MCTR1
(Synonyms: 13-glutathionyl-14-hydroxy Docosahexaenoic Acid, Maresin Conjugates in Tissue Regeneration 1, Maresin Sulfido Conjugate 1) 目录号 : GC44138
A specialized pro-resolving mediator
Cas No.:1784701-61-6
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
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Maresin conjugates in tissue regeneration 1 (MCTR1) is a specialized pro-resolving mediator (SPM) synthesized from docosahexaenoic acid in macrophages at the site of inflammation. DHA is oxidized to maresin 1 , which is then converted to MCTR1 by glutathione S-transferase Mu 4 or leukotriene C4 synthase. MCTR1 accelerates tissue regeneration in planaria (1 and 100 nM). Pretreatment with MCTR1 (50 ng/mouse, i.p.) prior to E. coli administration reduces neutrophil infiltration, shortens the inflammatory resolution period, and increases phagocytosis of E. coli by macrophages. When administered at a dose of 100 ng 12h post E. coli infection in a mouse model of peritonitis, MCTR1 reduces the amount of eicosanoids in the exudate.
| Cas No. | 1784701-61-6 | SDF | |
| 别名 | 13-glutathionyl-14-hydroxy Docosahexaenoic Acid, Maresin Conjugates in Tissue Regeneration 1, Maresin Sulfido Conjugate 1 | ||
| Canonical SMILES | O[C@@H](C/C=C\C/C=C\CC)[C@H](SC[C@H](NC(CC[C@H](N)C(O)=O)=O)C(NCC(O)=O)=O)/C=C/C=C/C=C\C/C=C\CCC(O)=O | ||
| 分子式 | C32H47N3O9S | 分子量 | 649.8 |
| 溶解度 | DMF: 50 mg/ml,DMSO: 50 mg/ml,Ethanol: 1 mg/ml,PBS (pH 7.2): 100µ g/ml | 储存条件 | Store at -80°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。 |
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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。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 1.5389 mL | 7.6947 mL | 15.3894 mL |
| 5 mM | 0.3078 mL | 1.5389 mL | 3.0779 mL |
| 10 mM | 0.1539 mL | 0.7695 mL | 1.5389 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。
MCTR1 inhibits ferroptosis by promoting NRF2 expression to attenuate hepatic ischemia-reperfusion injury
Am J Physiol Gastrointest Liver Physiol 2022 Sep 1;323(3):G283-G293.PMID:35916424DOI:10.1152/ajpgi.00354.2021.
Hepatic ischemia-reperfusion injury (HIRI) can lead to poor prognosis in patients undergoing liver transplantation or extensive liver resection. Maresin conjugate in tissue regeneration 1 (MCTR1) exerts a protective effect in several inflammatory disease models, but its role in HIRI remains unknown. In this study, we examined the effect of MCTR1 on HIRI and its underlying mechanism. HIRI mice and oxygen-glucose deprivation/reperfusion (OGD/R) AML12 cell models were used to evaluate the effects of MCTR1 at different doses on HIRI. Histological changes, inflammatory mediators, and ferroptosis-associated markers including iron content, oxidative stress and antioxidant activity, cell death marker (LDH), and the expression of Nuclear factor erythroid-derived 2-like 2 (NRF2) were analyzed. The results showed that MCTR1 treatment significantly ameliorated liver tissue damage and AST/ALT levels in HIRI mice. It also ameliorated ferroptosis in both HIRI mice and OGD/R AML12 cells, including a decrease in iron content, serum LDH release levels, reactive oxygen species (ROS), MDA, IL-1β levels, and COX2 and transferrin receptor (TFRC) expression. In addition, it increased the levels of IL-10, the antioxidant stress markers SOD and GSH, and the expression of GPX4. With respect to the underlying mechanism, the expression of NRF2 in HIRI mice and OGD/R AML12 cells was significantly inhibited. MCTR1 treatment restored the inhibition of NRF2 expression caused by ischemia-reperfusion, and NRF2 inhibitors significantly inhibited nuclear aggregation of NRF2 promoted by MCTR1. In conclusion, the MCTR1 ameliorates ferroptosis-induced hepatic ischemia-reperfusion injury by promoting NRF2 expression and may represent a therapeutic strategy for treating HIRI.NEW & NOTEWORTHY MCTR1 exerts a protective effect in several inflammatory disease models, but its role in hepatic HIRI remains unknown. We confirm that the MCTR1 ameliorates ferroptosis-induced hepatic ischemia-reperfusion injury by promoting NRF2 expression. Our study illustrates the mechanism that MCTR1 protects from HIRI and identifies a therapeutic target for liver transplantation ischemia-reperfusion injury from the perspective of ferroptosis.
MCTR1 Intervention Reverses Experimental Lung Fibrosis in Mice
J Inflamm Res 2021 May 11;14:1873-1881.PMID:34007201DOI:10.2147/JIR.S304811.
Purpose: Pulmonary fibrosis (PF) is a progressing lethal disease, effective curative therapies remain elusive and mortality remains high. Maresin conjugates in tissue regeneration 1 (MCTR1) is a DHA-derived lipid mediator promoting inflammation resolution produced in macrophage. However, the effect of MCTR1 on PF remains unknown. Material and methods: We established a lung fibrosis model in mice induced by intratracheal administration of bleomycin (BLM). On day 7 after lung fibrosis model establishment, treatment with MCTR1 up to day 21. The body weight of each mouse was recorded every day and survival curves were plotted. Histological staining was used to detect pulmonary inflammation and fibrosis. Lung sections were examined with transmission electron microscope to evaluate the ultrastructure of cells and deposit of collagen. Inflammatory cytokines in lung tissues were tested by ELISA. q-PCR and Western blot were used to evaluate the mRNA and the protein levels of EMT-related markers. Results: We found that MCTR1 intervention attenuated BLM-induced lung inflammatory and fibrotic response. Furthermore, MCTR1 protected BLM-induced epithelial cell destroy and reversed epithelial-to-mesenchymal transition phenotype into an epithelial one in lung fibrosis mice. Most importantly, post-treatment with MCTR1 restored BLM-induced lung dysfunction and enhanced survival rate significantly. Conclusion: Posttreatment with MCTR1 attenuated BLM-induced inflammation and fibrosis changes in mice, suggested MCTR1 may serve as a novel therapeutic strategy for fibrosis-related diseases.
Maresin conjugates in tissue regeneration-1 suppresses ferroptosis in septic acute kidney injury
Cell Biosci 2021 Dec 27;11(1):221.PMID:34961563DOI:10.1186/s13578-021-00734-x.
Background: Ferroptosis is unique among different types of regulated cell death and closely related to organ injury. Whether ferroptosis occurs in sepsis-associated acute kidney injury (SA-AKI) is not clear. Nuclear factor-erythroid-2-related factor 2 (Nrf2) is crucial to the regulation of ferroptosis. We and others have shown that Maresin conjugates in tissue regeneration 1 (MCTR1) or other members of specialized pro-resolving mediators (SPMs) can actively regulate inflammation resolution and protect organs against injury in inflammatory diseases by activating the Nrf2 signaling. The aim of this study was to determine whether ferroptosis occurs in SA-AKI. Furthermore, we investigated the potential role and mechanism of MCTR1 in the regulation of ferroptosis in SA-AKI, which mainly focus on the Nrf2 signaling. Results: We demonstrated for the first time that ferroptosis is present in SA-AKI. Moreover, MCTR1 effectively suppressed ferroptosis in SA-AKI. Meanwhile, MCTR1 upregulated the expression of Nrf2 in the kidney of septic mice. Nrf2 inhibitor ML-385 reversed MCTR1-regulated ferroptosis and AKI, implying that Nrf2 is involved in the inhibitory effects of MCTR1 on ferroptosis in SA-AKI. Further, MCTR1 inhibited ferroptosis and elevated the expression of Nrf2 in LPS-induced HK-2 cells. However, Nrf2 siRNA offset the effect of MCTR1 on ferroptosis. Finally, we observed that MCTR1 ameliorates multi-organ injury and improves survival in animal models of sepsis. Conclusions: These data demonstrate that MCTR1 suppresses ferroptosis in SA-AKI through the Nrf2 signaling. Our study enriches the pathophysiological mechanism of SA-AKI and provides new therapeutic ideas and potential intervention targets for SA-AKI.
MCTR1 alleviates lipopolysaccharide-induced acute lung injury by protecting lung endothelial glycocalyx
J Cell Physiol 2020 Oct;235(10):7283-7294.PMID:32037554DOI:10.1002/jcp.29628.
Endothelial glycocalyx degradation, critical for increased pulmonary vascular permeability, is thought to facilitate the development of sepsis into the multiple organ failure. Maresin conjugates in tissue regeneration 1 (MCTR1), a macrophage-derived lipid mediator, which exhibits potentially beneficial effects via the regulation of bacterial phagocytosis, promotion of inflammation resolution, and regeneration of tissue. In this study, we show that MCTR1 (100 ng/mouse) enhances the survival of mice with lipopolysaccharide (LPS)-induced (15 mg/kg) sepsis. MCTR1 alleviates LPS (10 mg/kg)-induced lung dysfunction and lung tissue inflammatory response by decreasing inflammatory cytokines (tumor necrosis factor-α, interleukin-1β [IL-1β], and IL-6) expression in serum and reducing the serum levels of heparan sulfate (HS) and syndecan-1. In human umbilical vein endothelial cells (HUVECs) experiments, MCTR1 (100 nM) was added to the culture medium with LPS for 6 hr. MCTR1 treatment markedly inhibited HS degradation by downregulating heparanase (HPA) protein expression in vivo and in vitro. Further analyses indicated that MCTR1 upregulates sirtuin 1 (SIRT1) expression and decreases NF-κB p65 phosphorylation. In the presence of BOC-2 or EX527, the above effects of MCTR1 were abolished. These results suggest that MCTR1 protects against LPS-induced sepsis in mice by attenuating pulmonary endothelial glycocalyx injury via the ALX/SIRT1/NF-κB/HPA pathway.
MCTR1 enhances the resolution of lipopolysaccharide-induced lung injury through STAT6-mediated resident M2 alveolar macrophage polarization in mice
J Cell Mol Med 2020 Sep;24(17):9646-9657.PMID:32757380DOI:10.1111/jcmm.15481.
Acute respiratory distress syndrome (ARDS) is a fatal disease characterized by excessive infiltration of inflammatory cells. MCTR1 is an endogenously pro-resolution lipid mediator. We tested the hypothesis that MCTR1 accelerates inflammation resolution through resident M2 alveolar macrophage polarization. The mice received MCTR1 via intraperitoneal administration 3 days after LPS stimulation, and then, the bronchoalveolar lavage (BAL) fluid was collected 24 hours later to measure the neutrophil numbers. Flow cytometry was used to sort the resident and recruited macrophages. Post-treatment with MCTR1 offered dramatic benefits in the resolution phase of LPS-induced lung injury, including decreased neutrophil numbers, reduced BAL fluid protein and albumin concentrations and reduced histological injury. In addition, the expression of the M2 markers Arg1, FIZZ1, Remlα, CD206 and Dectin-1 was increased on resident macrophages in the LPS + MCTR1 group. Resident macrophage depletion abrogated the therapeutic effects of MCTR1, and reinjection of the sorted resident macrophages into the lung decreased neutrophil numbers. Finally, treatment with MCTR1 increased STAT6 phosphorylation. The STAT6 inhibitor AS1517499 abolished the beneficial effects of MCTR1. In conclusion, MCTR1 promotes resident M2 alveolar macrophage polarization via the STAT6 pathway to accelerate resolution of LPS-induced lung injury.