Poly-L-lysine hydrobromide (MW 150000-300000) is a high-molecular-weight, positively charged synthetic polypeptide widely used to enhance cell adhesion to culture surfaces. Poly-L-lysine hydrobromide exhibits excellent water solubility and biocompatibility and serves as an essential reagent for the culture of primary neurons, epithelial cells, and stem cells[1-2]. When coated onto substrates, Poly-L-lysine hydrobromide forms a stable, uniform layer that resists detachment during long-term culture[3], and Poly-L-lysine hydrobromide is also employed as a drug-delivery vehicle[4].
In vitro, Poly-L-lysine hydrobromide (20μg/mL) applied to HeLa cells for 30min–2h significantly inhibits tumor-cell DNA, RNA, and protein synthesis, alters membrane permeability, induces leakage of intracellular small molecules, and causes cell rounding, granulation, and lysis[5]. Treatment of Jurkat T-cells, THLE-3 hepatocyte-like cells, and human umbilical vein endothelial cells (HUVEC) with Poly-L-lysine hydrobromide(10–30μg/ml) for 24h markedly induces apoptosis, as evidenced by mitochondrial membrane potential loss, cytochrome c release, and activation of caspase-9 and caspase-3.[6].
In vivo, Poly-L-lysine hydrobromide (50mg/kg/day; i.v.) administered to C57BL/6 mice bearing subcutaneous B16F10 melanoma on days 1 and 2 post-inoculation markedly suppresses tumor neovascularization, induces widespread tumor-cell apoptosis/necrosis, and delays solid-tumor growth[7]. A single intraluminal insertion of a 5-0 monofilament nylon suture coated with 0.1%w/v Poly-L-lysine hydrobromide into the internal carotid artery of C57BL/6 mice produces 30–180min middle-cerebral-artery occlusion followed by 24h reperfusion, resulting in 100% consistent infarcts in expected ipsilateral regions (striatum, thalamus, hippocampus, frontoparietal cortex) and time-dependent neurological deficits[8].
References:
[1] Olivera-Ardid S, Bello-Gil D, Tuzikov A et al, et al. Poly-L-Lysine-Based αGal-Glycoconjugates for Treating Anti-αGal IgE-Mediated Diseases. Front Immunol. 2022 Mar 31;13:873019.
[2] Hatcher JM, Zwirek M, Sarhan AR, et al. Development of a highly potent and selective degrader of LRRK2. Bioorg Med Chem Lett. 2023 Oct 1;94:129449.
[3] Tengberg JF, Russo F, Benned-Jensen T, et al. LRRK2 and RAB8A regulate cell death after lysosomal damage in macrophages through cholesterol-related pathways. Neurobiol Dis. 2024 Nov;202:106728.
[4] Harsiddharay RK, Gupta A, Singh PK, et al. Poly-L-lysine Coated Oral Nanoemulsion for Combined Delivery of Insulin and C-Peptide. J Pharm Sci. 2022 Dec;111(12):3352-3361.
[5] Arnold LJ Jr, Dagan A, Gutheil J, et al. Antineoplastic activity of poly(L-lysine) with some ascites tumor cells. Proc Natl Acad Sci U S A. 1979 Jul;76(7):3246-50.
[6] Symonds P, Murray JC, Hunter AC, et al. Low and high molecular weight poly(L-lysine)s/poly(L-lysine)-DNA complexes initiate mitochondrial-mediated apoptosis differently. FEBS Lett. 2005 Nov 7;579(27):6191-8.
[7] Al-Jamal KT, Al-Jamal WT, Akerman S, et al. Systemic antiangiogenic activity of cationic poly-L-lysine dendrimer delays tumor growth. Proc Natl Acad Sci U S A. 2010 Mar 2;107(9):3966-71.
[8] Belayev L, Busto R, Zhao W, et al. Middle cerebral artery occlusion in the mouse by intraluminal suture coated with poly-L-lysine: neurological and histological validation. Brain Res. 1999 Jul 3;833(2):181-90.
Poly-L-lysine hydrobromide (MW 150000-300000)是一种高分子量、带正电的合成多肽，常用于增强细胞对培养表面的黏附，具有良好的水溶性和生物相容性，是原代神经元、上皮细胞和干细胞培养中的重要工具试剂[1-2]。Poly-L-lysine hydrobromide可在培养表面形成稳定、均一的包被层，使细胞在长期培养的过程中不易脱落[3]，Poly-L-lysine hydrobromide还常被当成递送药物的载体[4]。
在体外，Poly-L-lysine hydrobromide（20μg/mL）处理作用于HeLa细胞30min–2h，可显著抑制肿瘤细胞DNA、RNA及蛋白合成，诱导膜通透性改变及胞内小分子外漏，并导致细胞形态变圆、颗粒化甚至溶解[5]。Poly-L-lysine hydrobromide（10–30μg/ml）处理Jurkat T细胞、THLE-3肝细胞样细胞及人脐静脉内皮细胞（HUVEC）24h，可显著诱导细胞凋亡，表现为线粒体膜电位下降、细胞色素c释放、caspase-9及caspase-3激活[6]。
在体内，Poly-L-lysine hydrobromide（50mg/kg/天）经尾静脉给予B16F10黑色素瘤皮下接种的C57BL/6小鼠，于后第1、2天各注射一次，显著抑制肿瘤新生血管形成，诱导肿瘤细胞广泛凋亡/坏死，并延迟实体瘤生长[7]。经Poly-L-lysine hydrobromide包被的5-0单丝尼龙线（0.1%w/v涂层）一次性经颈内动脉插入，阻断C57BL/6小鼠大脑中动脉30–180min，随后24h再灌注，可100%诱发同侧预期部位（纹状体、丘脑、海马及额顶皮质）的持续性梗死，并呈现时间依赖性神经功能缺损[8]。