ap39 (MedChemExpress)

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MedChemExpress ap39
$Fig. 3. <t>AP39</t> improves myocardial fibrosis in rats with myocardial infarction. (A): Masson’s staining of myocardial tissue in Control, ISO, ISO+AP39, ISO +AP39 +PAG, and AP39 groups of rats, 10 × 10 and 10 × 40 magnification (blue staining indicates collagen fibers), n = 3. (B): Immunohistochemical detection of Collagen III protein expression in myocardial tissue of each group of rats, 10 × 40 magnification, n = 3. (C-E): Western blot analysis of the expression changes of α-SMA and Collagen III in myocardial tissue of each group of rats. (F) Collagen volume fraction determined by Masson’s staining. (G) Collagen III volume fraction determined by immunohistochemistry, n = 3, * P < 0.05 vs Control; #P < 0.05 vs ISO; $P < 0.05 vs ISO+AP39.$
Ap39, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 10 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/ap39/AP39/pm37516015-65-0-7
Average 94 stars, based on 10 article reviews

ap39 - by Bioz Stars, 2026-11

94/100 stars

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1) Product Images from "AP39 inhibits ferroptosis by inhibiting mitochondrial autophagy through the PINK1/parkin pathway to improve myocardial fibrosis with myocardial infarction."

Article Title: AP39 inhibits ferroptosis by inhibiting mitochondrial autophagy through the PINK1/parkin pathway to improve myocardial fibrosis with myocardial infarction.

Journal: Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

doi: 10.1016/j.biopha.2023.115195

$Fig. 3. AP39 improves myocardial fibrosis in rats with myocardial infarction. (A): Masson’s staining of myocardial tissue in Control, ISO, ISO+AP39, ISO +AP39 +PAG, and AP39 groups of rats, 10 × 10 and 10 × 40 magnification (blue staining indicates collagen fibers), n = 3. (B): Immunohistochemical detection of Collagen III protein expression in myocardial tissue of each group of rats, 10 × 40 magnification, n = 3. (C-E): Western blot analysis of the expression changes of α-SMA and Collagen III in myocardial tissue of each group of rats. (F) Collagen volume fraction determined by Masson’s staining. (G) Collagen III volume fraction determined by immunohistochemistry, n = 3, * P < 0.05 vs Control; #P < 0.05 vs ISO; $P < 0.05 vs ISO+AP39.$
Figure Legend Snippet: Fig. 3. AP39 improves myocardial fibrosis in rats with myocardial infarction. (A): Masson’s staining of myocardial tissue in Control, ISO, ISO+AP39, ISO +AP39 +PAG, and AP39 groups of rats, 10 × 10 and 10 × 40 magnification (blue staining indicates collagen fibers), n = 3. (B): Immunohistochemical detection of Collagen III protein expression in myocardial tissue of each group of rats, 10 × 40 magnification, n = 3. (C-E): Western blot analysis of the expression changes of α-SMA and Collagen III in myocardial tissue of each group of rats. (F) Collagen volume fraction determined by Masson’s staining. (G) Collagen III volume fraction determined by immunohistochemistry, n = 3, * P < 0.05 vs Control; #P < 0.05 vs ISO; $P < 0.05 vs ISO+AP39.

Techniques Used: Staining, Control, Immunohistochemical staining, Expressing, Western Blot, Immunohistochemistry

Fig. 4. AP39 increases CSE levels and mitochondrial membrane potential in myocardial tissue and cardiomyocytes of rats with myocardial infarction, while reducing ROS levels in cardiomyocytes. (A): Changes in the viability of H9c2 cardiomyocytes induced by different concentrations of CoCl2 as measured by the CCK8 assay. (B): Western blot analysis of CSE expression in H9c2 cardiomyocytes. (C): Western blot analysis of CSE expression in myocardial tissue of different groups of rats. n = 3, * P < 0.05 vs Control; #P < 0.05 vs ISO; $P < 0.05 vs ISO+AP39. (D): Mean gray value (IntDen/Area) determined by JC-1, n = 3, * P < 0.05 vs Control; #P < 0.05 vs CoCl2; $P < 0.05 vs CoCl2 +AP39. (E): First and Second line: Detection of H2S levels in mitochondria of H9c2 cardiomyocytes using a mitochondrial H2S probe (Mito- HS); Third line: Detection of ROS levels in H9c2 cardiomyocytes using a ROS fluorescence probe; Fourth and Fifth line: Assessment of mitochondrial membrane potential changes in H9c2 cardiomyocytes using a mitochondrial membrane potential assay kit (JC-1).

Figure Legend Snippet: Fig. 4. AP39 increases CSE levels and mitochondrial membrane potential in myocardial tissue and cardiomyocytes of rats with myocardial infarction, while reducing ROS levels in cardiomyocytes. (A): Changes in the viability of H9c2 cardiomyocytes induced by different concentrations of CoCl2 as measured by the CCK8 assay. (B): Western blot analysis of CSE expression in H9c2 cardiomyocytes. (C): Western blot analysis of CSE expression in myocardial tissue of different groups of rats. n = 3, * P < 0.05 vs Control; #P < 0.05 vs ISO; $P < 0.05 vs ISO+AP39. (D): Mean gray value (IntDen/Area) determined by JC-1, n = 3, * P < 0.05 vs Control; #P < 0.05 vs CoCl2; $P < 0.05 vs CoCl2 +AP39. (E): First and Second line: Detection of H2S levels in mitochondria of H9c2 cardiomyocytes using a mitochondrial H2S probe (Mito- HS); Third line: Detection of ROS levels in H9c2 cardiomyocytes using a ROS fluorescence probe; Fourth and Fifth line: Assessment of mitochondrial membrane potential changes in H9c2 cardiomyocytes using a mitochondrial membrane potential assay kit (JC-1).

Techniques Used: Membrane, CCK-8 Assay, Western Blot, Expressing, Control, Fluorescence

Fig. 5. AP39 inhibits mitochondrial autophagy in hypoxic H9c2 cardiomyocytes. (A-B): RT-qPCR analysis of PINK1 and P62 mRNA changes in H9c2 cardiomyocytes of each group. n = 3, * P < 0.05 vs Control; #P < 0.05 vs CoCl2; $P < 0.05 vs CoCl2 +AP39. (C-G): Western blot analysis of PINK1, Parkin, P62, and LC3 protein expression changes in H9c2 cardiomyocytes. n = 3, * P < 0.05 vs Control; #P < 0.05 vs CoCl2; $P < 0.05 vs CoCl2 +AP39.

Figure Legend Snippet: Fig. 5. AP39 inhibits mitochondrial autophagy in hypoxic H9c2 cardiomyocytes. (A-B): RT-qPCR analysis of PINK1 and P62 mRNA changes in H9c2 cardiomyocytes of each group. n = 3, * P < 0.05 vs Control; #P < 0.05 vs CoCl2; $P < 0.05 vs CoCl2 +AP39. (C-G): Western blot analysis of PINK1, Parkin, P62, and LC3 protein expression changes in H9c2 cardiomyocytes. n = 3, * P < 0.05 vs Control; #P < 0.05 vs CoCl2; $P < 0.05 vs CoCl2 +AP39.

Techniques Used: Quantitative RT-PCR, Control, Western Blot, Expressing

Fig. 6. AP39 increases mitochondrial membrane potential, while inhibiting the expression of PINK1 and Parkin in hypoxic primary rat cardiomyocytes. First and Second line: Assessment of mitochondrial membrane potential changes in primary rat cardiomyocytes using a mitochondrial membrane potential assay kit (JC-1). Third to Sixth line: The expression of PINK1 and Parkin in primary rat cardiomyocytes using Immunofluorescence Staining. (A-B): Mean gray value(IntDen/Area) determined by JC-1 and Immunofluorescence Staining, n = 3, *P < 0.05 vs Control; #P < 0.05 vs CoCl2; $P < 0.05 vs CoCl2 +AP39.

Figure Legend Snippet: Fig. 6. AP39 increases mitochondrial membrane potential, while inhibiting the expression of PINK1 and Parkin in hypoxic primary rat cardiomyocytes. First and Second line: Assessment of mitochondrial membrane potential changes in primary rat cardiomyocytes using a mitochondrial membrane potential assay kit (JC-1). Third to Sixth line: The expression of PINK1 and Parkin in primary rat cardiomyocytes using Immunofluorescence Staining. (A-B): Mean gray value(IntDen/Area) determined by JC-1 and Immunofluorescence Staining, n = 3, *P < 0.05 vs Control; #P < 0.05 vs CoCl2; $P < 0.05 vs CoCl2 +AP39.

Techniques Used: Membrane, Expressing, Immunofluorescence, Staining, Control

Fig. 7. AP39 inhibits mitochondrial autophagy in rat myocardial infarction heart tissue. (A-E): Western blot analysis of the expression changes of PINK1, Parkin, P62, and LC3 in rat myocardial tissue. n = 3, * P < 0.05 vs Control; #P < 0.05 vs ISO; $P < 0.05 vs ISO+AP39. (F): Transmission electron microscopy observation of mitochondrial morphology and mitochondrial autophagy in rat myocardial infarction heart tissue.

Figure Legend Snippet: Fig. 7. AP39 inhibits mitochondrial autophagy in rat myocardial infarction heart tissue. (A-E): Western blot analysis of the expression changes of PINK1, Parkin, P62, and LC3 in rat myocardial tissue. n = 3, * P < 0.05 vs Control; #P < 0.05 vs ISO; $P < 0.05 vs ISO+AP39. (F): Transmission electron microscopy observation of mitochondrial morphology and mitochondrial autophagy in rat myocardial infarction heart tissue.

Techniques Used: Western Blot, Expressing, Control, Transmission Assay, Electron Microscopy

Fig. 8. AP39 inhibits myocardial ferroptosis in rat myocardial tissue and CoCl2-induced hypoxic damage in H9c2 myocardial cells. (A-C): Western blot analysis of the expression changes of GPX4 and SLC7a11 in rat myocardial tissue. n = 3, * P < 0.05 vs Control; #P < 0.05 vs ISO; $P < 0.05 vs ISO+AP39. (D-F): Western blot analysis of the expression changes of GPX4 and SLC7a11 in H9c2 myocardial cells. n = 3, * P < 0.05 vs Control; #P < 0.05 vs CoCl2; $P < 0.05 vs CoCl2 +AP39. (G-H): RT-qPCR analysis of the mRNA level changes of GPX4 and SLC7a11 in H9c2 myocardial cells. n = 3, * P < 0.05 vs Control; #P < 0.05 vs CoCl2; $P < 0.05 vs CoCl2 +AP39. (I): Detection of changes in the content of free Fe2+ in myocardial cell mitochondria using the mitochondrial Fe2+ fluorescent probe (Mito-FerroGreen).

Figure Legend Snippet: Fig. 8. AP39 inhibits myocardial ferroptosis in rat myocardial tissue and CoCl2-induced hypoxic damage in H9c2 myocardial cells. (A-C): Western blot analysis of the expression changes of GPX4 and SLC7a11 in rat myocardial tissue. n = 3, * P < 0.05 vs Control; #P < 0.05 vs ISO; $P < 0.05 vs ISO+AP39. (D-F): Western blot analysis of the expression changes of GPX4 and SLC7a11 in H9c2 myocardial cells. n = 3, * P < 0.05 vs Control; #P < 0.05 vs CoCl2; $P < 0.05 vs CoCl2 +AP39. (G-H): RT-qPCR analysis of the mRNA level changes of GPX4 and SLC7a11 in H9c2 myocardial cells. n = 3, * P < 0.05 vs Control; #P < 0.05 vs CoCl2; $P < 0.05 vs CoCl2 +AP39. (I): Detection of changes in the content of free Fe2+ in myocardial cell mitochondria using the mitochondrial Fe2+ fluorescent probe (Mito-FerroGreen).

Techniques Used: Western Blot, Expressing, Control, Quantitative RT-PCR

Fig. 9. AP39 can antagonize ferroptosis in hypoxic myocardial cells by inhibiting mitochondrial autophagy through the PINK1/Parkin pathway. (A-E): Western blot analysis of the expression changes of PINK1, Parkin, GPX4, and SLC7a11 in H9c2 myocardial cells. n = 3, * P < 0.05 vs Control; #P < 0.05 vs CoCl2; $P < 0.05 vs CoCl2 +AP39.

Figure Legend Snippet: Fig. 9. AP39 can antagonize ferroptosis in hypoxic myocardial cells by inhibiting mitochondrial autophagy through the PINK1/Parkin pathway. (A-E): Western blot analysis of the expression changes of PINK1, Parkin, GPX4, and SLC7a11 in H9c2 myocardial cells. n = 3, * P < 0.05 vs Control; #P < 0.05 vs CoCl2; $P < 0.05 vs CoCl2 +AP39.

Techniques Used: Western Blot, Expressing, Control

Fig. 10. AP39 inhibits ferroptosis and downregulates the expression of fibrosis-related proteins in hypoxic myocardial cells. (A-F): Western blot analysis of the expression changes of GPX4, SLC7a11, Collagen I, TGF-β, and α-SMA in H9c2 myocardial cells. n = 3, * P < 0.05 vs Control; #P < 0.05 vs CoCl2; $P < 0.05 vs CoCl2 +AP39.

Figure Legend Snippet: Fig. 10. AP39 inhibits ferroptosis and downregulates the expression of fibrosis-related proteins in hypoxic myocardial cells. (A-F): Western blot analysis of the expression changes of GPX4, SLC7a11, Collagen I, TGF-β, and α-SMA in H9c2 myocardial cells. n = 3, * P < 0.05 vs Control; #P < 0.05 vs CoCl2; $P < 0.05 vs CoCl2 +AP39.

Techniques Used: Expressing, Western Blot, Control

Control:

Article Title: UW Supplementation with AP39 Improves Liver Viability Following Static Cold Storage
Article Snippet: .. The liver was immediately weighed, and subsequently either perfused for 6 hours at 37°C as described below (fresh control, n = 4), or ushed Page 5/19 with UW with 200 nM AP39 (MedChemExpress, Monmouth Junction NJ, USA, n = 6) or vehicle (0.13% v/v dichloromethane) and stored on ice in the same respective solution for 3 days. ..

Article Title: TorPause: Efficient Static Organ Preservation for Transplants
Article Snippet: .. Perfusate defined the treatment group: UW alone (Control), or UW containing AP39 (3 μM, MedChemExpress, Monmouth Junction, NJ), GSK212 (2 μM, MedChemExpress, Monmouth Junction, NJ), or AP39 (3 μM) plus GSK212 (2 μM) (Combination); small molecules were diluted from DMSO stocks, with Control perfusate matched for DMSO (0.1% v/v). ..

Article Title: UW supplementation with AP39 improves liver viability following static cold storage
Article Snippet: .. The liver was immediately weighed, and subsequently either perfused for 6 h at 37 °C as described below (fresh control, n = 4), or flushed with UW with 200 nM AP39 (MedChemExpress, Monmouth Junction NJ, USA, n = 6) or vehicle (0.13% v/v dichloromethane, n = 6) and stored at 4 °C in the same respective solution for 3 days. ..

other:

Article Title: A Mitochondria-Modulating Nanosystem for Rheumatoid Arthritis Immunotherapy via Inflammatory Cascade Disruption.
Article Snippet: Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by chronic inflammation within joints, where macrophage-driven inflammatory cascade caused by mitochondrial dysfunction significantly contributes to the pathogenesis.. Through recruitment and activation of neutrophils from circulation, these macrophages promote the release of neutrophil extracellular traps (NETs) and generation of reactive oxygen species (ROS), leading to synovitis exacerbation and tissue damage.. To disrupt this closely linked cycle, we present a mitochondria-modulating nanosystem (NM@APDAase) targeting the inflammatory cascade for RA immunotherapy.