| In vitro: |
| Stem Cells Dev. 2014 Jan 15;23(2):146-54. | | Curculigoside improves osteogenesis of human amniotic fluid-derived stem cells.[Pubmed: 24007307 ] | Curculigoside, a phenolic glycoside, is the main active compound of Curculigo orchioides (Amaryllidaceae, rhizome). C. orchioides is a traditional Chinese herbal medicine and has been commonly used to treat orthopedic disorders and bone healing in Asia. This study evaluated the effect of Curculigoside on osteogenic differentiation of human amniotic fluid-derived stem cells (hAFSCs).
METHODS AND RESULTS:
The results showed that Curculigoside stimulated alkaline phosphatase activity and calcium deposition of hAFSCs during osteogenic differentiation in a dose-dependent manner (1-100 μg/mL), while the effects were reduced at the higher concentration of 200 μg/mL. From reverse transcriptase-polymerase chain reaction analysis, the osteogenic genes osteopontin (OPN) and Collagen I were upregulated with Curculigoside treatment (1-100 μg/mL). Concurrently, the ratio of osteoprotegerin (OPG) to receptor activator of nuclear factor kappa-B ligand (RANKL) was increased, indicating the inhibition of osteoclastogenesis by Curculigoside. Moreover, the role of Wnt/β-catenin signaling during Curculigoside treatment was revealed by the upregulation of β-catenin and Cyclin D1.
CONCLUSIONS:
In summary, Curculigoside improved osteogenesis and inhibited osteoclastogenesis of hAFSCs, suggesting its potential use to regulate hAFSC osteogenic differentiation for treating bone disorders.
| | J Ethnopharmacol. 2010 Oct 28;132(1):233-9. | | Curculigoside attenuates human umbilical vein endothelial cell injury induced by H2O2.[Pubmed: 20713149] | Vessel endothelium injury caused by reactive oxygen species (ROS) including H(2)O(2) plays a critical role in the pathogenesis of cardiovascular disorders. Therefore, agents or antioxidants that can inhibit production of ROS has highly clinical values in cardiovascular therapy. Curculigoside is the major bioactive compounds present in Curculigo orchioides, and possess potent antioxidant properties against oxidative stress insults through undefined mechanism(s). The present study was designed to test the hypothesis that Curculigoside can inhibit H(2)O(2)-induced injury in human umbilical vein endothelial cells.
METHODS AND RESULTS:
Human umbilical vein endothelial cells (HUVECs) were treated with Curculigoside in the presence/absence of hydrogen peroxide (H(2)O(2)). The protective effects of Curculigoside OP-D against H(2)O(2) were evaluated.
HUVECs incubated with 400 μM H(2)O(2) had significantly decreased the viability of endothelial cells, which was accompanied with apparent cells apoptosis, the activation of caspase-3 and the upregulation of p53 mRNA expression. In addition, H(2)O(2) treatment induced a marked increase of MDA, LDH content and in intracellular ROS, decreased the content of nitric oxide (NO) and GSH-Px activities in endothelial cells. However, pretreatment with 0.5.5,10 μM Curculigoside resulted in a significant recovery from H(2)O(2)-induced cell apoptosis. Also, it decreased other H(2)O(2)-induced damages in a concentration-dependent manner. Furthermore, pretreatment with Curculigoside decreased the activity of caspase-3 and p53 mRNA expression, which was known to play a key role in H(2)O(2)-induced cell apoptosis.
CONCLUSIONS:
The present study shows that Curculigoside can protect endothelial cells against oxidative injury induced by H(2)O(2), suggesting that this compound may constitute a promising intervention against cardiovascular disorders. | | Arch Pharm Res. 2009 Oct;32(10):1433-9. | | The effect of curculigoside on the expression of matrix metalloproteinase-1 in cultured human skin fibroblasts.[Pubmed: 19898807 ] | The dried rhizomes of Curculigo orchioides G. yielded two phenolic glycosides, Curculigoside (1), orcinol-beta-D-glucoside (4), and two cycloartane saponins, curculigosaponin G (2), curculigosaponin I (3). The structures were determined using spectroscopic methods.
METHODS AND RESULTS:
Among these isolates, compound 1 exhibited potent inhibitory activity against matrix metalloproteinase-1 in cultured human skin fibroblasts. In addition, it increased the level of Bcl-2 protein expression and decreased the level of Bax protein expression. Compound 4 was isolated from this plant for the first time. | | Mol Med Rep . 2019 Mar;19(3):2057-2064. | | Curculigoside exerts significant anti‑arthritic effects in vivo and in vitro via regulation of the JAK/STAT/NF‑κB signaling pathway[Pubmed: 30664158] | | Abstract
The present study aimed to investigate the anti‑arthritic effects of Curculigoside isolated from the rhizome of Curculigo orchioides Gaertn in vivo and in vitro, as well as to determine the potential underlying mechanisms. A rat model of arthritis was induced with type II collagen. Arthritic rats were treated with Curculigoside (50 mg/kg) and blood samples were collected to determine serum levels of tumor necrosis factor (TNF)‑α, interleukin (IL)‑1β, IL‑6, IL‑10, IL‑12 and IL‑17A. Furthermore, indices of the thymus and spleen were determined. The anti‑proliferative effects of Curculigoside were detected with Cell Counting kit‑8 assays in rheumatoid arthritis‑derived fibroblast‑like synoviocyte MH7A cells. In addition, expression levels of Janus kinase (JAK)1, JAK3, signal transducer and activator of transcription (STAT)3, nuclear factor (NF)‑κB p65 and its inhibitor (IκB) were determined by western blotting. The results revealed that Curculigoside inhibited paw swelling and arthritis scores in type II collagen‑induced arthritic (CIA) rats. Additionally, Curculigoside decreased serum levels of TNF‑α, IL‑1β, IL‑6, IL‑10, IL‑12 and IL‑17A in CIA rats. Curculigoside also significantly inhibited MH7A cell proliferation in a time and concentration‑dependent manner. Furthermore, treatment downregulated the expression of JAK1, JAK3 and STAT3, and upregulated cytosolic nuclear factor (NF)‑κB p65 and IκB. In conclusion, the results of the present study indicated that Curculigoside exhibited significant anti‑arthritic effects in vivo and in vitro, and the molecular mechanism may be associated with the JAK/STAT/NF‑κB signaling pathway. |
|
| In vivo: |
| J Pharm Pharmacol. 2013 Jul;65(7):1005-13. | | Curculigoside promotes osteogenic differentiation of bone marrow stromal cells from ovariectomized rats.[Pubmed: 23738728 ] | Curculigoside, a natural compound isolated from the medicinal plant Curculigo orchioides has been reported to prevent bone loss in ovariectomized rats. However, the underlying molecular mechanisms are largely unknown. This study investigated the effects of Curculigoside on proliferation and osteogenic differentiation of bone marrow stromal cells (BMSCs).
METHODS AND RESULTS:
The toxicity, proliferation and osteogenic differentiation of BMSCs cultured with various concentrations (0 as control, 10, 100 and 500 μm) of Curculigoside were measured by viability assay, MTT analysis, alkaline phosphatase (ALP) activity assay, alizarin red staining and mineralization assay, real-time PCR analysis on osteogenic genes including ALP, type I collagen (Col I), osteocalcin (OCN) and osteoprotegerin (OPG), runt-related transcription factor 2 (Runx2), as well as OPG enzyme-linked immunosorbent assay.
No significant cytotoxicity was observed for BMSCs after supplementation with Curculigoside. The proliferation of BMSCs was enhanced after administration of Curculigoside, especially 100 μm Curculigoside. Moreover, the osteogenic gene expression was significantly enhanced with 100 μm Curculigoside treatment. Importantly, Curculigoside significantly increased OPG secretion.
CONCLUSIONS:
The data indicate that Curculigoside could promote BMSC proliferation and induce osteogenic differentiation of BMSCs. The most profound response was observed with 100 μm Curculigoside. These findings may be valuable for understanding the mechanism of the effect of Curculigoside on bone, especially in relation to osteoporosis.
|
|
Cell. 2018 Jan 11;172(1-2):249-261.e12. doi: 10.1016/j.cell.2017.12.019.IF=36.216(2019)
Cell Metab. 2020 Mar 3;31(3):534-548.e5. doi: 10.1016/j.cmet.2020.01.002.IF=22.415(2019)
Mol Cell. 2017 Nov 16;68(4):673-685.e6. doi: 10.1016/j.molcel.2017.10.022.IF=14.548(2019)
ACS Nano. 2018 Apr 24;12(4): 3385-3396. doi: 10.1021/acsnano.7b08969.IF=13.903(2019)
Nature Plants. 2016 Dec 22;3: 16206. doi: 10.1038/nplants.2016.205.IF=13.297(2019)
Sci Adv. 2018 Oct 24;4(10): eaat6994. doi: 10.1126/sciadv.aat6994.IF=12.804(2019)