The following compounds were used under indicated conditions: Ro-3306 (CDK1 inhibitor, 9 μM, 20 h, S7747; Selleck Chemicals, Houston, TX); anisomycin (500 nM, 24 h, sc-3524; Santa Cruz Biotechnology, Dallas, TX, USA); thapsigargin (100 nM, 24 h, 586005; Sigma-Aldrich); metformin (1 mM, 24 h, 136-18662; FUJIFILM Wako Pure Chemical Corporation); SIN-1 (1 mM, 3 h, ab141525; Abcam); TNF-α (50 ng/ml, 24 h, 300-01 A; PeproTech, Rocky Hill, NJ); cisplatin (2 μM, 24 h, S1166; Selleck Chemicals); doxorubicin (2 μM, 24 h, ab120629; Abcam); SP600125 (JNK inhibitor, 5 μM, 36 h, S1460; Selleck Chemicals); SB203580 (p38 inhibitor, 5 μM, 36 h, S1076; Selleck Chemicals).
S1460
Manufactured by Selleck Chemicals
Sourced in United States
S1460 is a laboratory equipment designed for general use in chemical and scientific research settings. It is a multi-purpose device that can be utilized for various applications. The core function of S1460 is to provide a controlled environment for conducting experiments and analyses.
Automatically generated - may contain errors
Lab products found in correlation
Sp600125, by Selleck Chemicals (2 mentions)
Anisomycin, by Santa Cruz Biotechnology (1 mentions)
Doxorubicin, by Abcam (1 mentions)
Ab120629, by Abcam (1 mentions)
Cisplatin, by Selleck Chemicals (1 mentions)
S1166, by Selleck Chemicals (1 mentions)
Metformin, by Fujifilm (1 mentions)
Ro 3306, by Selleck Chemicals (1 mentions)
S7747, by Selleck Chemicals (1 mentions)
S1076, by Selleck Chemicals (1 mentions)
Tnf α, by Thermo Fisher Scientific (1 mentions)
Sb203580, by Selleck Chemicals (1 mentions)
Thapsigargin, by Merck Group (1 mentions)
P8765, by Merck Group (1 mentions)
T3434, by Merck Group (1 mentions)
Pd98059, by Merck Group (1 mentions)
D5942, by Merck Group (1 mentions)
Galaxy 48r, by Eppendorf (1 mentions)
S1039, by Selleck Chemicals (1 mentions)
Envirus, by Engreen Biosystem (1 mentions)
6 protocols using s1460
1
Evaluating Small Molecule Responses
2
Hypoxic Injury Mechanisms in Neonatal Rat Cardiomyocytes
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Neonatal rat CMs were plated in 6-well plates. To mimic the hypoxic injury of myocardium, cells were maintained in a 5% O2 incubator (Galaxy 48R, Eppendorf, Germany) for various periods of time, and then harvested for associated experiments. Before hypoxic treatment, hypoxia (5% O2)-balanced DMEM/F-12 medium was changed. To further understand the mechanisms underlying hypoxia-induced Jagged1 expression in CMs, the following inhibitors were used: YC-1 (HIF-1α inhibitor, 10 μmol/L; Y102, Sigma), PD98059 [extracellular-regulated signal kinase (ERK) inhibitor, 50 nmol/L; sc-3532, Santa Cruz Biotechnology, Dallas, TX, USA], PTDC [nuclear factor κB (NF-κB) inhibitor, 10 μmol/L; P8765, Sigma), DAPT (Notch inhibitor, 10 μmol/L; D5942, Sigma), SP600125 [c-Jun N-terminal kinase (JNK) inhibitor, 25 μmol/L; S1460, Selleck Chemicals, Houston, TX, USA], AG490 [Janus kinase (JAK) inhibitor, 25 μmol/L; T3434, Sigma), and Stattic [signal transducer and activator of transcription 3 (STAT3) inhibitor,10 μmol/L; S7949, Sigma]. Dimethyl sulfoxide (DMSO; 0.1%, v/v) was used as a solvent control.
3
Modeling Liver Cirrhosis to Hepatocarcinoma
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To establish a model of the progression of liver cirrhosis to hepatocarcinoma, 8-week-old male Axin2Cre;Rosa26EGFP SD rats were injected intraperitoneally with 50 mg/kg diethylinitrosamine (N0258-1G; Sigma-Aldrich, Shanghai, China) twice per week for 8 weeks. The rats were fed a regular diet for an additional 4 weeks. The rats were biopsied to evaluate the presence of liver cirrhosis and autophagy status. Rats with non-autophagic liver cirrhosis were intraperitoneally injected with rapamycin (2 mg/kg, S1039; Selleck, Shanghai, China) twice per week for 4 weeks. Rats with aberrant autophagic liver cirrhosis were then number randomized and injected intravenously with 1 × 109 TU/ml shRNA-vector, shRNA-Atg3, shRNA-Atg7 and shRNA-HGF lentiviruses in transduction enhancement reagent (Envirus; Engreen Biosystem, Beijing, China) twice per week for 4 weeks. In addition, the rats also received chloroquine (50 mg/kg, an inhibitor of the late stage of autophagy; Sigma-Aldrich) weekly, with SP600125 (a JNK inhibitor, 15 mg/kg, S1460; Selleck) or stattic (a STAT3 inhibitor, 2 mg/kg, S7024; Selleck) administered twice per week by intraperitoneal injection for 4 weeks. A group of normal rats or rats with vehicle injection served as the control where appropriate. The rats were killed after an additional 4-week observation after the final treatment. The entire experimental period was 20 weeks.
4
Exploring MAPK and PI3K/mTOR Pathway Inhibition in HCC
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5 × 105 HCC cell lines were seeded into 6-well plates with complete medium. The following day, cells were cultured in 0% FBS-DMEM for 24 h with: Trametinib, MK2206, AZD8055, SP600125, Vx-11e and Temuterkib (S2673, S1078, S1555, S1460, S7709, S8534, Selleck Chemicals). Supernatants were collected to determine the secreted GM-CSF levels. Cell pellets were used for protein or RNA isolation.
Cell growth was determined by IncuCyte ZOOM (Essen BioScience) assays as previously described in ref. 111 (link). Briefly, 2 × 104NrasG12D/PtenKO HCC cells were seeded in 48-well plates and treated with the MAPK and PI3K/mTOR pathway drugs mentioned above in DMEM-FCS 0%. Cells were imaged every 4 h and phase-contrast images were analyzed to determine the relative cell growth based on cell confluency.
Cell growth was determined by IncuCyte ZOOM (Essen BioScience) assays as previously described in ref. 111 (link). Briefly, 2 × 104NrasG12D/PtenKO HCC cells were seeded in 48-well plates and treated with the MAPK and PI3K/mTOR pathway drugs mentioned above in DMEM-FCS 0%. Cells were imaged every 4 h and phase-contrast images were analyzed to determine the relative cell growth based on cell confluency.
5
Acute Liver Injury Modulation in Mice
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Mice (male, 8–10 weeks old) were randomized into 8 groups (n = 3/group): Control group, Creatinine group, APAP group, APAP + Creatinine group, APAP + N-acetyl-L-cysteine (NAC) group, APAP + Creatinine + NAC group, APAP + SP600125 group and APAP + Creatinine + SP600125 group. For the creatinine pre-treatment groups, the mice were injected intraperitoneally with creatinine (C4255, Sigma-Aldrich, United States ) at the dose of 16 mg/g for 1 week before APAP treatment. For the APAP-induced acute liver injury model, mice were fasted overnight and then administered with APAP (A7085, Sigma-Aldrich, United States ) intraperitoneally at the dose of 400 mg/kg. The other groups were intraperitoneally administrated with equal volume of 0.9% saline solution. In some experiments, mice were given 150 mg/kg of NAC (A7250, Sigma-Aldrich, United States ) 1 h before the APAP administration to minimize the effect of ROS. In some cases, the pharmacologic inhibitor SP600125 (S1460, Selleck, United States ) was used at a dose of 15 mg/kg 1 h prior to the APAP injection to inhibit the activation of JNK. Mice were finally intraperitoneal injected with 1% pentobarbital (50 mg/kg) for anaesthetization and sacrificed at 6 h for flow cytometric assay and 24 h for biochemical and histological detection.
6
Investigating JNK Regulation in HUVEC Dysfunction
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HUVEC line was purchased from ATCC and cultured in F‐12K medium (Procell, Wuhan, China) with 10% fetal bovine serum (FBS; HyClone, USA), 1% penicillin/streptomycin (Biosharp, Heifei, China), heparin (0.1 mg/mL) and endothelial cell growth supplement (ECGs, 0.05 mg/mL). Cells were maintained at 37 ºC in a humid environment with 5% CO2 and used between passages 4–6 for experiments. HUVECs were stimulated with HG (33 mM)/PA (100 μM; HY-N0830, MCE, USA) for 48 h. Mannitol [MAN, 33 mM: 5.5 mM of glucose + 27.5 mM of D-mannitol (M4125, Sigma-Aldrich, USA)] was used as the osmotic control for the HG/PA. JNK inhibitor SP600125 (20 μM, 24 h; S1460, Selleck, USA) and JNK activator Anisomycin (10 μM, 24 h; S7409, Selleck, USA) were used to inhibit and induce JNK activation in HUVECs, respectively. For the protein stability and degradation assay, HUVECs were treated with cycloheximide (CHX, 20 μM; A8244, ApexBio, USA) for indicated duration or proteasome inhibitor MG132 (10 μM; A2585, ApexBio, USA) for 6 h, or lysosome inhibitor chloroquine (CQ, 50 μΜ; Sigma-Aldrich, USA) for 24 h. Each experimental result was repeated for three independent biological replicates.
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