DMSO : 250 mg/mL (241.74 mM; Need ultrasonic)
HS Code Reference
Personal Projective Equipment
For Reference Standard and R&D, Not for Human Use Directly.
provides coniferyl ferulate(CAS#:17406-45-0) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
The mechanism of SlMYC2, involved in methyl jasmonate (MJ)-induced tomato fruit resistance to pathogens, was investigated. The data indicated that MJ treatment enhanced the accumulation of total phenolics and flavonoids, as well as individual phenolic acids and flavonoids, which might be caused by the increased phenylalanine ammonia-lyase and polyphenol oxidase activities, induced pathogenesis-related gene (PR) expression, β-1,3-glucanase and chitinase activities, as well as α-tomatine, by inducing GLYCOALKALOID METABOLISM gene expression. These effects, induced by MJ, partly contributed to tomato fruit resistance to Botrytis cinerea. Nevertheless, the induction effects of MJ were almost counteracted by silence of SlMYC2, and the disease incidence and lesion diameter in MJ + SlMYC2-silenced fruit were higher than those in MJ-treated fruit. These observations are the first evidence that SlMYC2 plays vital roles in MJ-induced fruit resistance to Botrytis cinerea, possibly by regulating defence enzyme activities, SlPRs expression, α-tomatine, special phenolic acids and flavonoid compounds.
Disease resistance; MYC2 transcription factor; Methyl jasmonate; Tomato fruit.
SlMYC2 are required for methyl jasmonate-induced tomato fruit resistance to Botrytis cinerea
Dedong Min 1, Fujun Li 1, Xixi Cui 1, Jingxiang Zhou 1, Jiaozhuo Li 1, Wen Ai 1, Pan Shu 1, Xinhua Zhang 2, Xiaoan Li 1, Demei Meng 3, Yanyin Guo 1, Jian Li 4
Background: Despite of the most effective surgical removal of malignant tumors, metastasis makes cancer treatment difficult. The studies on natural compounds to inhibit this metastasis have been actively performed until now. However, the effect of tomatidine on metastasis remains unclear.
Method: The effect of tomatidine on antioxidative activity was measured with DPPH radical assay and reducing power assay. After treatment with tomatidine, the viability of human fibrosarcoma cells (HT1080 cells) was evaluated with MTT assay. The effect of tomatidine on the inhibition of matrix metalloproteinase-2 (MMP-2) and MMP-9, gelatinases related to metastasis, was analyzed using gelatin zymography, western blot and immunofluorescence staining. Cell invasion assay was used to investigate anti-metastasis activity of tomatidine.
Result: Tomatidine showed no DPPH radical scavenging effect and showed 8% of reduction power at 8 μM. Furthermore, tomatidine below 8 μM showed more than 80% of cell viability in MTT assay. The inhibition of tomatidine on MMP-2 activity and its protein expression levels were observed by gelatin zymography, western blot and immunofluorescence. It was observed that tomatidine inhibited not only p38 and ERK but also cell invasion.
Conclusion: Above results suggest that tomatidine could use as a potential candidate for cancer prevention and metastasis through the inhibitory effect on gelatinase.
AP-1; ERK; Gelatinase; Metastasis; Tomatidine; p38.
Tomatidine inhibits cell invasion through the negative modulation of gelatinase and inactivation of p38 and ERK
Sojeong Jeon 1, Moon-Moo Kim 2
2019 Nov 1
Plasma membrane damage commonly occurs during cellular growth and development. To counteract these potentially lethal injuries, membrane repair mechanisms have evolved, which promote the integrity of the lipid bilayer. Although the membrane of fungi is the target of important clinical drugs and agricultural fungicides, the molecular mechanisms which mediate membrane repair in these organisms remain elusive. Here we identify the penta-EF-hand protein PEF1 of the genetic model fungus Neurospora crassa as part of a cellular response mechanism against different types of membrane injury. Deletion of the pef1 gene in the wild type and different lysis-prone gene knockout mutants revealed a function of the protein in maintaining cell integrity during cell-cell fusion and in the presence of pore-forming drugs, such as the plant defense compound tomatine. By fluorescence and live-cell imaging we show that green fluorescent protein (GFP)-tagged PEF1 accumulates at the sites of membrane injury in a Ca2+-dependent manner. Site-directed mutagenesis identified Ca2+-binding domains essential for the spatial dynamics and function of the protein. In addition, the subcellular localization of PEF1 revealed that the syncytial fungal colony undergoes compartmentation in response to antifungal treatment. We propose that plasma membrane repair in fungi constitutes an additional line of defense against membrane-disturbing drugs, thereby expanding the current model of fungal drug resistance mechanisms.
Neurospora crassa; antifungal drug; cell fusion; membrane repair; penta-EF-hand protein.
Plasma Membrane Integrity During Cell-Cell Fusion and in Response to Pore-Forming Drugs Is Promoted by the Penta-EF-Hand Protein PEF1 in Neurospora crassa
Marcel Rene Schumann 1, Ulrike Brandt 1, Christian Adis 1, Lisa Hartung 1, Andre Fleißner 2
Combination of α-Tomatine and Curcumin Inhibits Growth and Induces Apoptosis in Human Prostate Cancer Cells. PUMID/DOI：DOI: 10.1371/journal.pone.0144293 PLoS One. 2015 Dec 2;10(12):e0144293. a-Tomatine is a glycoalkaloid found in tomatoes and curcumin is a major yellow pigment of turmeric. In the present study, the combined effect of these two compounds on prostate cancer cells was studied. Treatment of different prostate cancer cells with curcumin or a-tomatine alone resulted in growth inhibition and apoptosis in a concentration-dependent manner. Combinations of a-tomatine and curcumin synergistically inhibited the growth and induced apoptosis in prostate cancer PC-3 cells. Effects of the a-tomatine and curcumin combination were associated with synergistic inhibition of NF-?B activity and a potent decrease in the expression of its downstream gene Bcl-2 in the cells. Moreover, strong decreases in the levels of phospho-Akt and phosphor-ERK1/2 were found in PC-3 cells treated with a-tomatine and curcumin in combination. In animal experiment, SCID mice with PC-3 xenograft tumors were treated with a-tomatine and curcumin. Combination of a-tomatine and curcumin more potently inhibited the growth of PC-3 tumors than either agent alone. Results from the present study indicate that a-tomatine in combination with curcumin may be an effective strategy for inhibiting the growth of prostate cancer. Protective effect of tomatine against hydrogen peroxide-induced neurotoxicity in neuroblastoma (SH-SY5Y) cells. PUMID/DOI：DOI: 10.1111/jphp.12205 J Pharm Pharmacol. 2014 Jun;66(6):844-54. OBJECTIVES:Reactive oxygen species can induce cell apoptosis, and oxidative stress has been implicated in a variety of neurodegenerative disorders. Tomatine, which is a naturally occurring steroidal glycoalkaloid isolated from Solanum cathayanum, has shown potent anti-oxidant properties.METHODS:In this study, we used the SH-SY5Y cell line as an in vitro model and investigated the protective effect of tomatine against hydrogen peroxide (H2 O2 )-induced neurotoxicity in SH-SY5Y cells.KEY FINDINGS:Tomatine might inhibit the release of cellular lactate dehydrogenase, increase anti-oxidant enzyme activity and glutathione content, reverse the downregulated protein expression of the brain-derived neurotrophic factor (BDNF), inhibit expression of Bax and activations of caspase-3 and caspase-9 in H2 O2 -induced SH-SY5Y cells.CONCLUSIONS:Tomatine exerted beneficially neuroprotective effect on H2 O2 -induced SH-SY5Y cells, mainly enhancing intracellular anti-oxidant enzyme activity and BDNF expression, inhibiting H2 O2 -induced oxidative stress as well as expression of Bax and activations of caspase-3 and caspase-9, alleviating H2 O2 -induced SH-SY5Y cell injury and cell death. Suppression of 12-O-tetradecanoylphorbol-13-acetate-induced MCF-7 breast adenocarcinoma cells invasion/migration by α-tomatine through activating PKCα/ERK/NF-κB-dependent MMP-2/MMP-9 expressions. PUMID/DOI：DOI: 10.1007/s12013-012-9465-8 Cell Biochem Biophys. 2013 May;66(1):161-74. a-Tomatine, isolated from Lycopersicon esculentum Linn., is a naturally occurring glycoalkaloids in immature green tomatoes. Some reports demonstrated that a-tomatine had various anti-carcinogenic properties. First, the result demonstrated a-tomatine could inhibit TPA-induced the abilities of the adhesion, morphology/actin cytoskeleton arrangement, invasion, and migration by cell-matrix adhesion assay, immunofluorescence stain assay, Boyden chamber invasion assay, and wound-healing assay. Data also showed a-tomatine could inhibit the activation of extracellular signal-regulated kinase 1 and 2 (ERK1/2) and protein kinase C-a (PKCa) involved in the downregulation of the enzyme activities and messenger RNA levels of matrix metalloproteinase-2/9 (MMP-2/MMP-9) induced by TPA. Next, a-tomatine also strongly inhibited TPA-induced the activation of nuclear factor kappa B (NF-?B) and phospho-inhibitor of kappa Ba (phospho-I?Ba). In addition, TPA-induced translocation of PKC-a from cytosol to membranes, and suppression of TPA elicited the expression of PKC-a by adding the PKC-a inhibitors, GF-109203X and G?6983. The treatment of specific inhibitor for ERK (U0126) to MCF-7 cells could inhibit TPA-induced MMP-2/MMP-9 and phospho-ERK along with an inhibition on cell invasion and migration. Application of a-tomatine to prevent the invasion/migration of MCF-7 cells through blocking PKCa/ERK/NF-?B activation is first demonstrated herein. α-Tomatine suppresses invasion and migration of human non-small cell lung cancer NCI-H460 cells through inactivating FAK/PI3K/Akt signaling pathway and reducing binding activity of NF-κB. PUMID/DOI：DOI: 10.1007/s12013-011-9152-1 Cell Biochem Biophys. 2011 Jul;60(3):297-310. α-Tomatine, isolated from Lycopersicon esculentum Linn., is a naturally occurring steroidal glycoalkaloid in immature green tomatoes. Some reports demonstrated that α-tomatine had various anticarcinogenic properties. The purpose of this study is to investigate the anti-metastatic effect of α-tomatine in NCI-H460 human non-small cell lung cancer cells. First, the results showed that α-tomatine significantly suppressed the abilities of the adhesion, invasion, and migration of NCI-H460 cells under non-cytotoxic concentrations. Molecular data also showed α-tomatine could inhibit the activation of focal adhesion kinase (FAK) and phosphatidylinositol 3-kinase (PI3K)/Akt signal involve in the downregulation the enzyme activities, protein and messenger RNA levels of matrix metalloproteinase-7 (MMP-7). Next, α-tomatine also strongly inhibited the degradation of inhibitor of kappaBα (IκBα) and the nuclear levels of nuclear factor kappa B (NF-κB). Also, a dose-dependent inhibition on the binding ability of NF-κB by α-tomatine treatment was further observed. Furthermore, α-tomatine significantly decreased the levels of phospho-Akt and MMP-7 in Akt1-cDNA-transfected cells concomitantly with a marked reduction on cell invasion and migration. Presented results indicated α-tomatine might be further application for treating cancer metastasis. Lowering of plasma LDL cholesterol in hamsters by the tomato glycoalkaloid tomatine. PUMID/DOI：10942315 Food Chem Toxicol. 2000 Jul;38(7):549-53. Tomatoes contain the steroidal glycoalkaloid tomatine, which has been reported to form strong, insoluble complexes with cholesterol in vitro. To determine whether tomatine can reduce dietary cholesterol absorption and plasma levels of cholesterol and triglycerides, we fed hamsters a high-fat, high-cholesterol diet with 0.05-0.2% added tomatine in the diet. The tomatine diets induced lowering of serum low-density lipoprotein (LDL) without changing high-density lipoprotein (HDL) cholesterol. Compared to the control diets, four- to fivefold more labeled dietary cholesterol and coprostanol was excreted in the feces of the tomatine-fed hamsters. The amount of cholesterol excreted in the feces corresponded to the amount of tomatine in the diet. These observations suggest that due to the formation of an insoluble tomatine-cholesterol complex and its excretion in the feces, very little dietary tomatine is absorbed from the digestive tract into the blood stream. They are also consistent with the reported low oral toxicity of tomatine compared to other glycoalkaloids. Tomatidine inhibits iNOS and COX-2 through suppression of NF-kappaB and JNK pathways in LPS-stimulated mouse macrophages. PUMID/DOI：DOI: 10.1016/j.febslet.2008.05.049 FEBS Lett. 2008 Jul 9;582(16):