Curcumin attenuates Concanavalin A-induced liver injury in mice by inhibition of Toll-like receptor (TLR) 2, TLR4 and TLR9 expression

Tu, Caixia; Han, Bing; Yao, Qunyan; Zhang, Yi-an; Liu, Hongchun; Zhang, Shuncai

doi:10.1016/j.intimp.2011.11.005

Cited by 74 publications

(55 citation statements)

References 41 publications

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“…In addition, there is biochemical evidence indicating that curcumin can inhibit both ligand-induced and ligand-independent dimerization of TLR4 (Youn et al, 2006). The beneficial effect of curcumin is partly mediated by reducing the expression levels of TNF through inhibition of the expression of TLR2, TLR4 and TLR9 in mouse liver (Tu et al, 2012). Curcumin also binds with sub-micromolar affinity to the myeloid differentiation protein-2 (MD-2), which is the LPS-binding component of the endotoxin surface receptor complex MD-2/TLR4 (Gradisar et al, 2007).…”

Section: Suppression Of Tnf-a Production By Curcumin In Vitromentioning

confidence: 99%

“…Decreased TNF-a levels have also been noted in tumour-bearing animals treated with this polyphenol (Leyon and Kuttan, 2003). In addition to cancer, down-regulation of TNF-a by curcumin has been associated with protection from various pro-inflammatory diseases, including sub-chronic inflammation (Nandal et al, 2009;Nishida et al, 2010), cardiovascular diseases (Yao et al, 2004;Mito et al, 2011;Avci et al, 2012), diabetes (Jain et al, 2009;El-Azab et al, 2011;El-Moselhy et al, 2011), acute pancreatitis (Gulcubuk et al, 2006), enterocolitis (Jia et al, 2010), enteritis (Song et al, 2010), prostatitis (Zhang et al, 2010b), diabetic neuropathy (Sharma et al, 2007b), hepatic injury (Yun et al, 2010), Th1-type ileitis (Bereswill et al, 2010), hepatic fibrosis (Shu et al, 2007;Zeng et al, 2011), radiationinduced lung fibrosis , asthma (Ammar el et al, 2011), alcohol-induced liver disease (Nanji et al, 2003), non-alcoholic steatohepatitis (Ramirez-Tortosa et al, 2009), concanavalin A-induced liver injury (Tu et al, 2012), renal injury (Hashem et al, 2008;Pan et al, 2012), infection (Allam, 2009), fatigue (Gupta et al, 2009), bone turnover (Yang et al, 2011) and high-fat diet-induced hyperglycaemia (El-Moselhy et al, 2011). Curcumin has also been found to…”

Section: Suppression Of Tnf By Curcumin In Vivomentioning

confidence: 99%

“…• Attenuated concanavalin A-induced liver injury in mice by inhibition of TNF expression through TLR-2, TLR-4 and TLR-9 expression (Tu et al, 2012).…”

Section: Figurementioning

confidence: 99%

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Curcumin: an orally bioavailable blocker of TNF and other pro‐inflammatory biomarkers

Aggarwal

Gupta

Sung

2013

British J Pharmacology

344

239

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TNFs are major mediators of inflammation and inflammation-related diseases, hence, the United States Food and Drug Administration (FDA) has approved the use of blockers of the cytokine, TNF-a, for the treatment of osteoarthritis, inflammatory bowel disease, psoriasis and ankylosis. These drugs include the chimeric TNF antibody (infliximab), humanized TNF-a antibody (Humira) and soluble TNF receptor-II (Enbrel) and are associated with a total cumulative market value of more than $20 billion a year. As well as being expensive ($15 000-20 000 per person per year), these drugs have to be injected and have enough adverse effects to be given a black label warning by the FDA. In the current report, we describe an alternative, curcumin (diferuloylmethane), a component of turmeric (Curcuma longa) that is very inexpensive, orally bioavailable and highly safe in humans, yet can block TNF-a action and production in in vitro models, in animal models and in humans. In addition, we provide evidence for curcumin's activities against all of the diseases for which TNF blockers are currently being used. Mechanisms by which curcumin inhibits the production and the cell signalling pathways activated by this cytokine are also discussed. With health-care costs and safety being major issues today, this golden spice may help provide the solution. LINKED ARTICLESThis article is part of a themed section on Emerging Therapeutic Aspects in Oncology. To view the other articles in this section visit http://dx

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Section: Suppression Of Tnf-a Production By Curcumin In Vitromentioning

confidence: 99%

Section: Suppression Of Tnf By Curcumin In Vivomentioning

confidence: 99%

See 1 more Smart Citation

Curcumin: an orally bioavailable blocker of TNF and other pro‐inflammatory biomarkers

Aggarwal

Gupta

Sung

2013

British J Pharmacology

344

239

View full text Add to dashboard Cite

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“…Studies have suggested that TLR-mediated signals are involved in almost all liver diseases [13,[18][19][20], and recent studies implicating TLR2 and TLR4 signaling in ConAinduced liver injury are of particular importance [14,19,21,22]. Also, expression of TLR2 and TLR4 is upregulated in liver cells during ConA-induced hepatic injury [14,19,22].…”

Section: Introductionmentioning

confidence: 99%

Quercetin Protects Mice from ConA-Induced Hepatitis by Inhibiting HMGB1-TLR Expression and Down-Regulating the Nuclear Factor Kappa B Pathway

Liu

Yao

et al. 2015

Inflammation

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The dietary flavonoid quercetin has hepatoprotective effects. We analyzed the effects of quercetin on concanavalin A (ConA)-induced hepatitis in mice and its underlying molecular mechanisms of action. Mice were administered quercetin (50 mg/kg body weight, i.p.) or vehicle 30 min before intravenous administration of ConA. Quercetin pretreatment significantly reduced the ConA-induced elevations in plasma aminotransferase concentrations and liver necrosis, as well as reducing serum concentrations of the pro-inflammatory cytokines tumor necrosis factor (TNF)-α, interferon-γ, and interleukin-4. Quercetin pretreatment also reduced expression of high-mobility group box 1 protein (HMGB1) and toll-like receptor (TLR)-2 and TLR-4 messenger RNA (mRNA) and protein in liver tissues. Quercetin pretreatment significantly inhibited degradation of inhibitory kappa B alpha and modulated ConA-induced nuclear translocation in the liver of nuclear factor kappa B (NF-κB) p65. These results demonstrate that quercetin protects against ConA-mediated hepatitis in mice by attenuating the HMGB1-TLRs-NF-κB signaling pathway.

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“…UDCA inhibited CpG-induced immunoglobulin production by B cells [348] cytokine (IL-2, IL-4, IFN-J) release by mononuclear cells when challenged with LPS [349] and intrahepatic TNF-α and MIP-2 in the concanavalin A model of liver damage in experimental animals [350] . These findings suggest that UDCA modifies TLR TLR4 and TLR9 signaling pathways, therefore reducing inflammation [351] . The anti-inflammatory properties of UDCA might, in addition, be mediated by activation of the vitamin D receptor in cholangiocytes to promote the secretion of antimicrobial peptides in human bile [352,353] .…”

Section: Mode Of Action Of Udcamentioning

confidence: 80%

Primary biliary cirrhosis: From bench to bedside

Notas

2015

WJGPT

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Primary biliary cirrhosis (PBC) is a chronic nonsuppurative destructive intrahepatic cholangitis leading to cirrhosis after a protractive non cirrhotic stage. The etiology and pathogenesis are largely unknown and autoimmne mechanisms have been implicated to explain the pathological lesions. Many epitopes and autoantigens have been reported as crucial in the pathophysiology of the disease and T and B cells abnormalities have been described, the exact pathways leading to the destruction of small intrahepatic ductules are mostly speculative. In this review we examined the various epidemiologal and geoepidemiological data as well as the complex pathogenetic aspects of this disease, focusing on recent in vivo and in vitro studies in this field. Initiation and progression of PBC is believed to be a multifactorial process with strong infuences from the patient's genetic background and by various environmental factors. The role of innate and adaptive immunity, including cytokines, chemokines, macrophages and the involvement of apoptosis and reactive oxygen species are outlined in detailed. The current pathogenetic aspects are presented and a novel pathogenetic theory unifying the accumulated clinical information with in vitro and in vivo data is formulated.A review of clinical manifestations and immunological and pathological diagnosis was presented. Treatment modalities, including the multiple mechanisms of action of ursodeoxycholate were finally discussed. Core tip: Primary biliary cirrhosis (PBC) is a chronic nonsuppurative destructive intrahepatic cholangitis leading to cirrhosis of largely unknown pathophysiology. We examined the epidemiological and geoepidemiological data as well as the pathogenetic aspects of PBC. A novel pathogenetic theory unifying the accumulated clinical information with in vitro and in vivo data is formulated.

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Curcumin attenuates Concanavalin A-induced liver injury in mice by inhibition of Toll-like receptor (TLR) 2, TLR4 and TLR9 expression

Cited by 74 publications

References 41 publications

Curcumin: an orally bioavailable blocker of TNF and other pro‐inflammatory biomarkers

Curcumin: an orally bioavailable blocker of TNF and other pro‐inflammatory biomarkers

Quercetin Protects Mice from ConA-Induced Hepatitis by Inhibiting HMGB1-TLR Expression and Down-Regulating the Nuclear Factor Kappa B Pathway

Primary biliary cirrhosis: From bench to bedside

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