LQVTDSGLYRCVIYHPP
目录号 : GC66404
LQVTDSGLYRCVIYHPP是一种髓系细胞触发受体1（TREM-1）抑制肽。
Cas No.:887255-16-5
Sample solution is provided at 25 µL, 10mM.
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LQVTDSGLYRCVIYHPP is a myeloid cell triggered receptor 1 (TREM-1) inhibitory peptide [1]. LQVTDSGLYRCVIYHPP inhibits downstream inflammatory signaling pathways by competitively binding to TREM-1 and blocking its activation, thereby exerting anti-inflammatory effects [2]. LQVTDSGLYRCVIYHPP can be used in the study of infectious diseases, inflammatory diseases and tumor immunoregulation [3].
In macrophages, treatment with LQVTDSGLYRCVIYHPP (50μM; 24h) significantly reduced the relative levels of LPS-stimulated IL-6, TNFα, CD14 and TREM-1 mRNA transcripts [4]. In microglial, LQVTDSGLYRCVIYHPP (10μM; 24h) substantially decreased mRNA levels of proinflammatory cytokines (NLRP3, IL-1β, IL-18, IL-6, CD16, CD32, and iNOS) and chemokines (MCP-1, CXCL-1, and CXCL-2) [5]. In human corneal epithelial cells, LQVTDSGLYRCVIYHPP (50μM; 24h) induced TREM-1 blockage significantly inhibited the production of TNF-α, IL-1β, IL-6, and IL-8 upon A. fumigatus infection THCEs [6].
In mice cerebral ischemia/reperfusion (I/R) model, after pharmacologic inhibition of TREM-1 with synthetic peptide LQVTDSGLYRCVIYHPP (1mg/kg; intranasal administration; 3d), ischemia-induced infarction and neuronal injury were substantially alleviated [5]. Cecal ligation and puncture (CLP)-induced sepsis rat model, LQVTDSGLYRCVIYHPP (3.5mg/kg; iv; single injection) inhibits the elevation of proinflammatory cytokines TNF-α, IL-6, and IL-1β, thereby alleviating systemic and distant inflammatory responses [7]. In subarachnoid hemorrhage model, TREM-1 inhibition with LQVTDSGLYRCVIYHPP (1mg/kg; intranasal administration; 24h) improved neurological deficits, mitigated brain water content, and preserved brain-blood barrier integrity 24h after SAH [8].
References:
[1]. Siskind S, Brenner M, Wang P. TREM-1 modulation strategies for sepsis. Frontiers in Immunology. 2022 Jun 15; 13: 907387.
[2]. Fu L, Han L, Xie C, et al. Identification of extracellular actin as a ligand for triggering receptor expressed on myeloid cells-1 signaling. Frontiers in immunology. 2017 Aug 7; 8: 917.
[3]. Theobald V, Schmitt FC, Middel CS, et al. Triggering receptor expressed on myeloid cells-1 in sepsis, and current insights into clinical studies. Critical Care. 2024 Jan 9; 28(1): 17.
[4]. Liu M, Zhang Y, Xiong JY, et al. Etomidate Mitigates Lipopolysaccharide-Induced CD14 and TREM-1 Expression, NF-κB Activation, and Pro-inflammatory Cytokine Production in Rat Macrophages. Inflammation. 2016 Feb; 39(1): 327-335.
[5]. Xu P, Zhang X, Liu Q, et al. Microglial TREM-1 receptor mediates neuroinflammatory injury via interaction with SYK in experimental ischemic stroke. Cell death & disease. 2019 Jul 19; 10(8): 555.
[6]. Hu LT, Du ZD, Zhao GQ, et al. Role of TREM-1 in response to Aspergillus fumigatus infection in corneal epithelial cells. International Immunopharmacology. 2014 Nov 1; 23(1): 288-293.
[7]. Shi X, Zhang Y, Wang H, et al. Effect of triggering receptor expressed on myeloid cells 1 (TREM-1) blockade in rats with cecal ligation and puncture (CLP)-induced sepsis. Medical Science Monitor: International Medical Journal of Experimental and Clinical Research. 2017 Oct 23; 23: 5049.
[8]. Xu P, Hong Y, Xie Y, et al. TREM-1 exacerbates neuroinflammatory injury via NLRP3 inflammasome-mediated pyroptosis in experimental subarachnoid hemorrhage. Translational Stroke Research. 2021 Aug; 12: 643-659.
LQVTDSGLYRCVIYHPP是一种髓系细胞触发受体1（TREM-1）抑制肽 [1]。LQVTDSGLYRCVIYHPP 通过竞争性结合TREM-1并阻断其活化来抑制下游炎症信号通路，从而发挥抗炎作用 [2]。LQVTDSGLYRCVIYHPP可用于研究传染病、炎症性疾病和肿瘤免疫调节 [3]。
在巨噬细胞中，LQVTDSGLYRCVIYHPP（50μM；24h）处理可显著降低LPS刺激的IL-6、TNFα、CD14和TREM-1 mRNA转录物的相对水平 [4]。在小胶质细胞中，LQVTDSGLYRCVIYHPP（10μM；24h）显著降低了促炎细胞因子（NLRP3、IL-1β、IL-18、IL-6、CD16、CD32和iNOS）以及趋化因子（MCP-1、CXCL-1和CXCL-2）的mRNA水平 [5]。在人角膜上皮细胞中，LQVTDSGLYRCVIYHPP（50μM；24h）诱导的TREM-1阻断显著抑制了烟曲霉感染THCE后TNF-α、IL-1β、IL-6和IL-8的产生 [6]。
在小鼠脑缺血/再灌注（I/R）模型中，用合成肽LQVTDSGLYRCVIYHPP（1mg/kg；鼻腔给药；3d）药物抑制TREM-1后，缺血引起的梗死和神经元损伤得到显著减轻 [5]。在盲肠结扎穿刺（CLP）诱发的脓毒症大鼠模型中，LQVTDSGLYRCVIYHPP（3.5mg/kg；iv；单次注射）可抑制促炎细胞因子TNF-α、IL-6和IL-1β的升高，从而减轻全身和远处的炎症反应 [7]。在蛛网膜下腔出血（SAH）模型中，用LQVTDSGLYRCVIYHPP（1mg/kg；鼻内给药；24h）抑制TREM-1可改善神经功能缺损，降低脑含水量，并在SAH后24小时维持脑血屏障完整性 [8]。
| Cell experiment [1]: | |
Cell lines | Macrophages cells |
Preparation Method | The isolated macrophages (1.5×105/mL) were cultured in 96-well plates and treated in triplicate with vehicle, consisting of <0.1% dimethyl sulphoxide (DMSO) incomplete medium (control), 1μg/mL LPS for 48h (LPS group) or1μg/mL LPS for 24h and then with 5 or2.5μM etomidate for another 24h (the L+5E or L+2.5E group, respectively). Etomidate was freshly dissolved in DMSO. Some macrophages were cultured in complete medium without LPS stimulation for 24h and then treated with 5 or 2.5μM etomidate (as the 5E or 2.5E group) and 100ng/mL of LQVTDSGLYRCVIYHPP (as the LQVTDSGLYRCVIYHPP group) for 24h.Some macrophages were treated with 1μg/mL of LPS for 24h and then with 5μM etomidate and/or 50μM of LQVTDSGLYRCVIYHPP or control peptide for another 24h (as the L+5E, L+LQVTDSGLYRCVIYHPP and L+LQVTDSGLYRCVIYHPP+5E groups), respectively. |
Reaction Conditions | 50μM; 24h |
Applications | Treatment with LQVTDSGLYRCVIYHPP significantly reduced the relative levels of LPS-stimulated IL-6, TNFα, CD14 and TREM-1 mRNA transcripts in macrophages. |
| Animal experiment [2]: | |
Animal models | Cecal ligation and puncture (CLP)-induced sepsis rat model |
Preparation Method | Polymicrobial sepsis was induced using the cecal ligation and puncture (CLP). Rat was anesthetized with intraperitoneal injection of 40mg/kg thiopental. A small midline incision was made to expose the cecum through the skin and peritoneum under aseptic conditions. Approximately 1.5cm of the cecal appendage was ligated midway between the cecal base and the distal pole, using 4/0 surgical silk. Then, double punctures were made using an 18-gauge needle and expelling a small amount of feces. After cecum repositioning and skin closure, resuscitation was achieved through subcutaneous injection of 1mL pre-warmed saline (0.9% saline). Normal SD Rats receiving 0.1mL saline (1mg in 0.1mL of saline) served as the normal control group (NC). Rats with sepsis induced by CLP were allocated randomly to received scramble peptide (3.5mg/kg; CLP-Scrambled) or LQVTDSGLYRCVIYHPP (3.5mg/kg; CLP-LQVTDSGLYRCVIYHPP) via the jugular vein. |
Dosage form | 3.5mg/kg; iv; single injection |
Applications | LQVTDSGLYRCVIYHPP inhibits the elevation of proinflammatory cytokines TNF-α, IL-6, and IL-1β, thereby alleviating systemic and distant inflammatory responses. |
References: | |
| Cas No. | 887255-16-5 | SDF | Download SDF |
| 分子式 | C89H137N23O25S | 分子量 | 1961.25 |
| 溶解度 | DMso : 25 mg/mL (12.75 mM; Need ultrasonic)H20 : 5 mg/mL (2.55 mM; ultrasonic and adjust pH to 2 with HCI) | 储存条件 | Store at -20°C, protect from light |
| 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 | 0.5099 mL | 2.5494 mL | 5.0988 mL |
| 5 mM | 0.102 mL | 0.5099 mL | 1.0198 mL |
| 10 mM | 0.051 mL | 0.2549 mL | 0.5099 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。
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Quality Control & SDS
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- Purity: >98.00%
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