12031a h89 mce cat (MedChemExpress)
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12031a H89 Mce Cat, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 97/100, based on 226 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/h+89/H-89/pm42585016-166-130-132
Average 97 stars, based on 226 article reviews
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Inhibition:Article Title: CaRPOOL: a pooled calcium‑recording CRISPR screening platform identifies CCR7 as a modulator of cellular osmomechanosensing Article Snippet: .. For adenylyl cyclase or protein kinase A inhibition, cells were seeded and incubated overnight, then treated with SQ22536 (100 μM; MCE, HY‐100396) or Incubation:Article Title: CaRPOOL: a pooled calcium‑recording CRISPR screening platform identifies CCR7 as a modulator of cellular osmomechanosensing Article Snippet: .. For adenylyl cyclase or protein kinase A inhibition, cells were seeded and incubated overnight, then treated with SQ22536 (100 μM; MCE, HY‐100396) or Control:Article Title: Activation of the TGR5/cAMP/PKA/CREB axis in cholangiocytes mediates epithelial-mesenchymal transition and fibrosis in hepatolithiasis Article Snippet: When cell confluence reached approximately 70–80%, cells were treated with 500 μM taurodeoxycholic acid (TDCA; Sigma, Cat# T4009) for 24 h to establish a bile acid-induced biliary fibrosis model. Each condition was tested in triplicate, and the entire experiment was independently repeated twice to ensure reproducibility and data reliability. .. Based on the TDCA-induced cholangiocyte fibrosis cell model, additional pharmacological intervention groups were established as follows (3 technical replicates per group; each experiment was independently repeated twice): Control group (Control): no TDCA induction and no drug treatment; Model group (Model): treated with 500 μM TDCA for 24 h; Forskolin treatment group (Model + Forskolin): cells were co-treated with 500 μM TDCA and 50 μM forskolin (HY-15371, MCE) for 24 h [ ]; Article Title: Activation of the TGR5/cAMP/PKA/CREB axis in cholangiocytes mediates epithelial-mesenchymal transition and fibrosis in hepatolithiasis. Article Snippet: When cell 244 confluence reached approximately 70-80%, cells were treated with 500 μM taurodeoxycholic acid 245 (TDCA; Sigma, Cat# T4009) for 24 hours to establish a bile acid-induced biliary fibrosis model. 246 Each condition was tested in triplicate, and the entire experiment was independently repeated twice 247 to ensure reproducibility and data reliability. .. 248 249 AR TIC LE IN Injection:Article Title: Therapeutic effects of alprostadil on CCl 4 -induced hepatic fibrosis in rats and investigation of its molecular mechanisms. Article Snippet: Extended author information available on the last page of the article Abstract Hepatic fibrosis (HF) is driven by hepatic stellate cell (HSC) activation.. Although cyclic adenosine monophosphate (cAMP) is a key antifibrotic signal, whether pharmacological cAMP elevation acts through protein kinase A (PKA) or exchange protein directly activated by cAMP 1 (EPAC1) remains unclear.. Alprostadil (PGE1) elevates intracellular cAMP, but its antifibrotic mechanism is undefined. CCK-8 Assay:Article Title: Therapeutic effects of alprostadil on CCl 4 -induced hepatic fibrosis in rats and investigation of its molecular mechanisms. Article Snippet: Extended author information available on the last page of the article Abstract Hepatic fibrosis (HF) is driven by hepatic stellate cell (HSC) activation.. Although cyclic adenosine monophosphate (cAMP) is a key antifibrotic signal, whether pharmacological cAMP elevation acts through protein kinase A (PKA) or exchange protein directly activated by cAMP 1 (EPAC1) remains unclear.. Alprostadil (PGE1) elevates intracellular cAMP, but its antifibrotic mechanism is undefined. Article Title: Activation of the TGR5/cAMP/PKA/CREB axis in cholangiocytes mediates epithelial-mesenchymal transition and fibrosis in hepatolithiasis. Article Snippet: When cell 244 confluence reached approximately 70-80%, cells were treated with 500 μM taurodeoxycholic acid 245 (TDCA; Sigma, Cat# T4009) for 24 hours to establish a bile acid-induced biliary fibrosis model. 246 Each condition was tested in triplicate, and the entire experiment was independently repeated twice 247 to ensure reproducibility and data reliability. .. 248 249 AR TIC LE IN Reverse Transcription:Article Title: Therapeutic effects of alprostadil on CCl 4 -induced hepatic fibrosis in rats and investigation of its molecular mechanisms. Article Snippet: Extended author information available on the last page of the article Abstract Hepatic fibrosis (HF) is driven by hepatic stellate cell (HSC) activation.. Although cyclic adenosine monophosphate (cAMP) is a key antifibrotic signal, whether pharmacological cAMP elevation acts through protein kinase A (PKA) or exchange protein directly activated by cAMP 1 (EPAC1) remains unclear.. Alprostadil (PGE1) elevates intracellular cAMP, but its antifibrotic mechanism is undefined. Real-time Polymerase Chain Reaction:Article Title: Therapeutic effects of alprostadil on CCl 4 -induced hepatic fibrosis in rats and investigation of its molecular mechanisms. Article Snippet: Extended author information available on the last page of the article Abstract Hepatic fibrosis (HF) is driven by hepatic stellate cell (HSC) activation.. Although cyclic adenosine monophosphate (cAMP) is a key antifibrotic signal, whether pharmacological cAMP elevation acts through protein kinase A (PKA) or exchange protein directly activated by cAMP 1 (EPAC1) remains unclear.. Alprostadil (PGE1) elevates intracellular cAMP, but its antifibrotic mechanism is undefined. Lysis:Article Title: Therapeutic effects of alprostadil on CCl 4 -induced hepatic fibrosis in rats and investigation of its molecular mechanisms. Article Snippet: Extended author information available on the last page of the article Abstract Hepatic fibrosis (HF) is driven by hepatic stellate cell (HSC) activation.. Although cyclic adenosine monophosphate (cAMP) is a key antifibrotic signal, whether pharmacological cAMP elevation acts through protein kinase A (PKA) or exchange protein directly activated by cAMP 1 (EPAC1) remains unclear.. Alprostadil (PGE1) elevates intracellular cAMP, but its antifibrotic mechanism is undefined. Protease Inhibitor:Article Title: Therapeutic effects of alprostadil on CCl 4 -induced hepatic fibrosis in rats and investigation of its molecular mechanisms. Article Snippet: Extended author information available on the last page of the article Abstract Hepatic fibrosis (HF) is driven by hepatic stellate cell (HSC) activation.. Although cyclic adenosine monophosphate (cAMP) is a key antifibrotic signal, whether pharmacological cAMP elevation acts through protein kinase A (PKA) or exchange protein directly activated by cAMP 1 (EPAC1) remains unclear.. Alprostadil (PGE1) elevates intracellular cAMP, but its antifibrotic mechanism is undefined. Bicinchoninic Acid Protein Assay:Article Title: Therapeutic effects of alprostadil on CCl 4 -induced hepatic fibrosis in rats and investigation of its molecular mechanisms. Article Snippet: Extended author information available on the last page of the article Abstract Hepatic fibrosis (HF) is driven by hepatic stellate cell (HSC) activation.. Although cyclic adenosine monophosphate (cAMP) is a key antifibrotic signal, whether pharmacological cAMP elevation acts through protein kinase A (PKA) or exchange protein directly activated by cAMP 1 (EPAC1) remains unclear.. Alprostadil (PGE1) elevates intracellular cAMP, but its antifibrotic mechanism is undefined. SDS Page:Article Title: Therapeutic effects of alprostadil on CCl 4 -induced hepatic fibrosis in rats and investigation of its molecular mechanisms. Article Snippet: Extended author information available on the last page of the article Abstract Hepatic fibrosis (HF) is driven by hepatic stellate cell (HSC) activation.. Although cyclic adenosine monophosphate (cAMP) is a key antifibrotic signal, whether pharmacological cAMP elevation acts through protein kinase A (PKA) or exchange protein directly activated by cAMP 1 (EPAC1) remains unclear.. Alprostadil (PGE1) elevates intracellular cAMP, but its antifibrotic mechanism is undefined. Immunoprecipitation:Article Title: Therapeutic effects of alprostadil on CCl 4 -induced hepatic fibrosis in rats and investigation of its molecular mechanisms. Article Snippet: Extended author information available on the last page of the article Abstract Hepatic fibrosis (HF) is driven by hepatic stellate cell (HSC) activation.. Although cyclic adenosine monophosphate (cAMP) is a key antifibrotic signal, whether pharmacological cAMP elevation acts through protein kinase A (PKA) or exchange protein directly activated by cAMP 1 (EPAC1) remains unclear.. Alprostadil (PGE1) elevates intracellular cAMP, but its antifibrotic mechanism is undefined. Magnetic Beads:Article Title: Therapeutic effects of alprostadil on CCl 4 -induced hepatic fibrosis in rats and investigation of its molecular mechanisms. Article Snippet: Extended author information available on the last page of the article Abstract Hepatic fibrosis (HF) is driven by hepatic stellate cell (HSC) activation.. Although cyclic adenosine monophosphate (cAMP) is a key antifibrotic signal, whether pharmacological cAMP elevation acts through protein kinase A (PKA) or exchange protein directly activated by cAMP 1 (EPAC1) remains unclear.. Alprostadil (PGE1) elevates intracellular cAMP, but its antifibrotic mechanism is undefined. Enzyme-linked Immunosorbent Assay:Article Title: Therapeutic effects of alprostadil on CCl 4 -induced hepatic fibrosis in rats and investigation of its molecular mechanisms. Article Snippet: Extended author information available on the last page of the article Abstract Hepatic fibrosis (HF) is driven by hepatic stellate cell (HSC) activation.. Although cyclic adenosine monophosphate (cAMP) is a key antifibrotic signal, whether pharmacological cAMP elevation acts through protein kinase A (PKA) or exchange protein directly activated by cAMP 1 (EPAC1) remains unclear.. Alprostadil (PGE1) elevates intracellular cAMP, but its antifibrotic mechanism is undefined. AST Assay:Article Title: Therapeutic effects of alprostadil on CCl 4 -induced hepatic fibrosis in rats and investigation of its molecular mechanisms. Article Snippet: Extended author information available on the last page of the article Abstract Hepatic fibrosis (HF) is driven by hepatic stellate cell (HSC) activation.. Although cyclic adenosine monophosphate (cAMP) is a key antifibrotic signal, whether pharmacological cAMP elevation acts through protein kinase A (PKA) or exchange protein directly activated by cAMP 1 (EPAC1) remains unclear.. Alprostadil (PGE1) elevates intracellular cAMP, but its antifibrotic mechanism is undefined. Western Blot:Article Title: Therapeutic effects of alprostadil on CCl 4 -induced hepatic fibrosis in rats and investigation of its molecular mechanisms. Article Snippet: Extended author information available on the last page of the article Abstract Hepatic fibrosis (HF) is driven by hepatic stellate cell (HSC) activation.. Although cyclic adenosine monophosphate (cAMP) is a key antifibrotic signal, whether pharmacological cAMP elevation acts through protein kinase A (PKA) or exchange protein directly activated by cAMP 1 (EPAC1) remains unclear.. Alprostadil (PGE1) elevates intracellular cAMP, but its antifibrotic mechanism is undefined. other:Article Title: Propranolol alleviates cerebral infarction through the β2-AR-mediated ERK/NLRP3 pathway Article Snippet: H-89 , |

![Hesperetin and Naringenin increased cAMP level and [Ca 2+ ] i after glucose stimulation in murine L cells. (A,B) Intracellular cAMP levels from GLUTag cells in response to 10 μM Hesperetin (A) or 10 μM Naringenin (B) (n = 5). (C,D) GLP-1 secretion from GLUTag cells in response to 10 μM Hesperetin (C) or 10 μM Naringenin (D) with 10 μM <t>H89</t> or vehicle (n = 5). (E) The intracellular calcium concentration ([Ca 2+ ] i ) of GLUTag cells stimulated with 20 mM glucose plus vehicle or 10 μM Hesperetin was detected by using a Ca 2+ indicator, Fluo‐4 (n = 10). The change of fluorescence after stimulation was normalized to the basal fluorescence (ΔF/F 0 ) was measured by area under the curve (AUC). (F) GLP-1 secretion from GLUTag cells in response to 10 μM Hesperetin with 5 μM Nifedipine or vehicle (n = 5). (G) The intracellular calcium concentration ([Ca 2+ ] i ) of GLUTag cells stimulated with 20 mM glucose plus vehicle or 10 μM Naringenin was detected by using a Ca 2+ indicator, Fluo‐4 (n = 10). The change of fluorescence after stimulation was normalized to the basal fluorescence (ΔF/F 0 ). (H) GLP-1 secretion from GLUTag cells in response to 10 μM Naringenin with 5 μM Nifedipine or vehicle (n = 5). Black arrows indicated the initial time of glucose stimulation. ** p < 0.01, *** p < 0.001 by Mann-Whitney U-test, ns means not significant. Data are expressed as the mean ± SEM.](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_2436/pmc13272436/pmc13272436__fphar-17-1838267-g003.jpg)