Alisol B
Alisol B, a novel inhibitor of the sarcoplasmic/endoplasmic reticulum Ca(2+) ATPase pump, induces autophagy, endoplasmic reticulum stress, and apoptosis.Alisol B may be a potential novel therapeutic molecule for bone disorders through targeting the differentiation of osteoclasts as well as their functions. Alisol B also inhibited RANKL-induced expression of NFATc1 and c-Fos, which are key transcription factors for osteoclastogenesis.
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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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Zhongguo Zhong Xi Yi Jie He Za Zhi. 2012 Oct;32(10):1407-12.
Alisol B inhibited complement 3a-induced human renal tubular epithelial to mesenchymal transition[Pubmed:
23163157]
To study whether Alisol B could inhibit complement 3a (C3a) induced renal tubular epithelial-mesenchymal transition (EMT).
METHODS AND RESULTS:
The in vitro cultured human renal tubular epithelial HK-2 cells were intervened with 5 ng/mL transforming growth factor-beta (TGF-beta), 0.1 micromol C3a, and 0.1 micromol C3a + 10 micromol Alisol B, respectively. The mRNA and protein expressions of alpha-SMA, E-cadherin, and C3 were detected using RT-PCR, Western blot, and immunofluorescence, respectively.
The mRNA and protein expressions of C3 in HK-2 cells were up-regulated after intervention of C3a (P < 0.01), the mRNA and protein expressions of alpha-SMA in HK-2 cells were obviously enhanced (P < 0.01), the mRNA and protein expressions of E-cadherin obviously decreased (P < 0.01). When compared with the group intervened by exogenous C3a, after intervention of Alisol B, the mRNA and protein expressions of alpha-SMA in HK-2 cells were obviously reduced (P < 0.01), the mRNA and protein expressions of E-cadherin obviously increased (P < 0.05).
CONCLUSIONS:
Exogenous C3a could induce renal tubular EMT. Alisol B was capable of suppressing C3a induced EMT.
Biochem Pharmacol. 2010 Aug 1;80(3):352-61.
Alisol-B, a novel phyto-steroid, suppresses the RANKL-induced osteoclast formation and prevents bone loss in mice.[Pubmed:
20412788]
Osteoclasts, bone-resorbing multinucleated cells, are differentiated from hemopoietic progenitors of the monocyte/macrophage lineage. Bone resorption by osteoclasts is considered a potential therapeutic target to the treatment of erosive bone diseases, including osteoporosis, rheumatoid arthritis, and periodontitis.
METHODS AND RESULTS:
In the present study, we found that Alisol B, a phyto-steroid from Alisma orientale Juzepczuk, exhibited inhibitory effects on osteoclastogenesis both in vitro and in vivo. Although RT-PCR analysis showed that Alisol B did not affect the 1alpha,25(OH)(2)D(3)-induced expressions of RANKL, OPG and M-CSF mRNAs in osteoblasts, addition of Alisol B to co-cultures of mouse bone marrow cells and primary osteoblasts with 10(-8)M 1alpha,25(OH)(2)D(3) caused significant inhibition of osteoclastogenesis. We further examined the direct effects of Alisol B on osteoclast precursors. Alisol B strongly inhibited RANKL-induced osteoclast formation when added during the early stage of cultures, suggesting that Alisol B acts on osteoclast precursors to inhibit RANKL/RANK signaling. Among the RANK signaling pathways, Alisol B inhibited the phosphorylation of JNK, which are upregulated in response to RANKL in bone marrow macrophages, Alisol B also inhibited RANKL-induced expression of NFATc1 and c-Fos, which are key transcription factors for osteoclastogenesis. In addition, Alisol B suppressed the pit-forming activity and disrupted the actin ring formation of mature osteoclasts. In a hypercalcemic mouse model induced by 2-methylene-19-nor-(20S)-1alpha,25(OH)(2)D(3) (2MD), an analog of 1alpha,25(OH)(2)D(3), administration of Alisol B significantly suppressed 2MD-induced hypercalcemia as resulting from the inhibition of osteoclastogenesis.
CONCLUSIONS:
Taken together, these findings suggest that Alisol B may be a potential novel therapeutic molecule for bone disorders by targeting the differentiation of osteoclasts as well as their functions.
Mol Cancer Ther. 2010 Mar;9(3):718-30.
Alisol B, a novel inhibitor of the sarcoplasmic/endoplasmic reticulum Ca(2+) ATPase pump, induces autophagy, endoplasmic reticulum stress, and apoptosis.[Pubmed:
20197400]
Emerging evidence suggests that autophagic modulators have therapeutic potential. This study aims to identify novel autophagic inducers from traditional Chinese medicinal herbs as potential antitumor agents.
METHODS AND RESULTS:
Using an image-based screen and bioactivity-guided purification, we identified Alisol B 23-acetate, alisol A 24-acetate, and Alisol B from the rhizome of Alisma orientale as novel inducers of autophagy, with Alisol B being the most potent natural product. Across several cancer cell lines, we showed that Alisol B-treated cells displayed an increase of autophagic flux and formation of autophagosomes, leading to cell cycle arrest at the G(1) phase and cell death. Alisol B induced calcium mobilization from internal stores, leading to autophagy through the activation of the CaMKK-AMPK-mammalian target of rapamycin pathway. Moreover, the disruption of calcium homeostasis induces endoplasmic reticulum stress and unfolded protein responses in Alisol B-treated cells, leading to apoptotic cell death. Finally, by computational virtual docking analysis and biochemical assays, we showed that the molecular target of Alisol B is the sarcoplasmic/endoplasmic reticulum Ca(2+) ATPase.
CONCLUSIONS:
This study provides detailed insights into the cytotoxic mechanism of a novel antitumor compound.
