HNGF6A是一种人工合成的多肽，属于人类素（Humanin）类似物。
Cas No.:1093111-54-6
Sample solution is provided at 25 µL, 10mM.
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HNGF6A is a synthetic polypeptide belonging to the Humanin analogue class[1-2]. HNGF6A improves glucose metabolism and inhibits the production of reactive oxygen species (ROS). HNGF6A is used in research related to diabetes, atherosclerosis, and osteoarthritis[3].
In vitro, meniscus cells were pretreated with HNGF6A (5–100ng/ml) for 48 hours and were then stimulated with TBHP (50µM) or IL-1β (10ng/ml). HNGF6A significantly restored the expression of extracellular matrix synthesis-related genes (COL1A1, COL3A1, ACAN) and inhibited the expression of degradation-related genes (MMP1, MMP3, ADAMTS5), while maintaining mitochondrial redox homeostasis, reducing ROS levels, and decreasing cell apoptosis[4]. Murine osteoblastic cell line MC3T3-E1 cells were pretreated with HNGF6A (5–50ng/mL) for 3 days and were then exposed to H₂O₂ (400µM) for 4 hours. HNGF6A significantly inhibited apoptosis, downregulated the expression of pro-apoptotic proteins (Caspase-3, Cyto C, Bax), and upregulated the expression of the anti-apoptotic protein (Bcl-2). HNGF6A also promoted the expression of osteoblast phenotype-related proteins (ALP, BMP-2, OCN, RUNX2), enhanced alkaline phosphatase (ALP) activity, and increased mineralization nodule formation[5].
In vivo, three-month-old Sprague-Dawley rats were treated with HNGF6A (0.07mg/kg/h) via continuous intravenous infusion for 2 hours. HNGF6A significantly increased the glucose infusion rate during a hyperglycemic clamp and caused a sustained increase in plasma insulin levels. C57BL/6N mice received a single intravenous injection of HNGF6A (2mg/kg) 10 minutes before a glucose tolerance test, which showed a trend toward increased first-phase insulin secretion[6]. Apolipoprotein E (ApoE)-deficient mice fed a high-cholesterol diet were treated with HNGF6A (0.4mg/kg/day) via daily intraperitoneal injection for 16 weeks. HNGF6A significantly improved acetylcholine-induced endothelium-dependent vasodilation, reduced atherosclerotic plaque size in the proximal aorta, decreased nitrotyrosine immunoreactivity and apoptosis within the plaques, and preserved endothelial nitric oxide synthase expression[7].
References:
[1] Ding Y, Feng Y, Zhu W, et al. [Gly14]-Humanin Prevents Lipid Deposition and Endothelial Cell Apoptosis in a Lectin-like Oxidized Low-density Lipoprotein Receptor-1-Dependent Manner. Lipids. 2019 Nov;54(11-12):697-705.
[2] Chin YP, Keni J, Wan J, et al. Pharmacokinetics and tissue distribution of humanin and its analogues in male rodents. Endocrinology. 2013 Oct;154(10):3739-44.
[3] Peña Agudelo JA, Pidre ML, et al. Mitochondrial Peptide Humanin Facilitates Chemoresistance in Glioblastoma Cells. Cancers (Basel). 2023 Aug 11;15(16):4061.
[4] Liu R, Du X, Chen Y, et al. HNGF6A ameliorates oxidative stress-mediated mitochondrial dysfunction in degenerative meniscus. Bone Joint Res. 2025 Apr 7;14(4):318-330.
[5] Zhu X, Zhao Z, Zeng C, et al. HNGF6A Inhibits Oxidative Stress-Induced MC3T3-E1 Cell Apoptosis and Osteoblast Phenotype Inhibition by Targeting Circ_0001843/miR-214 Pathway. Calcif Tissue Int. 2020 May;106(5):518-532.
[6] Kuliawat R, Klein L, Gong Z, et al. Potent humanin analog increases glucose-stimulated insulin secretion through enhanced metabolism in the β cell. FASEB J. 2013 Dec;27(12):4890-8.
[7] Oh YK, Bachar AR, Zacharias DG, et al. Humanin preserves endothelial function and prevents atherosclerotic plaque progression in hypercholesterolemic ApoE deficient mice. Atherosclerosis. 2011 Nov;219(1):65-73.
HNGF6A是一种人工合成的多肽，属于人类素（Humanin）类似物[1-2]。HNGF6A可改善糖代谢和抑制抑制活性氧的产生。HNGF6A用于糖尿病、动脉粥样硬化和骨关节炎的相关研究[3]。
在体外，HNGF6A（5–100ng/ml）预处理半月板细胞48小时，随后以TBHP（50μM）或IL-1β（10ng/ml）刺激。HNGF6A显著恢复细胞外基质合成相关基因（COL1A1，COL3A1，ACAN）的表达并抑制降解相关基因（MMP1，MMP3，ADAMTS5）的表达，同时维持线粒体氧化还原稳态、降低ROS水平、减少细胞凋亡[4]。HNGF6A（5–50ng/mL）预处理小鼠成骨细胞系MC3T3-E1细胞3天，随后以H₂O₂（400μM）刺激4小时。HNGF6A显著抑制细胞凋亡并下调促凋亡蛋白（Caspase-3，Cyto C，Bax）的表达、上调抗凋亡蛋白（Bcl-2）的表达，同时促进成骨细胞表型相关蛋白（ALP，BMP-2，OCN，RUNX2）的表达、增强碱性磷酸酶（ALP）活性及细胞矿化结节形成[5]。
在体内，HNGF6A（0.07mg/kg/h）通过持续2小时的静脉输注，用于处理3月龄的Sprague-Dawley大鼠。HNGF6A显著提高了高血糖钳夹实验期间的葡萄糖输注率，并持续增加了血浆胰岛素水平。HNGF6A（2mg/kg）在葡萄糖耐量试验前10分钟单次静脉注射，用于处理C57BL/6N小鼠，其第一时相胰岛素分泌有增加趋势[6]。HNGF6A（0.4mg/kg/day）通过每日腹腔注射，持续16周，用于处理喂食高胆固醇饮食的载脂蛋白E（ApoE）缺陷小鼠。HNGF6A显著改善了乙酰胆碱诱导的内皮依赖性血管舒张功能、减少了主动脉近端动脉粥样硬化斑块的大小，同时降低了斑块中的硝基酪氨酸免疫反应性和细胞凋亡、并维持了内皮型一氧化氮合酶的表达[7]。
| Cell experiment [1]: | |
Cell lines | MC3T3-E1 cells (murine osteoblastic cell line) |
Preparation Method | MC3T3-E1 cells were maintained in Dulbecco's Modified Eagle Medium (DMEM-H) supplemented with 10% fetal bovine serum (FBS), 100U/mL penicillin, and 100µg/mL streptomycin at 37°C under 5% CO₂. Cells were pretreated with HNGF6A (5–50ng/mL) for 3 days, and were then exposed to H₂O₂ (400µM) for 4 hours to induce oxidative stress. |
Reaction Conditions | 5–50ng/mL; 3 days. |
Applications | HNGF6A pretreatment significantly increased cell viability and reduced H₂O₂-induced apoptosis in MC3T3-E1 cells. HNGF6A promoted osteoblast phenotype by upregulating the expression of osteogenic markers (ALP, BMP-2, OCN, RUNX2), enhancing alkaline phosphatase (ALP) activity, and increasing mineralization nodule formation. Mechanistically, HNGF6A exerted its protective effects by decreasing Circ_0001843 expression, increasing miR-214 levels, and inhibiting the phosphorylation of p38 and JNK. |
| Animal experiment [2]: | |
Animal models | ApoE-deficient mice |
Preparation Method | Mice were fed a high cholesterol diet and received daily intraperitoneal injections of the HN analogue HNGF6A (0.4mg/kg/day) for 16 weeks. Vascular function, plaque size, and molecular markers in the aorta were analyzed at the end of the treatment period. |
Dosage form | 0.4mg/kg/day; i.p.; 16 weeks. |
Applications | Chronic administration of HNGF6A preserved endothelium-dependent vasorelaxation in response to acetylcholine, significantly decreased atherosclerotic plaque size in the proximal aorta, and reduced nitrotyrosine immunoreactivity (a marker of oxidative stress) and apoptosis within the plaques. HNGF6A also preserved the expression of endothelial nitric oxide synthase (eNOS). |
References: | |
| Cas No. | 1093111-54-6 | SDF | |
| 化学名 | (6S,7Z,10Z,12S,13Z,15S,16Z,18R,19Z,21S,22Z,24S,25Z,27S,28Z,30S,31Z,33S,34Z,37Z,39S,40Z,42S,43Z,45S)-1-amino-6-((Z)-(((S)-1-((S)-2-((Z)-((S)-2-amino-1-hydroxy-4-(methylthio)butylidene)amino)propanoyl)pyrrolidin-2-yl)(hydroxy)methylene)amino)-45-((Z)-(((S)- | ||
| Canonical SMILES | CC[C@]([C@@](/N=C(O)/[C@](/N=C(O)/C/N=C(O)/[C@](/N=C(O)/[C@](/N=C(O)/[C@](/N=C(O)/[C@](/N=C(O)/[C@](/N=C(O)/[C@](/N=C(O)/[C@](/N=C(O)/[C@](/N=C(O)/C/N=C(O)/[C@](/N=C(O)/[C@]1([H])CCCN1C([C@](/N=C(O)/[C@](N)([H])CCSC)([H])C)=O)([H])CCCNC(N)=N)([H])C)([H])C | ||
| 分子式 | C112 H198 N34 O31 S2 | 分子量 | 2581.13 |
| 溶解度 | Soluble to 1 mg/ml in Water | 储存条件 | Store at -20°C |
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| 1 mM | 387.4 μL | 1.9371 mL | 3.8743 mL |
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| 10 mM | 38.7 μL | 193.7 μL | 387.4 μL |
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