lfhp-1c Search Results


lfhp 1c  (MedChemExpress)
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MedChemExpress lfhp 1c
a PGAM5 <t>inhibitor,</t> <t>LFHP-1c</t> treatment suppresses erastin-induced ferroptosis and lipid peroxidation. AC16 cells were treated with erastin (20 μM) with or without LFHP-1c (2 μM) for 16 h for cell death measurement or 12 h for lipid ROS measurement. Cells were stained with Propidium Iodide (PI) and cell death was analyzed by flow cytometry. Cells treated as indicated were stained with BODIPY 581/591 C11, and lipid ROS levels were measured by flow cytometry. b Knockdown of PGAM5 blocked erastin-induced ferroptosis and lipid peroxidation. Western blot images confirm the expression of the indicated proteins. Cells, as indicated, were treated with erastin (20 μM) for 16 h for cell death measurement, or 12 h for lipid ROS measurement. Cell death and lipid ROS were measured as described in ( a ). c DRP1 was dramatically phosphorylated at serine 616 and de-phosphorylated at serine 637 in a time-dependent manner upon erastin treatment. AC16 cells were treated with erastin (20 μM) as indicated. Western blot images confirm the expression of the indicated proteins. d PGAM5 inhibitor LFPH-1c treatment suppresses erastin induced de-phosphorylation of DRP1 at serine 637. AC16 cells were treated with erastin (20 μM) with or without LFPH-1c (2 μM) for the indicated time. Western blot images confirm the expression of the indicated proteins. e Knockdown of PGAM5 blocks erastin-induced de-phosphorylation of DRP1 at serine 637. AC16 cells, as indicated, were treated with erastin (20 μM) for the indicated time. Western blot images confirm the expression of the indicated proteins. f Knockdown of PGAM5 blocks ferroptosis-associated mitochondrial fragmentation. SU9-GFP labeled AC16 cells were treated with erastin (20 μM) as indicated. SU9-GFP labeled mitochondria were imaged by using a confocal laser scanning microscope (scale bars in images of all figures were 10 μM). Quantification of mitochondria with different morphologies (fragmented, short, long). “Short” represents cells with a majority of mitochondria shorter than 10 µm, “Long” represents cells with a majority of mitochondria longer than 10 µm, “Fragmented” represents cells with a majority of granular mitochondria. At least 100 cells were counted for each sample. g Overexpression of PGAM5 suppresses erastin-induced ferroptosis and lipid peroxidation. Western blot images confirm the expression of the indicated proteins. AC16 cells, as indicated, were treated with erastin (20 μM) for 16 h for cell death measurement, or 12 h for lipid ROS measurement. Cell death and lipid ROS were measured as described in ( a ). h The level of PGAM5 influences erastin-induced ferroptosis. Different dose PGAM5-flag plasmids were transfected into AC16 cells, and AC16 cells were cultured for 48 h, and then treated with erastin (20 μM) for 16 h for cell death measurement, or 12 h for lipid ROS measurement. Cell death and lipid ROS were measured as described in ( a ). Western blot images confirmed the expression of the indicated proteins. Data are derived from three independent experiments, and each value represents the mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001, t test ( n = 3).
Lfhp 1c, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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lfhp-1c  (MuseChem Chemicals)
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LFHP-1c（Cat No.:I041198）is an investigational compound under development for its potential use in treating inflammatory diseases and conditions related to immune system dysregulation. It is designed to selectively target specific pathways involved in inflammation, aiming to
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lfhp-1c  (Aladdin Scientific Corporation)
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LFHP-1c is an PGAM5 inhibitor with neuroprotective activity in brain ischemic stroke. LFHP-1c protects blood-brain barrier integrity from ischemia-induced injury. LFHP-1c binds to endothelial PGAM5 to inhibit the activity of PGAM5 phosphatase and the interaction
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lfhp-1c  (TargetMol)
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Image Search Results


a PGAM5 inhibitor, LFHP-1c treatment suppresses erastin-induced ferroptosis and lipid peroxidation. AC16 cells were treated with erastin (20 μM) with or without LFHP-1c (2 μM) for 16 h for cell death measurement or 12 h for lipid ROS measurement. Cells were stained with Propidium Iodide (PI) and cell death was analyzed by flow cytometry. Cells treated as indicated were stained with BODIPY 581/591 C11, and lipid ROS levels were measured by flow cytometry. b Knockdown of PGAM5 blocked erastin-induced ferroptosis and lipid peroxidation. Western blot images confirm the expression of the indicated proteins. Cells, as indicated, were treated with erastin (20 μM) for 16 h for cell death measurement, or 12 h for lipid ROS measurement. Cell death and lipid ROS were measured as described in ( a ). c DRP1 was dramatically phosphorylated at serine 616 and de-phosphorylated at serine 637 in a time-dependent manner upon erastin treatment. AC16 cells were treated with erastin (20 μM) as indicated. Western blot images confirm the expression of the indicated proteins. d PGAM5 inhibitor LFPH-1c treatment suppresses erastin induced de-phosphorylation of DRP1 at serine 637. AC16 cells were treated with erastin (20 μM) with or without LFPH-1c (2 μM) for the indicated time. Western blot images confirm the expression of the indicated proteins. e Knockdown of PGAM5 blocks erastin-induced de-phosphorylation of DRP1 at serine 637. AC16 cells, as indicated, were treated with erastin (20 μM) for the indicated time. Western blot images confirm the expression of the indicated proteins. f Knockdown of PGAM5 blocks ferroptosis-associated mitochondrial fragmentation. SU9-GFP labeled AC16 cells were treated with erastin (20 μM) as indicated. SU9-GFP labeled mitochondria were imaged by using a confocal laser scanning microscope (scale bars in images of all figures were 10 μM). Quantification of mitochondria with different morphologies (fragmented, short, long). “Short” represents cells with a majority of mitochondria shorter than 10 µm, “Long” represents cells with a majority of mitochondria longer than 10 µm, “Fragmented” represents cells with a majority of granular mitochondria. At least 100 cells were counted for each sample. g Overexpression of PGAM5 suppresses erastin-induced ferroptosis and lipid peroxidation. Western blot images confirm the expression of the indicated proteins. AC16 cells, as indicated, were treated with erastin (20 μM) for 16 h for cell death measurement, or 12 h for lipid ROS measurement. Cell death and lipid ROS were measured as described in ( a ). h The level of PGAM5 influences erastin-induced ferroptosis. Different dose PGAM5-flag plasmids were transfected into AC16 cells, and AC16 cells were cultured for 48 h, and then treated with erastin (20 μM) for 16 h for cell death measurement, or 12 h for lipid ROS measurement. Cell death and lipid ROS were measured as described in ( a ). Western blot images confirmed the expression of the indicated proteins. Data are derived from three independent experiments, and each value represents the mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001, t test ( n = 3).

Journal: Cell Death & Disease

Article Title: Targeting mitochondrial phosphatase PGAM5 alleviates ferroptosis and acute pancreatitis by upregulating NRF2-mediated FSP1 expression

doi: 10.1038/s41419-026-08484-9

Figure Lengend Snippet: a PGAM5 inhibitor, LFHP-1c treatment suppresses erastin-induced ferroptosis and lipid peroxidation. AC16 cells were treated with erastin (20 μM) with or without LFHP-1c (2 μM) for 16 h for cell death measurement or 12 h for lipid ROS measurement. Cells were stained with Propidium Iodide (PI) and cell death was analyzed by flow cytometry. Cells treated as indicated were stained with BODIPY 581/591 C11, and lipid ROS levels were measured by flow cytometry. b Knockdown of PGAM5 blocked erastin-induced ferroptosis and lipid peroxidation. Western blot images confirm the expression of the indicated proteins. Cells, as indicated, were treated with erastin (20 μM) for 16 h for cell death measurement, or 12 h for lipid ROS measurement. Cell death and lipid ROS were measured as described in ( a ). c DRP1 was dramatically phosphorylated at serine 616 and de-phosphorylated at serine 637 in a time-dependent manner upon erastin treatment. AC16 cells were treated with erastin (20 μM) as indicated. Western blot images confirm the expression of the indicated proteins. d PGAM5 inhibitor LFPH-1c treatment suppresses erastin induced de-phosphorylation of DRP1 at serine 637. AC16 cells were treated with erastin (20 μM) with or without LFPH-1c (2 μM) for the indicated time. Western blot images confirm the expression of the indicated proteins. e Knockdown of PGAM5 blocks erastin-induced de-phosphorylation of DRP1 at serine 637. AC16 cells, as indicated, were treated with erastin (20 μM) for the indicated time. Western blot images confirm the expression of the indicated proteins. f Knockdown of PGAM5 blocks ferroptosis-associated mitochondrial fragmentation. SU9-GFP labeled AC16 cells were treated with erastin (20 μM) as indicated. SU9-GFP labeled mitochondria were imaged by using a confocal laser scanning microscope (scale bars in images of all figures were 10 μM). Quantification of mitochondria with different morphologies (fragmented, short, long). “Short” represents cells with a majority of mitochondria shorter than 10 µm, “Long” represents cells with a majority of mitochondria longer than 10 µm, “Fragmented” represents cells with a majority of granular mitochondria. At least 100 cells were counted for each sample. g Overexpression of PGAM5 suppresses erastin-induced ferroptosis and lipid peroxidation. Western blot images confirm the expression of the indicated proteins. AC16 cells, as indicated, were treated with erastin (20 μM) for 16 h for cell death measurement, or 12 h for lipid ROS measurement. Cell death and lipid ROS were measured as described in ( a ). h The level of PGAM5 influences erastin-induced ferroptosis. Different dose PGAM5-flag plasmids were transfected into AC16 cells, and AC16 cells were cultured for 48 h, and then treated with erastin (20 μM) for 16 h for cell death measurement, or 12 h for lipid ROS measurement. Cell death and lipid ROS were measured as described in ( a ). Western blot images confirmed the expression of the indicated proteins. Data are derived from three independent experiments, and each value represents the mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001, t test ( n = 3).

Article Snippet: Chemical reagents used were erastin (Selleck, Cat#S7242), ML385 (APE×BIO, Cat#B8300), LFHP-1c (MCE, Cat# HY139598 ), L -arginine (Sigma, Cat#74-79-3), and iFSP1 (MCE, Cat#HY-136057).

Techniques: Staining, Flow Cytometry, Knockdown, Western Blot, Expressing, De-Phosphorylation Assay, Labeling, Laser-Scanning Microscopy, Over Expression, Transfection, Cell Culture, Derivative Assay

a Schematic illustration of the experimental design of the mouse arginine-induced acute pancreatitis model. b LFHP-1c treatment protects against arginine-induced higher levels of serum α-AMS. n = 6. c LFHP-1c treatment protects against arginine-induced higher levels of serum LDH and ALT. n = 6. d LFHP-1c treatment blocks arginine-induced upregulation of pro-inflammatory cytokines (miL-1β, miL-6, and TNF-α) in pancreatic tissue. RT-qPCR analyzes the expression of indicated pro-inflammatory cytokines. n = 3. e Representative H&E sections obtained from the mouse pancreas in response to different treatments after 72 h. f LFHP-1c treatment suppresses arginine-induced upregulation of 4-HNE and activates AMPK and promotes the expression of NRF2 and FSP1 in pancreatic tissue. g LFHP-1c treatment suppresses the arginine-induced higher level of pancreatic tissue MDA. n = 6. h LFHP-1c treatment promotes the mRNA level of FSP1 in pancreatic tissue. RT-qPCR analyzes the expression of FSP1. i LFHP-1c treatment suppresses the elevated mRNA level of PTGS2 induced by arginine in pancreatic tissue. RT-qPCR analyzes the expression of PTGS2. n = 3. Data are derived from independent experiments, and each value represents the mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001, t test.

Journal: Cell Death & Disease

Article Title: Targeting mitochondrial phosphatase PGAM5 alleviates ferroptosis and acute pancreatitis by upregulating NRF2-mediated FSP1 expression

doi: 10.1038/s41419-026-08484-9

Figure Lengend Snippet: a Schematic illustration of the experimental design of the mouse arginine-induced acute pancreatitis model. b LFHP-1c treatment protects against arginine-induced higher levels of serum α-AMS. n = 6. c LFHP-1c treatment protects against arginine-induced higher levels of serum LDH and ALT. n = 6. d LFHP-1c treatment blocks arginine-induced upregulation of pro-inflammatory cytokines (miL-1β, miL-6, and TNF-α) in pancreatic tissue. RT-qPCR analyzes the expression of indicated pro-inflammatory cytokines. n = 3. e Representative H&E sections obtained from the mouse pancreas in response to different treatments after 72 h. f LFHP-1c treatment suppresses arginine-induced upregulation of 4-HNE and activates AMPK and promotes the expression of NRF2 and FSP1 in pancreatic tissue. g LFHP-1c treatment suppresses the arginine-induced higher level of pancreatic tissue MDA. n = 6. h LFHP-1c treatment promotes the mRNA level of FSP1 in pancreatic tissue. RT-qPCR analyzes the expression of FSP1. i LFHP-1c treatment suppresses the elevated mRNA level of PTGS2 induced by arginine in pancreatic tissue. RT-qPCR analyzes the expression of PTGS2. n = 3. Data are derived from independent experiments, and each value represents the mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001, t test.

Article Snippet: Chemical reagents used were erastin (Selleck, Cat#S7242), ML385 (APE×BIO, Cat#B8300), LFHP-1c (MCE, Cat# HY139598 ), L -arginine (Sigma, Cat#74-79-3), and iFSP1 (MCE, Cat#HY-136057).

Techniques: Quantitative RT-PCR, Expressing, Derivative Assay