Anti-cancer chalcones: Structural and molecular target perspectives.

http://eprints.gla.ac.uk/102064/1/102064.pdf

Broad targeting of angiogenesis for cancer prevention and therapy

From time immemorial, mushrooms have been valued by humankind as a culinary wonder and folk medicine in Oriental practice. The last decade has witnessed the overwhelming interest of western research fraternity in pharmaceutical potential of mushrooms. The chief medicinal uses of mushrooms discovered so far are as anti-oxidant, anti-diabetic, hypocholesterolemic, anti-tumor, anti-cancer, immunomodulatory, anti-allergic, nephroprotective, and anti-microbial agents. The mushrooms credited with success against cancer belong to the genus Phellinus, Pleurotus, Agaricus, Ganoderma, Clitocybe, Antrodia, Trametes, Cordyceps, Xerocomus, Calvatia, Schizophyllum, Flammulina, Suillus, Inonotus, Inocybe, Funlia, Lactarius, Albatrellus, Russula, and Fomes. The anti-cancer compounds play crucial role as reactive oxygen species inducer, mitotic kinase inhibitor, anti-mitotic, angiogenesis inhibitor, topoisomerase inhibitor, leading to apoptosis, and eventually checking cancer proliferation. The present review updates the recent findings on the pharmacologically active compounds, their anti-tumor potential, and underlying mechanism of biological action in order to raise awareness for further investigations to develop cancer therapeutics from mushrooms. The mounting evidences from various research groups across the globe, regarding anti-tumor application of mushroom extracts unarguably make it a fast-track research area worth mass attention.

/pdf/recent-developments-in-mushrooms-as-anti-cancer-therapeutics-5d5ic8qzx3.pdf

Recent developments in mushrooms as anti-cancer therapeutics: a review.

Aryl hydrocarbon receptor and intestinal immunity.

Indirubin plays an important role in the treatment of many chronic diseases and exhibits strong anti-inflammatory activity. However, the molecular mode of action during mastitis prophylaxis remains poorly understood. In this study, a lipopolysaccharide (LPS)-induced mastitis mouse model showed that indirubin attenuated histopathological changes in the mammary gland, local tissue necrosis, and neutrophil infiltration. Moreover, indirubin significantly downregulated the production of interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNF-α). We explored the mechanism whereby indirubin exerts protective effects against LPS-induced inflammation of mouse mammary epithelial cells (MMECs). The addition of different concentrations of indirubin before exposure of cells to LPS for 1 h significantly attenuated inflammation and reduced the concentrations of the three inflammatory cytokines in a dose-dependent manner. Indirubin downregulated LPS-induced cyclooxygenase-2 (COX-2) and Toll-like receptor 4 (TLR4) expression, inhibited phosphorylation of the LPS-induced nuclear transcription factor-kappa B (NF-kB) P65 protein and its inhibitor IkBα of the NF-kB signaling pathway. Furthermore, indirubin suppressed phosphorylation of P38, extracellular signal-regulated kinase (ERK), and c-Jun NH2-terminal kinase (JNK) of the mitogen-activated protein kinase (MAPK) signal pathways. Thus, indirubin effectively suppressed LPS-induced inflammation via TLR4 abrogation mediated by the NF-kB and MAPK signaling pathways and may be useful for mastitis prophylaxis.

Indirubin Inhibits LPS-Induced Inflammation via TLR4 Abrogation Mediated by the NF-kB and MAPK Signaling Pathways.

Background Celastrol, a quinone methide triterpenoid isolated from the Celastraceae family, exhibits various biological properties, including chemopreventive, antioxidant and neuroprotective effects. In this study, we showed that celastrol inhibits inflammatory reactions in macrophages and protects mice from skin inflammation. Materials and methods Anti-inflammatory effects of celastrol (0‐1 lM) were examined in lipopolysaccharide (LPS)-stimulated RAW 264AE7 macrophages. To investigate the effects of celastrol (0‐50 lg per mice) in vivo, activation of myeloperoxidase (MPO) and histological assessment were examined in the 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced mouse ear oedema model. Results Our in vitro experiments showed that celastrol suppressed not only LPS-stimulated generation of nitric oxide and prostaglandin E2, but also expression of inducible nitric oxide synthase and cyclooxygenase-2 in RAW264AE7 cells. Similarly, celastrol inhibited LPS-induced production of inflammatory cytokines, including tumour necrosis factor-a and interleukin-6. In an animal model, celastrol protected mice from TPA-induced ear oedema, possibly by inhibiting MPO activity and production of inflammatory cytokines. Conclusions Our data suggest that celastrol inhibits the production of inflammatory mediators and is a potential target for the treatment of various inflammatory diseases.

http://web.hallym.ac.kr/~jgjun/paper/eci_819(2009).pdf

Suppression of inflammatory responses by celastrol, a quinone methide triterpenoid isolated from Celastrus regelii

Chrysin, a natural flavone, improves murine inflammatory bowel diseases

Background: 3,3-Diindolylmethane (DIM) is a major in vivo product of acid-catalyzed oligomerization of indole-3-carbinol (I3C) derived from Brassica food plants. Although DIM is known as a chemopreventive and chemotherapeutic phytochemical, the effects of DIM on inflammation in vivo are still unknown. In the present study we investigated the antiinflammatory effects of DIM on experimental colitis and colitis-associated colorectal carcinogenesis.



Methods: To determine if DIM has an antiinflammatory effect in vivo, we examined the therapeutic effects of DIM in dextran sodium sulfate (DSS)-induced experimental colitis and colitis-associated colon carcinogenesis induced by azoxymethane (AOM)/DSS in BALB/c mice.



Results: Treatment with DIM significantly attenuated loss of body weight, shortening of the colon, and severe clinical signs in a colitis model. This was associated with a remarkable amelioration of the disruption of the colonic architecture and a significant reduction in colonic myeloperoxidase activity and production of prostaglandin E2, nitric oxide, and proinflammatory cytokines. Further, DIM administration dramatically decreased the number of colon tumors in AOM/DSS mice.



Conclusions: These results suggest that DIM-mediated antiinflammatory action at colorectal sites may be therapeutic in the setting of inflammatory bowel disease and colitis-associated colon cancer.



(Inflamm Bowel Dis 2009)

3,3'-diindolylmethane attenuates colonic inflammation and tumorigenesis in mice.

Antiangiogenic effect of licochalcone A.

Licochalcone A (LicA), a major phenolic constituent of licorice, has antiproliferative and anti-inflammatory properties in human and murine cell lines. We previously showed that LicA down-regulates the expression of cyclooxygenase (COX)-2 and inducible nitric oxide synthase (iNOS) via the modulation of nuclear factor-κB and activator protein-1 activation in cell culture. We therefore tested whether LicA inhibits carcinogenesis and metastasis in mouse models. To induce colon carcinogenesis, C57BL/6 mice were given a single intraperitoneal injection of azoxymethane (10 mg/kg body weight), followed by 1% dextran sulfate sodium in the drinking water. Additionally, we also assessed the effect of LicA on liver metastasis by intrasplenic injection of BALB/c mice with CT-26 cells. Feeding the mice with LicA (5, 15, and 30 mg/kg body weight) significantly reduced tumor formation as well as the number of cells expressing proliferating cell nuclear antigen, β-catenin, COX-2, and iNOS in the colon. LicA also decreased colon levels of proinflammatory cytokines and chemokines. In addition, LicA significantly increases survival of animals and inhibited liver metastasis as well as the expression of matrix metalloproteinase-9 in the liver. These preclinical studies indicate that LicA has potent antitumor and antimetastatic activity, suggesting that LicA could increase efficacy and improve patient outcomes in colorectal cancer.

Antitumor and antimetastatic effects of licochalcone A in mouse models.

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