Curcumin alleviates lipopolysaccharide induced sepsis and liver failure by suppression of oxidative stress-related inflammation via PI3K/AKT and NF-κB related signaling

Biomedicine and Pharmacotherapy

Volumn 83, Issue , 2016, Pages 302-313

  Zhong, Wenhui ^a   Qian, Kejian ^b   Xiong, Jibin ^a   Ma, Ke ^a   Wang, Aizhong ^a   Zou, Yan ^a  

^a SHANGHAI JIAO TONG UNIVERSITY AFFILIATED SIXTH PEOPLE S HOSPITAL   (China)

^b NANCHANG UNIVERSITY   (China)

Author keywords

Apoptosis; Curcumin; Inflammation; Lipopolysaccharides; Liver injury; Oxidative stress

Indexed keywords

ALANINE AMINOTRANSFERASE; ALKALINE PHOSPHATASE; ASPARTATE AMINOTRANSFERASE; CASPASE 3; CASPASE 6; CASPASE 9; CATALASE; COPPER ZINC SUPEROXIDE DISMUTASE; CURCUMIN; CYCLIC AMP RESPONSIVE ELEMENT BINDING PROTEIN; CYTOCHROME P450 2E1; GLUTATHIONE; GLUTATHIONE PEROXIDASE; I KAPPA B; IMMUNOGLOBULIN ENHANCER BINDING PROTEIN; INTERLEUKIN 18; INTERLEUKIN 1BETA; INTERLEUKIN 6; LIPOPOLYSACCHARIDE; MANGANESE SUPEROXIDE DISMUTASE; MITOGEN ACTIVATED PROTEIN KINASE 3; MITOGEN ACTIVATED PROTEIN KINASE P38; NITRIC OXIDE; PHOSPHATIDYLINOSITOL 3 KINASE; PROTEIN KINASE B; REACTIVE OXYGEN METABOLITE; STAT3 PROTEIN; STRESS ACTIVATED PROTEIN KINASE; TRANSCRIPTION FACTOR NRF2; TUMOR NECROSIS FACTOR ALPHA; MESSENGER RNA;

ACUTE LIVER FAILURE; ALANINE AMINOTRANSFERASE BLOOD LEVEL; ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ANTIOXIDANT ACTIVITY; APOPTOSIS; ARTICLE; ASPARTATE AMINOTRANSFERASE BLOOD LEVEL; CELL DAMAGE; CONTROLLED STUDY; CYTOPLASM; DOWN REGULATION; ENDOTOXEMIA; ENZYME INHIBITION; INFLAMMATION; INTRACELLULAR SPACE; LETHALITY; LIPOPOLYSACCHARIDE-INDUCED SEPSIS; LIVER FUNCTION; LIVER HISTOLOGY; LIVER PROTECTION; MALE; MOUSE; NONHUMAN; OXIDATIVE STRESS; PRIORITY JOURNAL; PROTEIN BLOOD LEVEL; PROTEIN EXPRESSION; STELLATE CELL; TRANSMISSION ELECTRON MICROSCOPY; UPREGULATION; ANIMAL; BLOOD; C57BL MOUSE; DRUG EFFECTS; GENETICS; HEPATIC STELLATE CELL; LIVER FAILURE; METABOLISM; PATHOLOGY; SEPSIS; SIGNAL TRANSDUCTION;

ANIMALS; APOPTOSIS; CURCUMIN; HEPATIC STELLATE CELLS; INFLAMMATION; JNK MITOGEN-ACTIVATED PROTEIN KINASES; LIPOPOLYSACCHARIDES; LIVER FAILURE; MALE; MICE, INBRED C57BL; NF-KAPPA B; OXIDATIVE STRESS; PHOSPHATIDYLINOSITOL 3-KINASES; PROTO-ONCOGENE PROTEINS C-AKT; REACTIVE OXYGEN SPECIES; RNA, MESSENGER; SEPSIS; SIGNAL TRANSDUCTION;

EID: 84977615047     PISSN: 07533322     EISSN: 19506007     Source Type: Journal    
DOI: 10.1016/j.biopha.2016.06.036     Document Type: Article

References (39)

1. [1] Lang, M.B., Segersvard, R., Grundsten, M., et al. Management of alcohol use disorders in patients with chronic pancreatitis. JOP 13 (2012), 654–659.
2. [2] Purohit, V., Bode, J.C., Bode, C., et al. Alcohol, intestinal bacterial growth, intestinal permeability to endotoxin, and medical consequences: summary of a symposium. Alcohol 42 (2008), 349–361.
3. [3] Khan, A.Q., Nafees, S., Sultana, S., Perillyl alcohol protects against ethanol induced acute liver injury in Wistar rats by inhibiting oxidative stress, NFκ-B activation and proinflammatory cytokine production. Toxicology 279 (2011), 108–114.
4. [4] Boe, D.M., Richens, T.R., Horstmann, S.A., et al. Acute and chronic alcohol exposure impair the phagocytosis of apoptotic cells and enhance the pulmonary inflammatory response. Alcohol Clin. Exp. Res. 34 (2010), 1723–1732.
5. [5] Zhang, Z., Bagby, G.J., Stoltz, D., et al. Prolonged ethanol treatment enhances lipopolysaccharide/phorbol myristate acetate-induced tumor necrosis factor-α production in human monocytic cells. Alcohol Clin. Exp. Res. 25 (2001), 444–449.
6. [6] Zimmermann, H.W., Seidler, S., Gassler, N., et al. Interleukin-8 is activated in patients with chronic liver diseases and associated with hepatic macrophage accumulation in human liver fibrosis. PLoS One, 6, 2011, e21381.
7. [7] Kiecolt-Glaser, J.K., Preacher, K.J., MacCallum, R.C., et al. Chronic stress and age-related increases in the proinflammatory cytokine IL-6. Proc. Natl. Acad. Sci. U. S. A. 100 (2003), 9090–9095.
8. [8] Means, A.L., Meszoely, I.M., Suzuki, K., et al. Pancreatic epithelial plasticity mediated by acinar cell transdifferentiation and generation of nestin-positive intermediates. Development 132 (2005), 3767–3776.
9. [9] Raynard, B., Balian, A., Fallik, D., et al. Risk factors of fibrosis in alcohol-induced liver disease. Hepatology 35 (2002), 635–638.
10. [10] Mandrekar, P., Bala, S., Catalano, D., et al. The opposite effects of acute and chronic alcohol on lipopolysaccharide-induced inflammation are linked to IRAK-M in human monocytes. J. Immunol. 183 (2009), 1320–1327.
11. [11] Zhou, H., Yu, M., Fukuda, K., et al. IRAK-M mediates Toll-like receptor/IL-1R-induced NFκB activation and cytokine production. EMBO J. 32 (2013), 583–596.
12. [12] Sun, Z.J., Chen, G., Hu, X., et al. Activation of PI3K/Akt/IKK-alpha/NF-kappaB signaling pathway is required for the apoptosis-evasion in human salivary adenoid cystic carcinoma: its inhibition by quercetin. Apoptosis 15 (2010), 850–863.
13. [13] Shenoy, S., transplantation, Liver, in acute liver failure. Indian J. Gastroenterol. 25 (2006), S13–S18.
14. [14] Venkatesan, B., Valente, A.J., Prabhu, S.D., Shanmugam, P., Delafontaine, P., Chandrasekar, B., EMMPRIN activates multiple transcription factors in cardiomyocytes, and induces interleukin-18 expression via Rac1-dependent PI3K/Akt/IKK/NF-kappaB andMKK7/JNK/AP-1 signaling. J. Mol. Cell. Cardiol. 49 (2010), 655–663.
15. [15] Baker, R.G., Hayden, M.S., Ghosh, S., NF-(B, inflammation, and metabolic disease. Cell Metab. 13 (2011), 11–22.
16. [16] Tazi, K.A., Quioc, J.J., Saada, V., et al. Upregulation of TNF-alpha production signaling pathways in monocytes from patients with advanced cirrhosis: possible role of Akt and IRAK-M. J. Hepatol. 45 (2006), 280–289.
17. [17] Cuschieri, J., Maier, R.V., Mitogen-activated protein kinase (MAPK). Crit. Care Med. 33 (2005), S417–S419.
18. [18] Rahbari, N.N., Mehrabi, A., Mollberg, N.M., Müller, S.A., Koch, M., Büchler, M.W., Weitz, J., Hepatocellular carcinoma: current management and perspectives for the future. Ann. Surg. 253 (2011), 453–469.
19. [19] Bujold, A., Dawson, L.A., Stereotactic radiation therapy and selective internal radiation therapy for hepatocellular carcinoma. Cancer Radiother. 15 (2011), 54–63.
20. [20] Shin, J.W., Wang, J.H., Park, H.J., Choi, M.K., Kim, H.G., Son, C.G., Herbal formula CGX ameliorates LPS/D-galactosamine-induced hepatitis. Food Chem. Toxicol. 49 (2011), 1329–1334.
21. [21] Xing, W.W., Zou, M.J., Liu, S., Xu, T., Gao, J., Wang, J.X., Xu, D.G., Hepatoprotective effects of IL-22 on fulminant hepatic failure induced by d-galactosamine and lipopolysaccharide in mice. Cytokine 56 (2011), 174–179.
22. [22] Schiødt, F.V., Lee, W.M., Fulminant liver disease. Clin. Liver Dis. 7 (2003), 331–349.
23. [23] Mukherjee, S., Mahmoudi, T.M., Mukherjee, U., Liver transplant for viral hepatitis and fulminant hepatic failure. Minerva Gastroenterol. Dietol. 55 (2009), 83–100.
24. [24] Abdelrahman, M., Sharples, E.J., McDonald, M.C., Collin, M., Patel, N.S., Yaqoob, M.M., Thiemermann, C., Erythropoietin attenuates the tissue injury associated with hemorrhagic shock and myocardial ischemia. Shock 22 (2004), 63–69.
25. [25] Brines, M., Grasso, G., Fiordaliso, F., et al. Erythropoietin mediates tissue protection through an erythropoietin and common beta-subunit heteroreceptor. Proc. Natl. Acad. Sci. U. S. A. 101 (2004), 14907–14912.
26. [26] Brines, M., Cerami, A., Emerging biological roles for erythropoietin in the nervous system. Nat. Rev. Neurosci. 6 (2005), 484–494.
27. [27] Oztürk, E., Demirbilek, S., Köroğlu, A., et al. Propofol and erythropoietin antioxidant properties in rat brain injured tissue. Prog. Neuropsychopharmacol. Biol. Psychiatry 32 (2008), 81–86.
28. [28] Zou, W., Roth, R.A., Younis, H.S., Burgoon, L.D., Ganey, P.E., Oxidative stress is important in the pathogenesis of liver injury induced by sulindac and lipopolysaccharide cotreatment. Toxicology 272 (2010), 32–38.
29. [29] Jaeschke, H., Reactive oxygen and mechanisms of inflammatory liver injury: present concepts. J. Gastroenterol. Hepatol. 26:Suppl. 1 (2011), 173–179.
30. [30] Kudo, H., Takahara, T., Yata, Y., Kawai, K., Zhang, W., Sugiyama, T., Lipopolysaccharide triggered TNF-alpha-induced hepatocyte apoptosis in a murine non-alcoholic steatohepatitis model. J. Hepatol. 51 (2009), 168–175.
31. [31] Raval, C.M., Zhong, J.L., Mitchell, S.A., Tyrrell, R.M., The role of Bach1 in ultraviolet A-mediated human heme oxygenase 1 regulation in human skin fibroblasts. Free Radic. Biol. Med. 52 (2012), 227–236.
32. [32] Franco, R., Cidlowski, J.A., Glutathione efflux and cell death. Antioxid. Redox Signal. 17 (2012), 1694–1713.
33. [33] Cabiscol, E., Tamarit, J., Ros, J., Oxidative stress in bacteria and protein damage by reactive oxygen species. Int. Microbiol. 3 (2000), 3–8.
34. [34] Funato, Y., Michiue, T., Asashima, M., Miki, H., The thioredoxin-related redox-regulating protein nucleoredoxin inhibits Wnt-β-catenin signalling through dishevelled. Nat. Cell Biol. 8 (2006), 501–508.
35. [35] Ren, Y., Yang, X., Niu, X., Liu, S., Ren, G., Chemical characterization of the avenanthramide-rich extract from oat and its effect on d-galactose-induced oxidative stress in mice. J. Agric. Food Chem. 59 (2011), 206–211.
36. [36] Góth, L., Catalase deficiency and type 2 diabetes. Diabetes Care, 31, 2008, e93.
37. [37] Ackerley, D.F., Barak, Y., Lynch, S.V., Curtin, J., Matin, A., Effect of chromate stress on Escherichia coli K-12. J. Bacteriol. 188 (2006), 3371–3381.
38. [38] Jauniaux, E., Watson, A.L., Hempstock, J., Bao, Y.P., Skepper, J.N., Burton, G.J., Onset of maternal arterial blood flow and placental oxidative stress. A possible factor in human early pregnancy failure. Am. J. Pathol. 157 (2000), 2111–2122.
39. [39] Orrenius, S., Gogvadze, V., Zhivotovsky, B., Mitochondrial oxidative stress: implications for cell death. Annu. Rev. Pharmacol. Toxicol. 47 (2007), 143–183.