| Description: |
Tectorigenin has hepatoprotective, antifibrotic, anti-leukemia, antioxidant, and anti-inflammatory activities, it could sensitize paclitaxel-resistant human ovarian cancer cells through inactivation of the Akt/IKK/IκB/NFκB signaling pathway, and promise a new intervention to chemosensitize paclitaxel-induced cytotoxicity in ovarian cancer. |
| Targets: |
PPAR | NF-kB | IkB | TNF-α | p65 | IL Receptor | NOS | COX | NO | PGE | Caspase | Akt | IKK |
| In vitro: |
| Pharm Biol. 2015 Apr 9:1-9. | | Tectorigenin regulates adipogenic differentiation and adipocytokines secretion via PPARγ and IKK/NF-κB signaling.[Pubmed: 25856699] | Obesity is associated with a number of diseases with metabolic abnormalities such as type 2 diabetes (T2D). OBJECTIVE: We investigate the effects of Tectorigenin on 3T3-L1 preadipocyte differentiation and adipocytokines secretion.
METHODS AND RESULTS:
The effects of Tectorigenin on adipocyte differentiation were studied using Oil Red O staining. Effects of Tectorigenin on adipogenesis-related genes expression and adipocytokines secretion were measured by the real-time quantitative RT-PCR and ELISA method, respectively. Reporter gene assays were performed to determine the PPARγ and NF-κB transactivation. We also used [3H]-2-deoxy-d-glucose to study the glucose uptake, and the IKK/NF-κB signaling pathway was assessed by western blot analysis. HFD/STZ rats were used to evaluate the therapeutic efficacies of Tectorigenin. Tectorigenin 10, 25, 50, and 75 μM inhibited 3T3-L1 adipogenesis and related genes transcription. TNF-α-induced changes of IL-6, MCP-1, as well as adiponectin in 3T3-L1 were markedly reversed by Tectorigenin at 75 μM. Further investigation using reporter gene revealed that Tectorigenin was a partial PPARγ agonist with an IC50 value of 13.3 μM. Tectorigenin improved basal and insulin-stimulated glucose uptake in mature 3T3-L1 adipocytes. Moreover, Tectorigenin antagonized TNF-α-induced NF-κB transactivation and p65 nuclear translocation. Although Tectorigenin (50 and 100 mg/kg) displayed the ability to promote insulin sensitivity and improve glucose metabolism in HFD/STZ rats, it did not cause significant side effects such as body weight gain, fluid retention, or cardiac hypertrophy.
CONCLUSIONS:
These results suggest that Tectorigenin may ameliorate hyperglycemia by blocking preadipocyte differentiation and adipocytokines secretion in which PPARγ and NF-κB signaling pathways were involved. | | Arch. Pharm. Res., 2008, 31(11):1447-56. | | Tectorigenin inhibits IFN-γ/LPS-induced inflammatory responses in murine macrophage RAW 264.7 cells.[Reference: WebLink] | Tectorigenin (Tg) and tectoridin (Td) are the major compounds isolated from the rhizomes of iridaceous plant Belamcanda chinensis which is well known as a chinese traditional medicine for the treatment of inflammatory diseases.
METHODS AND RESULTS:
In this study we investigated whether Tectorigenin and tectoridin can be applied to the suppression of interferon-γ and lipopolysaccharide (IFN-γ/LPS)-induced inflammatory responses in macrophages. Anti-inflammatory activities of Tectorigenin and tectoridin were compared with genistein (Ge), well known isoflavonoid as a phytoestrogen and regarded as an emerging anti-inflammatory agent. Both compounds showed low cytotoxic effect. In Raw 264.7 cells activated with IFN-γ/LPS, pre-treated Tectorigenin was found to inhibit the expression of inducible nitric oxide synthase (iNOS), the production of nitric oxide (NO) and the secretion of interleukin (IL)-1β dose-dependently. Tectorigenin also decreased the expression of cyclooxigenase (COX)-2 and the production of prostaglandin E2 (PGE2) in dose-dependent manner. These inhibitory effects of Tectorigenin were found to be caused by the blocking of nuclear factor kappa-B (NF-κB) activation. Compared with genistein and tectoridin, Tectorigenin showed significant inhibitory effect for almost anti-inflammatory tests in this study.
CONCLUSIONS:
All these results clearly demonstrated that Tectorigenin appears to have the potential to prevent inflammation. |
|
| In vivo: |
| Chin J Nat Med. 2014 Nov;12(11):841-6. | | Tectorigenin inhibits the inflammation of LPS-induced acute lung injury in mice.[Pubmed: 25480515] | In a previous study, the anti-inflammatory effects of Tectorigenin were disclosed. In this study, the anti-inflammatory effects of Tectorigenin on acute lung injury using a lipopolysaccharide (LPS)-induced acute lung injury (ALI) mouse model were investigated.
METHODS AND RESULTS:
The cell-count in the bronchoalveolar lavage fluid (BALF) was measured. The animal lung edema degree was evaluated by the wet/dry weight (W/D) ratio. The superoxidase dismutase (SOD) activity and myeloperoxidase (MPO) activity was assayed using SOD and MPO kits, respectively. The levels of inflammatory mediators, including tumor necrosis factor-α (TNF-α), IL-1β, and IL-6 were assayed using an enzyme-linked immunosorbent assay method. Pathological changes of lung tissues were observed through HE staining. The inflammatory signal pathway related protein nuclear factor NF-κB p65 mRNA expression was measured by real-time PCR, and the protein level of NF-κB p65 was measured using Western blotting analysis. The data showed that treatment with the Tectorigenin markedly attenuated the inflammatory cell numbers in the BALF, decreased nuclear factor NF-κB p65 mRNA level and protein level in the lungs, and improved SOD activity and inhibited MPO activity. Histological studies showed that Tectorigenin substantially inhibited LPS-induced neutrophils in lung tissue compared with the model group.
CONCLUSIONS:
The results indicated that Tectorigenin had a protective effect on LPS-induced ALI in mice. | | J Ethnopharmacol. 2010 Aug 19;131(1):165-73. | | Tectorigenin inhibits the in vitro proliferation and enhances miR-338* expression of pulmonary fibroblasts in rats with idiopathic pulmonary fibrosis.[Pubmed: 20600766 ] | Tectorigenin is one of the main components in rhizomes of Iris tectorum, which is traditionally used to treat disorders such as hepatic cirrhosis caused by fibrosis. Idiopathic pulmonary fibrosis (IPF), one of the most common interstitial lung diseases, is caused by accumulation of fibroblasts in lungs.
In this work we sought to examine the effects of tectorigenin on pulmonary fibroblasts in the IPF animal model and investigated the molecular mechanism (microRNA regulation) of tectorigenin treatment.
METHODS AND RESULTS:
A well-known animal disease model of pulmonary fibrosis in rat was established by intratracheally instilling of bleomycin. In vitro cultured pulmonary fibroblasts in bleomycin-treated rats and in controls were treated with or without tectorigenin. Comparative analyses of cell proliferation, apoptosis and cell cycle of pulmonary fibroblasts in bleomycin-treated rats and in controls were performed. Expression of miR-338* and its candidate gene LPA1 related to IPF of tectorigenin-treated pulmonary fibroblasts in bleomycin-treated rats were further investigated.
Tectorigenin significantly inhibited the proliferation of pulmonary fibroblasts in bleomycin-treated rats but not in controls. However, no altered cell cycle and apoptosis of pulmonary fibroblasts in bleomycin-treated rats and in controls was observed after tectorigenin treatment. Tectorigenin remarkably enhanced miR-338* expression of pulmonary fibroblasts in bleomycin-treated rats and downregulated LPA1 in the protein level.
CONCLUSIONS:
Tectorigenin inhibits the proliferation of pulmonary fibroblasts in vitro and enhances miR-338* expression, which might in turn downregulate LPA1. This indicates a potential inhibitory role of tectorigenin on the pathogenesis of IPF. |
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