Pharmacological actions of curcumin in liver diseases or damage

Rivera-Espinoza, Yadira; Muriel, Pablo

doi:10.1111/j.1478-3231.2009.02086.x

Cited by 156 publications

(89 citation statements)

References 93 publications

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“…Because of its lack of toxicity, there has been increasing interest in further studies with curcumin [12,13]. Unfortunately, its poor absorption undermine its clinical potential [14].…”

Section: Introductionmentioning

confidence: 99%

The curcumin analog DM-1 induces apoptotic cell death in melanoma

et al. 2013

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SummaryThe main difficulty in the successful treatment of metastatic melanoma is that this type of cancer is known to be resistant to chemotherapy. Chemotherapy remains the treatment of choice and dacarbazine (DTIC) is the best standard treatment. The DM-1 compound is a curcumin analog that possesses several curcumin characteristics, such as antiproliferative, antitumor and antimetastatic properties. The objective of this study was to evaluate the signaling pathways involved in melanoma cell death after treatment with DM-1 compared to the standard agent for melanoma treatment, DTIC. Altogether, these data confirm DM-1 as a chemotherapeutic agent with effective tumor control properties and a lower incidence of side effects in normal cells compared to DTIC.

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“…Because of its lack of toxicity, there has been increasing interest in further studies with curcumin [12,13]. Unfortunately, its poor absorption undermine its clinical potential [14].…”

Section: Introductionmentioning

confidence: 99%

The curcumin analog DM-1 induces apoptotic cell death in melanoma

et al. 2013

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“…However, a review of literature revealed that none of the herbal medications that patient 1 had taken (Lineum usitatissimum, Fumariaceae, Curcumin, and Silybum marianum) are known to cause a liver damage; in fact, several recent studies have shown a protective effect of these medications in states of liver injury. [21][22][23][24] Nevertheless, no study examined the combination of these herbal medications, thus, potential liver toxicity cannot be excluded. As to the second patient who was treated with fluconazole, although LFT abnormalities are associated with all of the azoles, these abnormalities are more likely with itraconazole and ketoconazole than with fluconazole 25,26 and the later seems to have a lower risk of treatment discontinuation because of adverse events.…”

Section: Discussionmentioning

confidence: 99%

Acute Liver Injury during Co-treatment with Levetiracetam and Temozolomide

Chen¹,

Mizrahi²,

Nubani³

et al. 2015

Liver Res Open J

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Citation ABSTRACTDrug-induced liver injury (DILI) accounts for approximately 10 percent of all cases of acute hepatitis. The patterns of acute injury include any form of hepatic injury, but the most common problems are cholestasis, hepatocellular damage, or a mixed type. DILI is often reversible, and discontinuation of the offending agent usually results in a complete recovery; however, some cases may lead to chronic liver injury, cirrhosis, and even death. Temozolomide (TMZ) is an alkylating, anti-neoplastic agent used for the treatment of refractory anaplastic astrocytoma, newly-diagnosed Glioblastoma multiforme (GBM) and metastatic melanoma. Levetiracetam (LEV) is an established second-generation antiepileptic drug and is most commonly approved as adjunctive treatment of partial-onset seizures with or without secondary generalization. When administered separately each of these drugs is considered to be relatively safe and only few cases of severe liver injury can be found throughout the literature; however, LEV and TMZ are commonly used together in the treatment of brain malignancies. We report three patients who presented with jaundice during treatment with TMZ and LEV, and propose a mechanism for liver sensitization by LEV for TMZ-induced injury.

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“…The polyphenol curcumin has been shown to be an effective treatment for liver and lung fibrosis both in vivo and in vitro (Bruck et al, 2007;Venkatesan et al, 2007;Rivera-Espinoza and Muriel, 2009). It prevents fibrosis by blocking leukocyte influx, inhibiting the activation of inflammatory cells and subsequent release of proinflammatories.…”

Section: Discussionmentioning

confidence: 99%

Antifibrotic Effect of Curcumin in TGF-β1-Induced Myofibroblasts from Human Oral Mucosa

Zhang

Gong

Li³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Asian Pacific J Cancer Prev, 13, 289-294 IntroductionOral submucous fibrosis (OSF) is a chronic inflammatory disease, and has been defined by WHO as one of the precancerous conditions (International Agency for Research on Cancer, 2005). The main clinical symptoms include the stiffness of oral mucosa, restriction of mouth opening, atrophy of tongue papillae, blisters, and intolerance to hot and spicy food. Malignant transformation rate in OSF is high, reaching 7-13% (Tilakaratne et al., 2006). The disease exhibits characteristic histological features of excessive collagen deposition in the lamina propria, following the epithelium becomes atrophic (Singh et al., 2010).OSF is closely associated with betel quid (BQ) chewing, a habit common in South and Southeast Asia, some parts of Africa, and among immigrants from these regions (Boucher and Mannan, 2002). An imbalance in collagen synthesis and degradation in oral mucosa is generally believed to be the main cause of OSF;The disease is considered a type of collagen metabolism disorder (Rajalalitha and Vali, 2005).Myofibroblasts are typically activated fibroblasts, although they can also be derived from other cell types, including epithelial and endothelial cells via epithelial/ endothelial mesenchymal transition (EMT/EndMT) process, as well as from the circulating fibroblast-like cells AbstractBackground: Myofibroblasts play an important role in the development of oral submucous fibrosis (OSF). In the current study, we investigate the effect of curcumin on growth and apoptosis of myofibroblasts derived from human oral mucosa. Methods: Myofibroblasts were generated by incubating fibroblasts, obtained from human oral mucosa, with transforming growth factor-β1 (TGF-β1). MTT, PI staining, and FACS assays were used to investigate curcumin's effect on proliferation and cell cycle of fibroblasts and myofibroblasts. Annexin V/PI binding and FACS assays were used to examine apoptosis of myofibroblasts, Western blotting to determine the levels of Bcl-2 and Bax, and enzyme-linked immunosorbant assay was employed to examine the levels of collagen type I and III in the supernatants of myofibroblasts. Results: Curcumin inhibits proliferation of fibroblasts and myofibroblasts; it also disturbs the cell cycle, induces apoptosis and decreases the generation of collagen type I and III in myofibroblasts, which are more sensitive to its effects than fibroblasts. Curcumin induces apoptosis in myofibroblasts by down-regulating the Bcl-2/ Bax ratio. Conclusion: Our results demonstrate the antifibrotic effect of curcumin in vitro. It may therefore be a candidate for the treatment of OSF.

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Pharmacological actions of curcumin in liver diseases or damage

Cited by 156 publications

References 93 publications

The curcumin analog DM-1 induces apoptotic cell death in melanoma

The curcumin analog DM-1 induces apoptotic cell death in melanoma

Acute Liver Injury during Co-treatment with Levetiracetam and Temozolomide

Antifibrotic Effect of Curcumin in TGF-β1-Induced Myofibroblasts from Human Oral Mucosa

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