Hy 17589a

Manufactured by MedChemExpress

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HY-17589A is a laboratory equipment product manufactured by MedChemExpress. It is designed for use in scientific research and experiments. The core function of HY-17589A is to [Core function description].

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Chloroquine (HY-17589A) (9 citations) Chloroquine (CQ; HY-17589A) (5 citations) CQ (HY‐17589A) (3 citations)

12 protocols using hy 17589a

Rat Liver Graft Preservation Strategies

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Sprague Dawley (SD) rats were anesthetized by cardiac arrest through incision of the diaphragm after being heparinized to simulate donor warm ischemia time for 30 min in situ. Liver graft procurement at the end of the abdominal aorta was flushed. The rats were randomly divided into four different groups to analyze the effect of different preservation strategies on graft injury and survival (n = 6 each).
3-MA/CQ: The rats were injected intraperitoneally with CQ (60 mg/kg) or 3-MA (15 mg/kg) (HY-17589A, HY-19312, MedChemExpress, Monmouth Junction, NJ, USA) at 1 h before warm ischemia. The same volume of blank solution was used as the HOPE 1 h control, and the livers were exposed to warm ischemia for 30 min, followed by cold storage in HTK solution for 3 h and 1 h of hypothermic oxygenated machine perfusion (HOPE 1 h + 3-MA, HOPE 1 h + CQ).
We performed NMP as a simulated transplantation following hypothermic storage/perfusion to assess the viability of the grafts (n = 3 each).

Luo J., Hu Y., Qiao Y., Li H., Huang J., Xu K., Jiang L., Wu H., Hu X., Jia J., Zhou L., Xie H., Li J, & Zheng S. (2023). Hypothermic Oxygenated Machine Perfusion Promotes Mitophagy Flux against Hypoxia-Ischemic Injury in Rat DCD Liver. International Journal of Molecular Sciences, 24(6), 5403.

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Modulating Vascular Smooth Muscle Cell Calcification

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The mouse vascular smooth muscle cell line (MOVAS-1) was obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA). Cells were cultured in DMEM (Hyclone, Logan, UT, USA) containing 10% FBS (Gibco, Waltham, MA, USA) and 1% (v/v) penicillin/streptomycin at 37 °C in a humidified incubator with 5% CO₂. Cells between passages 6 and 8 were used for all experiments. VSMC calcification was induced according to previous protocols [20 (link), 21 (link)]. Briefly, VSMCs were cultured with growing medium in the presence of β-glycerophosphate (β-GP) (10 mM; G9422; Sigma, St. Louis, MO, USA) for 7 days. To investigate the role of Irisin in VSMC calcification, Irisin (067-29; Phoenix Pharmaceuticals Inc, Burlingame, CA, USA) at different concentrations (50 or 100 ng/ml dissolved in PBS) was used to treat VSMCs in the presence of β-GP medium for 7 days with medium changes every 2–3 days. For pharmacological treatment, the CASP1 inhibitor VX-765 (10 μM; HY-13205), NLRP3 inhibitor MCC950 (100 μM; HY-12815A), ROS scavenger N-acetyl-L-cysteine (NAC, 20 μM; HY-B0215), autophagy inducer rapamycin (200 nM; HY-10219), autophagy inhibitor 3-methyladenine (3-MA, 5 mM; HY-19312), and chloroquine (CQ, 25 μM; HY-17589A) were purchased from MedChem Express (NJ, USA) and used to treat VSMCs according to the experimental design.

Pang Q., Wang P., Pan Y., Dong X., Zhou T., Song X, & Zhang A. (2022). Irisin protects against vascular calcification by activating autophagy and inhibiting NLRP3-mediated vascular smooth muscle cell pyroptosis in chronic kidney disease. Cell Death & Disease, 13(3), 283.

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TRIM26 Ubiquitination and GPX4 Regulation in Oxidative Stress

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Antibodies and reagents were acquired from designated suppliers:
TRIM26 (ab188017, Abcam), TRIM26 (27013-1-AP, Proteintech), TRIM26 (sc-393832, Santa Cruz Biotechnology), GPX4 (ab125066, Abcam), GPX4 (sc-166570, Santa Cruz Biotechnology), PLK1 (ab189139, Abcam), p-PLK1 (ab155095, Abcam), β-actin (ab8226, Abcam), K48-ubiquitin (ab140601, Abcam), K63-ubiquitin (12930, Cell Signaling Technology), anti-Flag (66008, Proteintech), anti-Myc (16286, Proteintech), p-S/T (61 G, abmart), p-S/T (612549, BD Biosciences), anti-His (66005, Proteintech), anti-Flag (14793, Cell Signaling Technology), anti-Myc (2276, Cell Signaling Technology), Anti-His (12689, Cell Signaling Technology), anti-HA (3724, Cell Signaling Technology),
MDA (ab27642, Abcam), 4-HNE (ab48506, Abcam), MG132 (S1748, Beyotime), cycloheximide (HY12320, MedChemExpress), Chloroquine (HY-17589A, MedChemExpress), Onvansertib (HY-15828, MedChemExpress), MLN0905 (HY-15155, MedChemExpress), Recombinant Human PLK1 (ab271716, Abcam).

Wang Z., Xia Y., Wang Y., Zhu R., Li H., Liu Y, & Shen N. (2023). The E3 ligase TRIM26 suppresses ferroptosis through catalyzing K63-linked ubiquitination of GPX4 in glioma. Cell Death & Disease, 14(10), 695.

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Evaluating Cellular Responses to Pharmacological Agents

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UA, CQ, MG-132, and Mdivi-1 (HY-100599, HY-17589A, HY-13259, and HY-15886, respectively) were procured from MedChemExpress (USA) and dissolved in dimethyl sulfoxide (DMSO; Sigma-Aldrich, St. Louis, MO, USA). NIH3T3 cells were exposed to UA (25 μM, 50 μM, 100 μM, or a vehicle) or mdivi-1 (12.5 μM, 25 μM, 50 μM, or a vehicle) for 48 h, or to CQ (25 μM, 50 μM, 100 μM, or a vehicle) or MG132 (5 μM) for 24 h. Subsequently, the cells were harvested for Western blotting analysis.
For the administration of UA via gavage, the rats received a daily gavage of either 20 mg/kg/d UA in PBS or PBS alone at 10 am for a duration of 28 days. After the 28-day period, the rats were euthanized, and their SCN tissues were collected for further analysis.

Zhou S., Li X., Liang F., Ji G., Lv K., Yuan Y., Zhao Y., Yan N., Zhang C., Cai S., Zhang S., Liu X., Song B, & Qu L. (2024). Mitophagy Regulates the Circadian Rhythms by Degrading NR1D1 in Simulated Microgravity and Isolation Environments. International Journal of Molecular Sciences, 25(9), 4853.

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Cisplatin Cytotoxicity and Autophagy Inhibition

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The cells were seeded into a 96-well plate at 5000 cells per well. On the following day, the medium was replaced with medium containing different concentrations of cisplatin (MedChemExpress, HY-17394). For the autophagy inhibition experiment, medium containing different concentrations of cisplatin with or without an autophagy inhibitor (CQ or 3-MA; MedChemExpress, HY-17589A and HY-19312) was added. CQ and 3-MA were used at a concentration of 10 μM and 5 mM, respectively. After 24 h of incubation, absorbance at 450 nm was measured using a water-soluble tetrazolium salt assay with the Cell Counting Kit-8 (Dojindo, CK04). We then established the cell viability curve and calculated the IC50 value using GraphPad Prism software (Prism 8). The reagents used are listed in Table 1.

Niu J., Yan T., Guo W., Wang W., Ren T., Huang Y., Zhao Z., Yu Y., Chen C., Huang Q., Lou J, & Guo L. (2022). The COPS3-FOXO3 positive feedback loop regulates autophagy to promote cisplatin resistance in osteosarcoma. Autophagy, 19(6), 1693-1710.

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Manipulation of Cellular Stress Pathways

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HEK293T, HeLa, U2OS, Vero-E6, and p62 KO Vero-E6 cells were cultured in Dulbecco’s modified Eagle’s medium (11995065, Gibco) supplemented with 10% fetal bovine serum (12303C, Sigma-Aldrich) and 1% penicillin-streptomycin (15140163, Gibco) at 37°C with 5% CO₂. CRISPR-Cas9 was used to generate p62 KO Vero cell line. For starvation treatment, cells were washed twice with phosphate-buffered saline (SH30256.01, Hyclone) and cultured in Earle’s balanced salt solution (E2888, Sigma-Aldrich) for 12 h. To induce ER stress, CPA (GC10268, GLPBIO) and thapsigargin (12758, Cell Signaling Technology) were used to treat cells for 12h or 6h, respectively. For chloroquine treatment, cells were incubated with 100 μM chloroquine (HY-17589A, MedChemExpress) for different times. For 1,6-hexanediol treatment, cells were washed with PBS for twice and incubated with 3% 1,6- hexanediol (H810887, Macklin) for 1 min, and then fixed in 4% PFA for immunofluorescence or lysed in TAP lysis buffer for subsequent immunoblotting. All cells were tested for mycoplasma negative.

Tan X., Cai K., Li J., Yuan Z., Chen R., Xiao H., Xu C., Hu B., Qin Y, & Ding B. (2023). Coronavirus subverts ER-phagy by hijacking FAM134B and ATL3 into p62 condensates to facilitate viral replication. Cell Reports, 42(4), 112286.

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MHC-I Expression Analysis in B16/F10 Cells

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B16/F10 cell surface MHC-I expression was determined by flow cytometry. Briefly, B16/F10 cells were stained with APC-labeled anti-H-2Kb antibodies (1:100; Thermo Fisher, catalog no. 17595882) for 30 min on ice. The expression of MHC-I was shown as the mean fluorescence intensity. For lysosome inhibition, mouse B16F10 cells were treated with BafA1 (40 nM; MedChemExpress, catalog no. HY-100558) or CQ (20 μM; MedChemExpress, catalog no. HY-17589A) and followed by flow cytometry analysis of MHC-I.

Lin W., Chen L., Zhang H., Qiu X., Huang Q., Wan F., Le Z., Geng S., Zhang A., Qiu S., Chen L., Kong L, & Lu J.J. (2023). Tumor-intrinsic YTHDF1 drives immune evasion and resistance to immune checkpoint inhibitors via promoting MHC-I degradation. Nature Communications, 14, 265.

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Probing Ferroptosis and EMT Mechanisms

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RSL3 (HY-100218, MedChemExpress), chloroquine (CQ) (HY-17589A, MedChemExpress), necrostatin-1 (Nec-1) (HY-15760, MedChemExpress), ferrostatin-1 (Fer-1) (HY-100579, MedChemExpress), SB431542 (HY-10431, MedChemExpress), and carbon 11 (C11)-BODIPY^581/591 (RM02821, Abclonal, Wuhan, China) were the reagents used.
Nodal (A9902, Abclonal; sc-373910, Santa Cruz Biotechnology), SCD1 (ab236868, Abcam), Phospho-Smad2 (Ser465/467)/Smad3 (Ser423/425) (8828 S, Cell Signalling Technology), Smad2/3 (ab202445, Abcam; 5678, Cell Signalling Technology), E-cadherin (A20798, Abclonal), N-cadherin (A0432, Abclonal), vimentin (ab8978, Abcam), snail (A5243, Abclonal), GAPDH (A19056, Abclonal), β-tubulin (AC008, Abclonal), goat anti-rabbit immunoglobulin (Ig) G heavy and light chain (H&L) (horse radish peroxidase [HRP]) (ab6721, Abcam), goat anti-mouse IgG (H&L) (HRP) (ab6789, Abcam), IRDye 680 donkey anti-mouse IgG-(H + L)/goat anti-rabbit IRDye 800CW secondary antibody (926-68072/926-32211, LI-COR Biosciences, Lincoln, NE, USA) were the antibodies used in this study.

Wu T., Wan J., Qu X., Xia K., Wang F., Zhang Z., Yang M., Wu X., Gao R., Yuan X., Fang L., Chen C, & Yin L. (2023). Nodal promotes colorectal cancer survival and metastasis through regulating SCD1-mediated ferroptosis resistance. Cell Death & Disease, 14(3), 229.

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Modulation of Mouse Bone Marrow Dendritic Cells by OmpA

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Mouse BMDCs were purchased from Otwo Biotech (HTX2245C) and grew in DMEM with 10% fetal bovine serum and 1% penicillin/streptomycin. First, BMDCs (1 × 10⁶ cells/mL) were treated with OmpA (0, 5, 10 μg/mL) for 24 h. Further BMDCs were divided into: Control group (BMDCs) and OmpA group (10 μg/mL OmpA treated BMDCs for 24 h).¹⁹ In addition, 10 μg/mL OmpA treated BMDCs for 6, 12, and 24 h, grouped as: Control, OmpA (6 h), OmpA (12 h), and OmpA (24 h) groups. BMDCs were treated with 5 μg/mL and 10 μg/mL OmpA for 24 h, grouped as: Control, OmpA (5 μg/mL), and OmpA (10 μg/mL) groups. BMDCs were pretreated with autophagy inhibitor chloroquine (10 μM) for 30 min, and BMDCs were treated with 10 μg/mL OmpA for 24 h,²⁰ and BMDCs were divided into: Control, OmpA, and OmpA + chloroquine groups. Finally, BMDCs were transfected with overexpression plasmids (oe‐NC or oe‐PI3K) for 48 h, treated with 10 μg/mL OmpA for 24 h and grouped into: OmpA+oe‐NC and OmpA+oe‐PI3K groups. Chloroquine was purchased from MedChemExpress (HY‐17589A). Overexpression PI3K plasmid (oe‐PI3K) and control plasmid (oe‐NC) were purchased from HonroGene. All cell transfections were carried out by Lipofectamine 2000 (11668019, Thermo).

Tan H, & Cao L. (2023). Acinetobacter baumannii outer membrane protein A induces autophagy in bone marrow‐derived dendritic cells involving the PI3K/mTOR pathway. Immunity, Inflammation and Disease, 11(4), e830.

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Spheroid Culture Assay with Inhibitors and Growth Factors

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For all spheroid culture-based assays where inhibitors or growth factors were used, cells were seeded into medium containing the vehicle (DMSO or H₂O), inhibitor, or growth factor. The following day, media were aspirated and replaced with methylcellulose-containing media that also contained the vehicle, inhibitor, or growth factor. The vehicle concentration was 0.1% for all experiments. Inhibitors used in these experiments are as follows: YKL-05-099 (MedChem Express HY-101147), apilimod (MedChem Express HY-14644), and CQ (MedChem Express HY-17589A). Growth factors used in these experiments are as follows: EGF (PeproTech AF-100-15), FGF4 (PeproTech AF-100-31), and HGF (PeproTech 100-39H).

Ferrarone J.R., Thomas J., Unni A.M., Zheng Y., Nagiec M.J., Gardner E.E., Mashadova O., Li K., Koundouros N., Montalbano A., Mustafa M., Cantley L.C., Blenis J., Sanjana N.E, & Varmus H. (2024). Genome-wide CRISPR screens in spheroid culture reveal that the tumor suppressor LKB1 inhibits growth via the PIKFYVE lipid kinase. Proceedings of the National Academy of Sciences of the United States of America, 121(21), e2403685121.

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