Immunomodulatory effects of licochalcone A on experimental autoimmune encephalomyelitis

Fontes, Lívia Beatriz Almeida; Dias, Débora dos Santos; Carvalho, Lara Soares Aleixo de; Mesquita, Harleson Lopes de; Reis, Lívia da Silva; Dias, Alyria Teixeira; Filho, Ademar A. Da Silva; Corrêa, José Otávio do Amaral

doi:10.1111/jphp.12212

Cited by 36 publications

(28 citation statements)

References 31 publications

(59 reference statements)

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“…This protocol results in a chronic demyelinating disease predominantly driven by CD4 + T cell-mediated immunity, especially Th1 and Th17 cells, pointed as the main immunopathogenic cells in this model [6,7]. Th1 cells, stimulated by IL-12 or IFN-γ, secrete IFN-γ and TNF-α that have been considered primarily responsible for the induction of the inflammatory process in CNS during the development of MS and EAE [8].…”

Section: Parthenolide Modulates Immune Response In Cells From C57bl/6mentioning

confidence: 99%

“…Briefly, mice received a subcutaneous injection at the tail base with 100 µg of MOG 35-55 (≥ 97 % purity; Sigma-Aldrich) per animal emulsified in CFA (Sigma-Aldrich) (v/v) containing 400 µg of attenuated Mycobacterium tuberculosis H37RA (Difco). Immediately thereafter, and again 48 h later, the mice received an intraperitoneal (i. p.) injection of 300 ng/animal of pertussis toxin (Sigma-Aldrich) [6]. Non-immunized mice were used as controls.…”

Section: Induction Of Experimental Autoimmune Encephalomyelitismentioning

confidence: 99%

“…Immunized mice were observed daily for clinical signs of EAE up to 21 days after immunization. Animals were monitored daily and neurological impairment was quantified on a clinical scale of 0 to 5, according to the literature [4,6,7], as follows: 0, no disease; 1, limp tail; 2, hind limb weakness; 3, hind limb paralysis; 4, hind and forelimb paralysis; and 5, moribund state. Results are expressed as the mean ± SD for EAE clinical scores.…”

Section: Clinical Assessment and In Vitro Treatment With Parthenolidementioning

confidence: 99%

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Parthenolide Modulates Immune Response in Cells from C57BL/6 Mice Induced with Experimental Autoimmune Encephalomyelitis

et al. 2016

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Multiple sclerosis is a chronic inflammatory and autoimmune disease of the central nervous system that affects more than 2.5 million people worldwide. Experimental autoimmune encephalomyelitis is a murine autoimmune disease used to study multiple sclerosis. Parthenolide, a natural sesquiterpene lactone found in L., is known for its strong anti-inflammatory activity. Herein, we have investigated the immunomodulatory effects of parthenolide on cytokine production and nitric oxide in cultured cells from myelin oligodendrocyte glycoprotein 35-55 amino acid peptide mice. Experimental autoimmune encephalomyelitis was induced in C57BL/6 mice with myelin oligodendrocyte glycoprotein 35-55 amino acid peptide, and parthenolide was isolated from . Splenocytes and peritoneal cells were obtained from experimental autoimmune encephalomyelitis-induced mice and incubated with parthenolide (1, 5, and 20 µM). After treatment with parthenolide, supernatants were collected, and nitric oxide and cytokines were measured. The results suggested that parthenolide may regulate the activity of Th17 and Th1 cells, mainly by decreasing IL-17, TNF-, and interferon gamma production. This modulation may be related to the lower levels of IL-12p40 and IL-6 after treatment with parthenolide. It was shown, for the first time, that parthenolide presents immunomodulatory effects on inflammatory mediators produced by cells from experimental autoimmune encephalomyelitis-induced mice.

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Section: Parthenolide Modulates Immune Response In Cells From C57bl/6mentioning

confidence: 99%

Section: Induction Of Experimental Autoimmune Encephalomyelitismentioning

confidence: 99%

Section: Clinical Assessment and In Vitro Treatment With Parthenolidementioning

confidence: 99%

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Parthenolide Modulates Immune Response in Cells from C57BL/6 Mice Induced with Experimental Autoimmune Encephalomyelitis

et al. 2016

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“…Chalcone, (E)-1,3-diphenyl-2-propene-1-one, has been reported as being a precursor in flavonoid synthesis [1]. Similar to flavonoids, chalcones have already been documented as exhibiting several biological activities, including antioxidant [2], anti-inflammatory [3], antibacterial and antifungal [4], antiprotozooal [5], immunomodulatory [6], and antiangiogenic [7,8] effects. Furthermore, antiproliferative/antitumor activities of chalcones have also been intensively studied [9][10][11][12][13][14].…”

Section: Introductionmentioning

confidence: 99%

Antiproliferative Effect of Acridine Chalcone Is Mediated by Induction of Oxidative Stress

et al. 2020

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Chalcones are naturally occurring phytochemicals with diverse biological activities including antioxidant, antiproliferative, and anticancer effects. Some studies indicate that the antiproliferative effect of chalcones may be associated with their pro-oxidant effect. In the present study, we evaluated contribution of oxidative stress in the antiproliferative effect of acridine chalcone 1C ((2 E)-3-(acridin-9-yl)-1-(2,6-dimethoxyphenyl)prop-2-en-1-one) in human colorectal HCT116 cells. We demonstrated that chalcone 1C induced oxidative stress via increased reactive oxygen/nitrogen species (ROS/RNS) and superoxide production with a simultaneous weak adaptive activation of the cellular antioxidant defence mechanism. Furthermore, we also showed chalcone-induced mitochondrial dysfunction, DNA damage, and apoptosis induction. Moreover, activation of mitogen activated phosphokinase (MAPK) signalling pathway in 1C-treated cancer cells was also observed. On the other hand, co-treatment of cells with strong antioxidant, N-acetyl cysteine (NAC), significantly attenuated all of the above-mentioned effects of chalcone 1C, that is, decreased oxidant production, prevent mitochondrial dysfunction, DNA damage, and induction of apoptosis, as well as partially preventing the activation of MAPK signalling. Taken together, we documented the role of ROS in the antiproliferative/pro-apoptotic effects of acridine chalcone 1C. Moreover, these data suggest that this chalcone may be useful as a promising anti-cancer agent for treating colon cancer.

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“…Licochalcone A, an anti-inflammatory [1][2][3][4], immunomodulatory [5,6], and antimicrobial [3,5,[7][8][9] polyphenol extracted from Glycyrrhiza inflata [1][2][3]10], triggers apoptosis or inhibits proliferation and migration of tumor cells [11], including those of cervical cancer [12], oral squamous carcinoma [7,9,[13][14][15], esophageal carcinoma [16], gastric cancer [4,17,18], hepatocellular carcinoma [2,19], malignant pleural mesothelioma [20], bladder determined photometrically at 405 nm. The absorption of the supernatant of erythrocytes lysed in distilled water was defined as 100% hemolysis.…”

Section: Introductionmentioning

confidence: 99%

Licochalcone A Induced Suicidal Death of Human Erythrocytes

Egler

Läng

2015

Cell Physiol Biochem

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Background: The anti-inflammatory, immunomodulatory, and antimicrobial Glycyrrhiza inflata extract component licochalcone A triggers apoptosis of tumor cells and is thus considered for the treatment of malignancy. Similar to apoptosis of nucleated cells, erythrocytes may enter eryptosis, the suicidal erythrocyte death characterized by cell shrinkage and cell membrane scrambling with phosphatidylserine translocation to the erythrocyte surface. Signaling involved in the triggering of eryptosis includes Ca²⁺ entry with increase of cytosolic Ca²⁺ activity ([Ca²⁺]_i), and ceramide. The present study explored, whether and how licochalcone A induces eryptosis. Methods: Human erythrocytes drawn from healthy individuals were exposed for 24 hours to 1-10 µg/ml licochalcone A. Flow cytometry was subsequently employed to estimate phosphatidylserine exposure at the cell surface from annexin V binding, cell volume from forward scatter, [Ca²⁺]_i from Fluo3-fluorescence, and ceramide utilizing specific antibodies. In addition, hemolysis was quantified from hemoglobin release. Results: Licochalcone A significantly increased the percentage of annexin-V-binding cells (≥ 5 µg/ml), significantly decreased forward scatter (2.5 - 5 µg/ml), significantly increased Fluo3-fluorescence (≥ 7.5 µg/ml), and significantly increased ceramide abundance (10 µg/ml). The effect of licochalcone on annexin-V-binding was not significantly modified, but hemolysis significantly enhanced by removal of extracellular Ca²⁺. Conclusions: Licochalcone triggers cell shrinkage and phospholipid scrambling of the erythrocyte cell membrane, an effect independent from Ca²⁺ entry and presumably in part due to ceramide.

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Immunomodulatory effects of licochalcone A on experimental autoimmune encephalomyelitis

Abstract: LicoA possesses immunomodulatory effects on H2 O2 , NO, IFN-γ, TNF-α and IL-17 production in cells from EAE mice. It is suggested that LicoA acts on the mechanism of development of EAE by IFN-γ, IL-17 and TNF-α inhibition, modulating the immune response on both Th1 and Th17 cells.

Cited by 36 publications

References 31 publications

Parthenolide Modulates Immune Response in Cells from C57BL/6 Mice Induced with Experimental Autoimmune Encephalomyelitis

Parthenolide Modulates Immune Response in Cells from C57BL/6 Mice Induced with Experimental Autoimmune Encephalomyelitis

Antiproliferative Effect of Acridine Chalcone Is Mediated by Induction of Oxidative Stress

Licochalcone A Induced Suicidal Death of Human Erythrocytes

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