Tigogenin
Tigogenin is one of steroidal sapogenins which is widely used for synthesizing steroid drugs. It might have protective effect on bone and be helpful in preventing the development of osteoporosis.Tigogenin induces apoptosis, associated with overexpression of COX-2 correlated with overproduction of endogenous PGE2. Tigogenin inhibited of PPARgamma and via p38 MAPK pathway.
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Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to
24 months(2-8C).
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
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The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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Int J Mol Med. 2007 Oct;20(4):451-60.
Inhibition of human rheumatoid arthritis synovial cell survival by hecogenin and tigogenin is associated with increased apoptosis, p38 mitogen-activated protein kinase activity and upregulation of cyclooxygenase-2.[Pubmed:
17786275]
We conducted our study to assess the antiproliferative and proapoptotic potential of hecogenin and Tigogenin, two saponins which are structurally similar to diosgenin.
METHODS AND RESULTS:
We particularly focused our attention on mitogen-activated protein kinase (MAPK) activation in relation to apoptosis but also with the COX-2 expression and activity. Rheumatoid arthritis (RA) synoviocytes were isolated from fresh synovial biopsies obtained from five RA patients undergoing hip arthroplasty. Measurement of cell proliferation was determined using the MTT assay. Apoptosis was evaluated by studying caspase-8, caspase-9 and caspase-3 activities but also by quantification of DNA fragmentation. Quantification of human phospho-MAPKs was realized by ELISA. COX-2 expression was demonstrated by Western blot analysis and COX-2 activity by assay of endogenous prostaglandin E2 (PGE2) production. Tigogenin was more effective than hecogenin in inducing apoptosis in human RA fibroblast-like synoviocytes (FLS) which was caspase dependent but poly(ADP-ribose) polymerase independent and characterized by DNA fragmentation. Our results demonstrated hecogenin- and Tigogenin-induced apoptosis through activation of p38 without affecting the JNK and ERK pathways. Indeed, pretreatment with a p38 inhibitor decreased saponin-induced apoptosis with a significant decrease in DNA fragmentation. Furthermore, the rate of apoptosis induced by hecogenin or Tigogenin was associated with overexpression of COX-2 correlated with overproduction of endogenous PGE2.
CONCLUSIONS:
These new results provide strong evidence that a family of structurally similar plant steroids is capable of inducing apoptosis in human RA FLS with different rates and different signalling pathways. This study also confirms the discussed appearance of the downregulation or upregulation of COX-2 in cell apoptosis as a function of cell type.
Mol Cell Endocrinol. 2007 May 30;270(1-2):17-22.
Tigogenin inhibits adipocytic differentiation and induces osteoblastic differentiation in mouse bone marrow stromal cells.[Pubmed:
17363141]
We investigated the effect of Tigogenin on adipocytic and osteoblastic differentiation in mouse bone marrow stromal cells (BMSCs).
METHODS AND RESULTS:
Tigogenin enhanced the proliferation of BMSCs significantly. Tigogenin treatment reduced the adipogenic induction of lipid accumulation, visfatin secretion, and the expressions of peroxisome proliferation-activated receptor (PPAR)gamma2 and adipocyte fatty acid-binding protein (ap)2. Moreover, Tigogenin had no effect on the mitotic clonal expansion. On the other hand, Tigogenin significantly elevated alkaline phosphatase (ALP) activity and the expressions of Cbfa1, collagen type I (COL I) and osteocalcin (OCN), as well as the content of matrix calcium in BMSCs. Further, SB-203580 antagonized the Tigogenin-promoted osteogenesis.
CONCLUSIONS:
These observations suggested that Tigogenin may modulate differentiation of BMSCs to cause a lineage shift away from the adipocytes and toward the osteoblasts, which is at least mediated by inhibition of PPARgamma and via p38 MAPK pathway, and is a potential drug preventing the development of osteoporosis and the related disorders.
Carbohydr Res. 2014 Jan 13;383:21-6.
Efficient one-pot synthesis of tigogenin saponins and their antitumor activities.[Pubmed:
24239606]
CONCLUSIONS:
An efficient synthesis of naturally occurring Tigogenin triglycoside 1a and its three derivatives 1b-d bearing different carbohydrate moieties, as well as their antitumor activities, is described.
Partially protected thiogalactosides bearing unprotected 2,4-OH or 4-OH groups were used to facilitate regioselective reactions for one-pot sequential multi-step glycosylation, which has significantly simplified the target molecule synthesis.
CONCLUSIONS:
The synthetic saponins 1a-d exhibited much higher anti-tumor activities than the positive control cisplatin against the human epithelial cervical cancer cell (HeLa) as evaluated by CCK-8 assay.
