Dinoprost (Prostaglandin F2a)
(Synonyms: 地诺前列素; Prostaglandin F2α; PGF2α) 目录号 : GC30370
Dinoprost (Prostaglandin F2a)是一种口服有效的强效前列腺素受体 （FP 受体） 激动剂。Dinoprost刺激子宫肌层活动，放松宫颈，抑制黄体类固醇生成，并通过直接作用诱导黄体溶解。
Cas No.:551-11-1
Sample solution is provided at 25 µL, 10mM.
;)
,-1-7$$$37316672.jpg');)
;)
;)
$$$36806353.jpg');)
;33(7)%EF%BC%9A546-561$$$37156877.jpg');)
;)
;)
;)
%201124-1138.$$$35908550.jpg');)
%20766-780.$$$37100057.jpg');)
%20418-432.$$$36893736.jpg');)
%EF%BC%9A-240-255.$$$35108512.jpg');)
533-545$$$36543525.jpg');)
%201-13.$$$36600053.jpg');)
;)
Quality Control & SDS
- View current batch:
- Purity: >96.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
| Cell experiment [1]: | |
Cell lines | Bovine luteal cells |
Preparation Method | Bovine luteal cells were treated for 24 h with PGF2x (1μg/mL) ,dinoprost (1μg/mL) , luprostiol (1μg/mL), as well as luteinising hormone (positive control; 100ng/mL). |
Reaction Conditions | 1μg/mL; 24h |
Applications | Dinoprost stimulated P4 secretion ,luprostiol did not in uence P4 synthesis. The cytotoxic and pro-apoptotic effects were observed in the Dinoprost-treated cells. |
| Animal experiment [2]: | |
Animal models | Ischemia/ Reperfusion (I/R) damage model |
Preparation Method | A total of 24 rats were randomly divided into four groups:Control, Ischemia (Isch), I/R and Dino+I/R. Ischemia was induced by clamping the ovarian blood supply, followed by reperfusion. Dinoprost was administered before reperfusion in the Dino+I/R group. COX-2, IL-1β, and TNF-α expression levels were assessed through histochemical and immunochemical analyses. |
Dosage form | 6mg/kg; sc; 3d |
Applications | After Dinoprost treatment, COX-2 expression was decreased, IL-1β and TNF-α expressions did not change significantly, and the amount of bleeding was reduced. |
References: | |
Dinoprost (Prostaglandin F2a) is an orally active, potent prostaglandin receptor (FP receptor) agonist.Dinoprost stimulates myometrial activity, relaxes the cervix, inhibits corpus luteal steroidogenesis, and induces luteolysis by direct action[1].
Dinoprost (1μM; 24h) induces ER stress, autophagy, and apoptosis in goat luteal cells[2]. Dinoprost (1μg/mL; 24h) stimulated P4 secretion, luprostiol did not in uence P4 synthesis. The cytotoxic and pro-apoptotic effects were observed in the Dinoprost-treated cells[3].
After confirming that the corpus luteum is mature in the ewe, Dinoprost (12.5 mg; im) is injected. Half an hour later, the blood flow velocity of the ewe increases, and one hour later, the NO level rises rapidly, which has a negative impact on the corpus luteum[4]. In rats treated with Dinoprost (6mg/kg; sc; 3d) after ovarian I/R injury, the expression of COX-2 was reduced, the expression of IL-1β and TNF-α did not change significantly, and the amount of bleeding was reduced [5].
References:
[1].Wen X, Liu L, Li S, et al. Prostaglandin F2α induces goat corpus luteum regression via endoplasmic reticulum stress and autophagy[J]. Frontiers in Physiology, 2020, 11: 868.
[2].Thieme H, Schimmat C, Münzer G, et al. Endothelin antagonism: effects of FP receptor agonists prostaglandin F2α and fluprostenol on trabecular meshwork contractility[J]. Investigative ophthalmology & visual science, 2006, 47(3): 938-945.
[3]. Korzekwa A J, Lukasik K, Pilawski W, et al. Influence of prostaglandin F2α analogues on the secretory function of bovine luteal cells and ovarian arterial contractility in vitro[J]. The Veterinary Journal, 2014, 199(1): 131-137.
[4].El-Sherry T M, Senosy W, Mahmoud G B, et al. Effect of dinoprost and cloprostenol on serum nitric oxide and corpus luteum blood flow during luteolysis in ewes[J]. Theriogenology, 2013, 80(5): 513-518.
[5].Karakus S, Ozkaraca M. Investigating the protective potential of dinoprost in a rat model of ischemia-reperfusion[J]. 2023.
Dinoprost (Prostaglandin F2a)是一种口服有效的强效前列腺素受体 （FP 受体） 激动剂。Dinoprost刺激子宫肌层活动，放松宫颈，抑制黄体类固醇生成，并通过直接作用诱导黄体溶解[1]。
Dinoprost（1 μM；24 h）诱导山羊黄体细胞中的 ER 应激、自噬和细胞凋亡[2]。Dinoprost（1μg/mL；24 h）刺激 P4 分泌，在用Dinoprost处理的细胞中观察到细胞毒性和促细胞凋亡作用[3]。
确认母羊体内黄体成熟后，注射Dinoprost（12.5mg；im），半小时后母羊血流速度加快，1小时后NO水平迅速升高，对黄体产生负面影响[4]。大鼠卵巢I/R损伤后经Dinoprost（6mg/kg；sc；3d）治疗，大鼠COX-2表达降低，IL-1β和TNF-α表达无明显变化，出血量减少[5]。
| Cas No. | 551-11-1 | SDF | |
| 别名 | 地诺前列素; Prostaglandin F2α; PGF2α | ||
| Canonical SMILES | CCCCC[C@H](O)/C=C/[C@H]1[C@H](O)C[C@H](O)[C@@H]1C/C=C\CCCC(O)=O | ||
| 分子式 | C20H34O5 | 分子量 | 354.48 |
| 溶解度 | H2O : 100 mg/mL (282.10 mM; Need ultrasonic); DMSO : 100 mg/mL (282.10 mM; Need ultrasonic) | 储存条件 | Store at -20°C |
| 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。 |
||
| 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。 | ||
| 制备储备液 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 2.821 mL | 14.1052 mL | 28.2103 mL |
| 5 mM | 0.5642 mL | 2.821 mL | 5.6421 mL |
| 10 mM | 0.2821 mL | 1.4105 mL | 2.821 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 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 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
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，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
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。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Expression patterns of chemokine (C-C motif) ligand 2, prostaglandin F2A receptor and immediate early genes at mRNA level in the bovine corpus luteum after intrauterine treatment with a low dose of prostaglandin F2A
The present study evaluated expression patterns of chemokine (C-C motif) ligand 2 gene/Monocyte chemoattractant protein-1 gene (CCL2/MCP-1), prostaglandin F2 alpha receptor gene (PTGFR) and immediate early genes including nuclear receptor subfamily 4, group A, member 1 (NR4A1), early growth response 1 (EGR1) and FBJ murine osteosarcoma viral oncogene homolog (FOS) in cells of the bovine corpus luteum after intrauterine infusion of a low dose of prostaglandin F2α (PGF2A) aimed at enhancing our understanding of the mechanisms of luteolysis. Holstein dairy cows were superovulated (>6 corpora lutea [CL]) and on day 9 of the estrous cycle were infused with a low dose of PGF2A (0.5 mg PGF2A in 0.25 ml phosphate buffered saline) into the greater curvature of the uterine horn ipsilateral to the CL. Ultrasound-guided biopsy samples of different CL were collected at 0 min, 15 min, 30 min, 1h, 2h and 6h after PGF2A infusion. Expression profiles and localization of mRNA for PTGFR, CCL2/MCP-1, and immediate early genes (NR4A1, EGR1 and FOS), were investigated by using qPCR and in situ hybridization. The concentrations of early response genes including FOS, NR4A1, and EGR1 exhibited the greatest increase at 30 min after PGF2A, compared to other time points. Expression profile of CCL2 mRNA increased gradually after intrauterine infusion of PGF2A with maximal up-regulation for CCL2 at 6h. Abundance of PTGFR mRNA only increased at 15 min and significantly decreased at 6h, compared to 0 min. Cellular localizations of all studied genes except CCL2 (primarily localized to apparent immune cells) were predominantly visualized in large luteal cells. Interestingly, early response genes demonstrated a changing profile in cellular localization with initial responses appearing to be in both large luteal cells and endothelial cells, although no staining for PTGFR mRNA was observed in endothelial cells. Later, sustained responses, were only observed in large luteal cells, although PTGFR mRNA was decreasing in large luteal cells over time after PGF2A. The involvement of the immune system was also highlighted by the immediate increases in CCL2 mRNA that became much greater over time as there was an apparent influx of CCL2-positive immune cells. Thus, the temporal and cell-specific localization patterns for the studied mRNA demonstrate the complex pathways that are responsible for initiation of luteolysis in the bovine CL.
Interferon-Tau regulates a plethora of functions in the corpus luteum
The corpus luteum (CL) plays a vital role in regulating the reproductive cycle, fertility, and in maintaining pregnancy. Interferon-tau (IFNT) is the maternal recognition of a pregnancy signal in domestic ruminants; its uterine, paracrine actions, which extend the CL lifespan, are widely established. However, considerable evidence also suggests a direct, endocrine role for IFNT. The purpose of this review is to highlight the importance of IFNT in CL maintenance, acting directly and in a cell-specific manner. A transcriptomic study revealed a distinct molecular profile of IFNT-exposed day 18, pregnant bovine CL, compared to the non-pregnant gland. A substantial fraction of the differentially expressed genes was downregulated, many of which are known to be elevated by prostaglandin F2A (PGF2A). In vitro, IFNT was found to mimic changes observed in the luteal transcriptome of early pregnancy. Key luteolytic genes such as endothelin-1 (EDN1), transforming growth factor-B1 (TGFB1), thrombospondins (THBSs) 1&2 and serpine-1 (SERPINE1) were downregulated in luteal endothelial cells. Luteal steroidogenic large cells (LGCs) were also found to be a target for the antilutelotytic actions of IFNT. IFNT-treated LGCs showed a significant reduction in the expression of the proapoptotic, antiangiogenic THBS1&2, as well as TGFBR1 and 2. Furthermore, IFNT was shown to be a potent survival factor for luteal cells in vivo and in vitro, activating diverse pathways to promote cell survival while suppressing cell death signals. Pentraxin 3 (PTX3), robustly upregulated by IFNT in various luteal cell types, mediated many of the prosurvival effects of IFNT in LGCs. A novel reciprocal inhibitory crosstalk between PTX3 and THBS1 lends further support to their respective survival and apoptotic actions in the CL. Even though IFNT did not directly regulate progesterone synthesis, it could maintain its concentrations, by increasing luteal cell survival and by supporting vascular stabilization. The direct effects of IFNT in the CL, enhancing cell survival and vasculature stabilization while curbing luteolytic activities, may constitute an important complementary branch leading to the extension of the luteal lifespan during early pregnancy.
Urinary leukotriene E4 and prostaglandin F2a concentrations in children with migraine: a randomized study
Objectives: Pro-inflammatory mediators are thought to play both peripheral and central roles in migraine pathophysiology. Prostaglandins and leukotrienes, known as the eicosanoids, are degradation products of arachidonic acid and constitute signalization components of inflammatory pathways. This study was designed to assess concentrations of leukotriene E4 (LT-E4) and prostaglandin F2a (PG-F2a) in children with migraine.
Materials and methods: This study involved patients aged ≤18 years who presented to the Ondokuz Mayis University Children's Hospital with migrainous headache between January and October 2011. Urinary LT-E4 and PG-F2a concentrations were measured in patients during a headache episode and at a headache-free time and in a control group.
Results: The patient group consisted of 38 girls and 26 boys aged 5-18 years diagnosed with migraine and having at least 6 months of headache, whereas the control group consisted of 21 girls and 29 boys. Mean ± standard deviation (SD) urinary LT-E4 concentrations were significantly higher in patients during a migraine episode than in controls (1466.8±1052.5 pg/ml vs 811.6±460.0 pg/ml, P<0.001). In patients with migraine, both urinary LT-E4 (P<0.001) and PG-F2a (P=0.021) levels were significantly higher during headache than during non-headache periods.
Conclusion: Urinary LT-E4 and PG-F2a were both significantly higher in children with migraine during headache than during non-headache periods. The elevation in the levels of these inflammatory mediators was compatible with the hypothesis relating neuroinflammation in trigeminal vascular blood vessels with migraine pathophysiology. Leukotriene antagonists may be effective in the prophylaxis of migraine attacks.
Low-dose natural prostaglandin F2α (dinoprost) at timed insemination improves conception rate in dairy cattle
The primary objective was to determine if low doses of PGF2α (dinoprost) given intramuscularly (im) concurrent with timed artificial insemination (TAI) would improve conception rates in dairy cattle. A secondary objective was to determine if body condition score (BCS) and parity would influence conception rates, either independently or in interaction with PGF2α treatment. In experiment I, 307 lactating Holstein cows were randomly assigned to receive either 5-mg PGF2α im (PGF2α treated, n = 154) or 0-mg PGF2α (control, n = 153) at TAI (Day 0). Blood samples were obtained on Days -10, -3, 0, and 7 to determine plasma progesterone (P4) concentrations. Pregnancy was confirmed 30 to 32 days after insemination by transrectal ultrasonography. In experiment II, 451 cows were randomly assigned to receive either 10-mg PGF2α im (PGF2α treated, n = 226) or 0-mg PGF2α (control, n = 225) at TAI, and pregnancy was confirmed 45 to 50 days after TAI by palpation per rectum. Pregnancy data were analyzed by CATMOD (SAS). In experiment I, PGF2α treatment, BCS, and parity did not affect conception rate (35.7% vs. 37.0% for PGF2α treated vs. control; P > 0.05). However, in experiment II, conception rates were higher in cows given 10-mg PGF2α than those in control cows (45.8% vs. 36.0%; P < 0.05), in cows with high BCS than in cows with low BCS (52.1% vs. 30.4%; P < 0.01), and in primiparous than in multiparous cows (47.6% vs. 34.4%; P < 0.01), but their interaction with PGF2α treatment did not affect conception rates. In summary, 5 mg of PGF2α given im concurrent with TAI failed to enhance conception rate in lactating dairy cows, whereas 10 mg of PGF2α significantly increased conception rate.
Ureaplasma diversum infection in vitro alters prostaglandin E2 and prostaglandin F2a production by bovine endometrial cells without affecting cell viability
Bovine epithelial and stromal cells of the endometrium were inoculated with Ureaplasma diversum, pathogenic strain 2312, at 10(6) or 10(3) color-changing units (ccu)/ml in the presence of 1% fetal bovine serum (depleted of steroids by dextran-charcoal treatment) to assess the effect of infection on prostaglandin biosynthesis. When the inoculum of U. diversum was 10(6) ccu/ml, the concentration of U. diversum in the culture medium decreased with time. U. diversum was found on the epithelial and stromal cell monolayers, increasing in titer 100-fold, indicating that attachment and eventually growth occurred. When the inoculum was 10(3) ccu/ml, the titer of U. diversum remained the same or increased in the supernatant and increased on epithelial and stromal cells. The effect of infection was evaluated by measurement of the primary prostaglandin produced by each cell type, prostaglandin F2a for epithelial cells and prostaglandin E2 for stromal cells. Infection with U. diversum significantly decreased prostaglandin F2a accumulation, by 44.7% +/- 6.0% at 10(6) ccu/ml (P < or = 0.005) and 15.8% +/- 5.3% at 10(3) ccu/ml (P < or = 0.05) in epithelial cells. Prostaglandin E2 accumulation by stromal cells was decreased by 34.0% +/- 4.0% at 10(6) ccu/ml (P < or = 0.001) and by 13.5% +/- 2.7% at 10(3) ccu/ml (P < or = 0.005). Infection with 10(6) ccu/ml did not alter endometrial cell viability, as shown by protein measurement, trypan blue dye exclusion, and cell plating efficiency tests. Thus, alterations in prostaglandin production were not due to cell deterioration. These observations suggest that U. diversum can alter prostaglandin E2 and prostaglandin F2a patterns in primary cultures of bovine endometrial cells without affecting cell viability.