Sphondin
(Synonyms: 牛防风素) 目录号 : GC60345
Sphondin可从Heracleumlaciniatum中分离，对IL-1β诱导的A549细胞中COX-2蛋白和PGE2释放水平的升高具有抑制作用。
Cas No.:483-66-9
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
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- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Sphondin, isolated from Heracleum laciniatum, possesses an inhibitory effect on IL-1β-induced increase in the level of COX-2 protein and PGE2 release in A549 cells[1].
Pretreatment of A549 cells with Sphondin (10-50 μM) concentration-dependently attenuates IL-1β-induced COX-2 protein expression and PGE2 release[1].
[1]. Ling Ling Yang, et al. Effects of Sphondin, Isolated From Heracleum Laciniatum, on IL-1beta-induced cyclooxygenase-2 Expression in Human Pulmonary Epithelial Cells. Life Sci. 2002 Nov 29;72(2):199-213.
| Cas No. | 483-66-9 | SDF | |
| 别名 | 牛防风素 | ||
| Canonical SMILES | O=C1C=CC2=C(C3=C(OC=C3)C(OC)=C2)O1 | ||
| 分子式 | C12H8O4 | 分子量 | 216.19 |
| 溶解度 | DMSO : 25 mg/mL (115.64 mM; ultrasonic and warming and heat to 60°C) | 储存条件 | |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
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1 mg | 5 mg | 10 mg |
| 1 mM | 4.6256 mL | 23.1278 mL | 46.2556 mL |
| 5 mM | 0.9251 mL | 4.6256 mL | 9.2511 mL |
| 10 mM | 0.4626 mL | 2.3128 mL | 4.6256 mL |
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| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
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| % DMSO % % Tween 80 % saline | ||||||||||
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计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
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1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
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Sphondin efficiently blocks HBsAg production and cccDNA transcription through promoting HBx degradation
J Med Virol 2023 Mar;95(3):e28578.PMID:36846971DOI:10.1002/jmv.28578.
Hepatitis B surface antigen (HBsAg) loss and seroconversion, which is considered as functional cure of chronic Hepatitis B virus (HBV) infection, is rarely achieved even after long-term antiviral treatments. Therefore, new antiviral strategies interfering with other HBV replication steps are required, especially those that could efficiently inhibit HBsAg production. Here, we identified novel anti-HBV compounds that could potently block HBsAg expression from cccDNA by screening a natural compound library derived from Chinese traditional medical plants by a novel screening strategy. The combination of ELISA assay detecting the HBsAg and real-time PCR detecting HBV RNAs as indicator for cccDNA transcriptional activity were used. The antiviral activity of a candidate compound and underlying mechanism were evaluated in HBV-infected cells and a humanized liver mouse model. Herein, we selected a highly effective low-cytotoxic compound Sphondin, which could effectively inhibit both intracellular HBsAg production and HBV RNAs levels. Moreover, we found that Sphondin markedly inhibited cccDNA transcriptional activity without affecting cccDNA level. Mechanistic study found Sphondin preferentially bound to HBx protein by residue Arg72, which led to increased 26S proteasome-mediated degradation of HBx. Sphondin treatment significantly reduced the recruitment of HBx to cccDNA, which subsequently led to inhibition of cccDNA transcription and HBsAg expression. The absence of HBx or R72A mutation potently abrogated the antiviral effect induced by Sphondin in HBV-infected cells. Collectively, Sphondin may be considered as a novel and natural antiviral agent directly targeting HBx protein, which effectively inhibited cccDNA transcription and HBsAg expression.
Effects of Sphondin, isolated from Heracleum laciniatum, on IL-1beta-induced cyclooxygenase-2 expression in human pulmonary epithelial cells
Life Sci 2002 Nov 29;72(2):199-213.PMID:12417253DOI:10.1016/s0024-3205(02)02173-2.
Recently, under large-scale screening experiments, we found that Sphondin, a furanocoumarin derivative isolated from Heracleum laciniatum, possessed an inhibitory effect on IL-1beta-induced increase in the level of COX-2 protein and PGE(2) release in A549 cells. Accordingly, we examined in the present study the action mechanism of Sphondin on the inhibition of IL-1beta-induced COX-2 protein expression and PGE(2) release in a human pulmonary epithelial cell line (A549). Pretreatment of cells with Sphondin (10-50 microM) concentration-dependently attenuated IL-1beta-induced COX-2 protein expression and PGE(2) release. The IL-1beta-induced increase in COX-2 mRNA expression was also attenuated by Sphondin (50 microM). The selective COX-2 inhibitor, NS-398 (0.01-1 microM), inhibited the activity of the COX-2 enzyme in a concentration-dependent manner, while Sphondin (10-50 microM) had no effect. Sphondin (50 microM) did not affect the IL-1beta-induced activations of p44/42 MAPK, p38 MAPK, and JNK. Treatment of cells with Sphondin (50 microM) or the NF-kappaB inhibitor, PDTC (50 microM) partially inhibited IL-1beta-induced degradation of IkappaB-alpha in the cytosol and translocation of p65 NF-kappaB from the cytosol to the nucleus. Furthermore, IL-1beta-induced NF-kappaB-specific DNA-protein complex formation in the nucleus was partially inhibited by Sphondin (50 microM) or PDTC (50 microM). Taken together, we demonstrate that Sphondin inhibits IL-1beta-induced PGE(2) release in A549 cells; this inhibition is mediated by suppressing of COX-2 expression, rather than by inhibiting COX-2 enzyme activity. The inhibitory mechanism of Sphondin on IL-1beta-induced COX-2 expression may be, at least in part, through suppression of NF-kappaB activity. We conclude that Sphondin may have the therapeutic potential as an anti-inflammatory drug on airway inflammation.
Delayed phototoxic effects of 8-methoxypsoralen, khellin, and Sphondin inAedes aegypti
J Chem Ecol 1986 Apr;12(4):899-914.PMID:24306978DOI:10.1007/BF01020260.
At concentrations up to 6.7 ppm, 8-methoxypsoralen, Sphondin, and khellin are not toxic to first-instar larvae of the mosquitoAedes aegypti. The irradiation of sensitized larvae with long-wavelength ultraviolet light did not always produce any immediate toxicity enhancement, but delayed effects were clearly visible. These were observed over the development of the organisms from first-instar larvae to adults. No adverse effects were noted when larvae were irradiated in the absence of sensitizers, or when they were placed in solutions of sensitizers which had been previously irradiated with the same light sources. 8-Methoxypsoralen was slightly more phototoxic than its isomer Sphondin. Khellin, recently reported to undergo photoinduced cyclization with DNA components, showed minimal phototoxicity in the concentration range used.
Phototoxicity from furocoumarins (psoralens) of Heracleum laciniatum in a patient with vitiligo. Action spectrum studies on bergapten, pimpinellin, angelicin and Sphondin
Contact Dermatitis 1983 Sep;9(5):364-6.PMID:6627920DOI:10.1111/j.1600-0536.1983.tb04429.x.
Investigations on light reactions in a patient with vitiligo are presented. The minimal erythema dose (MED) in the UVB area was approximately 1/3 of that in persons of skin type II. The application of furocoumarins (psoralens) increased light tolerance by 1 MED at 300-310 nm. Action spectrum studies with furocoumarins from Heracleum laciniatum showed the following order of potency: bergapten, pimpinellin, angelicin and Sphondin. The efficacy was highest at 325-350 nm, with maxima at 330-335 nm. Pimpinellin was recently found to be phototoxic, but an action spectrum of Sphondin is reported for the first time.
Inducible nitric oxide synthase inhibitors of Chinese herbs. Part 2: naturally occurring furanocoumarins
Bioorg Med Chem 2000 Dec;8(12):2701-7.PMID:11131161DOI:10.1016/s0968-0896(00)00200-5.
Inducible nitric oxide synthase (iNOS)-dependent production of nitric oxide (NO) plays an important role in inflammation. The effects of various naturally occurring furanocoumarins on NO production in lipopolysaccharide (LPS)-activated RAW 264.7 macrophage cells were evaluated in vitro. The results showed that angelicin, pimpinellin, Sphondin, byakangelicol, oxypeucedanin, oxypeucedanin hydrate, xanthotoxin, and cnidilin are potential NO production inhibitors, and their IC50 values for inhibition of nitrite production were 19.5, 15.6, 9.8, 16.9, 16.8, 15.8, 16.6, and 17.7 microg/mL, respectively. Distinct structure-activity relationships were also revealed for the NO production inhibitory activities of these furanocoumarins. Activities of the angelicin type such as pimpinellin and Sphondin were more potent than those of the psoralen type. Presence of a methoxy at the C6 position in the angelicin type seemed to be essential to augment the activity. Western blot analysis demonstrated that only Sphondin dose-dependently inhibited the expression of the iNOS protein at 2.5-20 microg/mL. However, iNOS enzyme activity was stimulated with LPS for 12 h and Sphondin was administered (20 microg/mL) for 24 h, which did not reasonably inhibit iNOS enzyme activity. L-NAME (100 microM), a known specific inhibitor of iNOS, was employed as a positive control with the same protocol and showed more than 50% inhibition activity. The results demonstrate that the NO production inhibitory activity of Sphondin is due to the effect of iNOS expression, but not by direct inhibition of iNOS enzyme activity. Thus, Sphondin may act as a potent inhibitor of NO production under tissue-damaging inflammatory conditions.