult Sprague-Dawley rats living in atmospheric air or 10% oxygen for four weeks. Levels of serum alanine aminotransferase (ALT), 8-isoprostane and nitrotyrosine were measured. The activities of nuclear transcription factors and the expression of downstream genes (iNOS, eNOS, ET-1 and VEGF) were measured using RT-PCR, Western blotting and Gel shift analysis. Results showed that serum ALT level, 8-isoprostane level and formation of nitrotyrosine were within normal range at all time-points. In the hypoxic liver, DNAbinding activities of HIF-1α, NF-κB and AP-1 increased significantly. Expression levels of iNOS, VEGF and ET1 progressively increased from day 7 to day 28. eNOS was also elevated in the hypoxic liver. In conclusion, our study suggests that increased activity of HIF-1α, AP-1 and NF-κB may partly play a significant role in the hepatic response to oxidative stress and liver injury under chronic hypoxia. The increased expression of VEGF, ET-1, iNOS and eNOS may be partly due to the compensatory mechanism in the vascular beds of the liver in response to chronic hypoxia.

Published
2013

45. Role of nitric oxide in the regulation of fibrogenic factors in experimental liver fibrosis in mice

Author

Leung, Tung-Ming, Fung, Man-Lung, Liong, Emily C., Lau, Thomas Y.H., Nanji, Amin A., and Tipoe, George L.

Subjects
616 - Patología. Medicina clínica. Oncología, Liver fibrosis, Nitric oxide
Abstract

Previously, we have shown that an increased expression level of iNOS but a reduction in the expression of eNOS is associated with increased oxidative stress markers in CCl4-induced experimental liver fibrosis. The present study aimed to investigate the effect of L-arginine and 5-methylisothiourea hemisulfate (SMT) in the expression of profibrogenic factors in chronic liver injury. ICR mice were treated with CCl4 with or without treatment of L-arginine, an NO donor, or SMT, an iNOS inhibitor. The expression of matrix metalloptroteinases (MMPs), tissue inhibitors of metalloproteinases (TIMPs), α-smooth muscle actin (α- SMA), tumor necrosis factor-α (TNF-α) and cyclooxygenase-2 (COX-2) were investigated by RTPCR. The activity of the MMP-2 and MMP-9 were measured by zymography. Our results showed that CCl4- treated mice showed significant up-regulation of expression of pro-fibrogenic factors, TNF-α and COX-2. Treatment with L-arginine or SMT showed a significant reduction in CCl4-induced expression of these profibrogenic factors, TNF-α and COX-2. In conclusion, both SMT and L-arginine effectively attenuated the progression of CCl4-induced liver fibrosis. SMT suppresses iNOS mediated NO production. However, Larginine augments NO production. The similar effect of the two drugs on liver fibrosis indicates that there may be two distinct pathways of NOS mediated fibrogenesis in chronic liver injury by iNOS and eNOS. Our results suggest that eNOS-mediated liver fibrogenesis may play a more important role than that of iNOS in chronic liver injury. Taken together, these results support the contention that NO plays an active role in the progression of liver fibrosis and hepatocellular damage.

Published
2011

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