Hql 79

Manufactured by Cayman Chemical

Sourced in United States

HQL-79 is a laboratory equipment product. It is designed for general laboratory use. The core function of HQL-79 is to assist in the performance of various laboratory tasks and procedures.

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Lab products found in correlation

4 protocols using hql 79

Inhibition of COX-1/2 in Leukemia Stem Cell Transplantation

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Inhibition of COX-1/2 was accomplished by use of indomethacin (Cayman Chemicals, Ann Arbor, MI). indomethacin (0.00325%, w/v) was dissolved in ethanol (0.5%, v/v) and administered by means of oral drinking water for one week prior to bone marrow transplantation with BCR-ABL LSCs, as described previously (23 (link), 28 (link), 29 (link)). In a subset of Δ¹²-PGJ₃ rescue experiments, administration of exogenous Δ¹²-PGJ₃ was performed as described previously (2 (link)). In brief, mice were given daily intraperitoneal (i.p.) injection of Δ¹²-PGJ₃ (0.025mg/kg) in 500 µl of sterile PBS for seven days, starting at day-7 post-transplant until sacrifice at day-14. HQL-79 (Cayman Chemicals, Ann Arbor, MI) was used to inhibit the activity of H-PGDS. HQL-79 (30 mg/kg body weight) was administered by i.p. injection every other day (3–4 times/week) from day zero (day of transplant) until day 14 (total of seven injections). HQL-79 was resuspended in a solution of 0.05 mM citric acid and 11.1 mM hydroxypropyl beta-cyclodextrin (HPBCD; Sigma, St. Louis) and incubated for >10 minutes at 37 °C, until dissolved. Mice were injected with this formation within 10 minutes of preparation. All mice were euthanized on day 14 post-transplant.

Finch E.R., Kudva A.K., Quickel M.D., Goodfield L.L., Kennett M.J., Whelan J., Paulson R.F, & Prabhu K.S. (2015). Chemopreventive effects of dietary eicosapentaenoic acid supplementation in experimental myeloid leukemia. Cancer prevention research (Philadelphia, Pa.), 8(10), 989-999.

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Subconjunctival Injection for Ocular Treatments

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Subconjunctival injection is routinely used in clinical treatment and in experimental studies of ocular diseases (Wang et al., 2020a (link)). Anesthetized mice were injected subconjunctivally with 10 μL solution per injection. miR-223-5p antagomir (20 μmol/L) from GenePharma (Shanghai, China), miRNA antagomir negative control (NC) (20 μmol/L) from GenePharma (Shanghai, China). HQL-79 (50 μg/ml) (Cayman, 10134), and vehicle (2% methanol) were injected subconjunctivally 24 h before and 0 h after injury. At 24 h after wounding, corneas were collected for qRT-PCR, western blot and immunofluorescence staining. On the fifth day after the corneal epithelial debridement, corneas were used for corneal whole-mount staining and corneal sensitivity measurement. In the untreated normal and diabetic mice, the right eyes were untreated after injury.

Zhang Y., Dou S., Qi X., Zhang Z., Qiao Y., Wang Y., Xie J., Jiang H., Zhang B., Zhou Q., Wang Q, & Xie L. (2021). Transcriptional Network Analysis Reveals the Role of miR-223-5p During Diabetic Corneal Epithelial Regeneration. Frontiers in Molecular Biosciences, 8, 737472.

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Eosinophil Signaling Pathways Activation

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Purified human eosinophils or mouse eosinophils at 2 × 10⁶ cells/mL or 3 × 10⁶ cells/mL in Ca²⁺/Mg²⁺ HBSS (HBSS^+/+; pH 7.4) were pre-treated with the PI3K inhibitors wortmannin (1 μM; Biomol) and LY294002 (10 μM; Cayman Chemicals), PKC inhibitor calphostin C (1 μM; Biomol), pertussis toxin (PTX; 100 ng/mL), neutralizing monoclonal antibodies anti-CCL5 (10 μg/mL) and anti-CCR3 (10 μg/mL) (both from R&D), the PAF receptor antagonist BN52021 (10 μM), PGD₂ receptor antagonists BWA868c (200 nM; DP1 receptor) and Cay10471 (200 nM; DP2 receptor, or PGD₂ synthesis inhibitors HQL-79 (10 μM; H-PGDS) and AT-56 (10 μM; L-PGDS) (all from Cayman Chemicals) at 37°C for 30 min before stimulation with human recombinant (hr) or mouse recombinant (mr) leptin (0.5, 5, or 50 nM, as indicated; Peprotech) for 15 or 60 min in a water bath (37°C). Alternatively, eosinophils were also stimulated with PAF (1-O-hexadecyl-2-acetyl-sn-glyceryl-3-phosphorylcholine; 1 μM; Cayman Chemicals), hr CCL5 (also known as RANTES−100 ng/mL; R&D) or PGD₂ (25 nM; Cayman Chemicals). Each experimental condition was repeated at least three times with eosinophils purified from different donors or differentiated in vitro from different mouse bone marrows.

Amorim N.R., Luna-Gomes T., Gama-Almeida M., Souza-Almeida G., Canetti C., Diaz B.L., Weller P.F., Torres Bozza P., Maya-Monteiro C.M, & Bandeira-Melo C. (2018). Leptin Elicits LTC4 Synthesis by Eosinophils Mediated by Sequential Two-Step Autocrine Activation of CCR3 and PGD2 Receptors. Frontiers in Immunology, 9, 2139.

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Modulation of AML splenocyte function by IL-4 and cyclopentenone prostaglandins

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Splenocytes were isolated from either normal or AML mice and treated with rmIL-4 (10 ng/mL, 24hr) or CyPGs (Δ¹²-PGJ₂, 15d-PGJ₂, and Δ¹²-PGJ₃ at 100 nM in sterile PBS for 24hr) and incubated at 37 °C and 5% CO₂. Δ¹²-PGJ₂ and 15d-PGJ₂ were purchased from Cayman Chemical, Ann Arbor, MI, USA. Δ¹²-PGJ₃ was prepared in our laboratory as described previously.^{20 (link)} All three compounds were prepared fresh before use in sterile PBS and concentrations were calculated by liquid chromatography-mass spectrometry (not shown). For mRNA expression analysis, primary AML splenocytes were treated with rmIL-4 (10 ng/mL, 24hr); for protein expression analysis, primary AML splenocytes were treated with HQL79 (50 μM) and GW9662 (10 μM) in the presence of rmIL-4 (50 ng/mL) and incubated at 37°C and 5% CO₂ for 72 h. For the analyses of apoptosis and viability, primary AML splenocytes were treated with rmIL-4 (0, 50, 100 ng/mL) for 24, 48, and 72 h. At the time point of 48 h, GW9662 (10 μM) was added to the treatment of 50 ng/mL rmIL-4. HQL79 and GW9662 were purchased from Cayman Chemical, Ann Arbor, MI, USA, and reconstituted in cell-culture grade dimethyl sulfoxide (DMSO) (Sigma-Aldrich, St. Louis, MO, USA).

Qian F., Arner B.E., Kelly K.M., Annageldiyev C., Sharma A., Claxton D.F., Paulson R.F, & Prabhu K.S. (2022). Interleukin-4 treatment reduces leukemia burden in acute myeloid leukemia. FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 36(5), e22328.

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