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Proteintech anti rabbit inos
Anti Rabbit Inos, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1153 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+rabbit+inos/iNOS+Antibody/pm41915872-266-6-9
Average 96 stars, based on 1153 article reviews

anti rabbit inos - by Bioz Stars, 2026-10

96/100 stars

Images

Staining:

Article Title: IL-3 Modulates Microglia Polarization and Attenuates Neuroinflammation in Traumatic Brain Injury.
Article Snippet: .. The primary and secondary antibodies include anti-rabbit iNOS (18985-1-AP, Proteintech, 1:200), anti-rabbit NRF2 (ab62352, Abcam, 1:400), anti-rabbit P65 NF- κB (8242S, CST, 1:400), and anti-rabbit PRDX1 (15816-1-AP, Proteintech, 1:200), anti-mouse IL-3R (sc-74522, santa, 1:50), antimouse GFAP (3670, CST, 1:400), anti-rabbit IL-3 (PA5-115414, Invitrogen, 1:400), anti-mouse IBA1 (ab283319, abcam, 1:400), anti-rabbit IL-3R (GTX64388, GeneTex, 1:200), anti-mouse MBP (66003-1-Ig, Proteintech, 1:500), anti-mouse NEUN (MAB377, sigma, 1:1000), sheep anti-mouse IgG H&L secondary antibody (Abcam, Alexa Fluor 488, ab 150113, 1:200), sheep anti-mouse IgG H&L secondary antibody (Abcam, Alexa Fluor594, ab150116, 1:200), sheep anti-rabbit IgG H&L secondary antibody (Abcam, Alexa Fluor 488, ab150077, 1:200), sheep anti-rabbit IgG H&L secondary antibody (Abcam, Alexa Fluor 594, ab 150 080, 1:200), and Cell nuclei were stained with DAPI. .. Images were obtained using a Leica TCS SP8 confocal laser scanning microscope (Leica Microsystems, Wetzlar, Germany) and an electron microscope (Olympus, Tokyo, Japan).

Incubation:

Article Title: Anticolorectal Cancer Activity of Bilobalide in Patient-Derived Colorectal Cancer Organoids and AOM/DSS Mouse Model
Article Snippet: Cells or sections were immobilized using 4% paraformaldehyde (PFA) (Sigma-Aldrich, USA), permeabilized with 0.5% Triton X-100 (SigmaAldrich, USA) for 20min, and thereafter sealed with 5% bovine serum albumin (Gibco, Grand Island, NY) for 30min. .. Te cells were incubated overnight with anti-mouse Arg-1 (1 : 200-1 :1000 dilution, Proteintech, catalog number: 66129-1), anti-mouse CD206 (1 : 200-1 :1000 dilution, Proteintech, catalog number: 60143-1), anti-rabbit iNOS (1 : 200-1 :1000 dilution, Proteintech, catalog number: 22226- 1), and anti-rabbit Ki67 (1 : 200-1 :1000 dilution, Proteintech, catalog number: 27309-1) antibodies for immunostaining. .. Next, the cells were treated with Alexa Fluor 488/ Cy3-conjugated anti-mouse/rabbit immunoglobulin G (Life Technology, CA) for 2 h at 37°C.

Article Title: Ovariectomy Induces Microglial Cell Activation and Inflammatory Response in Rat Prefrontal Cortices to Accelerate the Chronic Unpredictable Stress-Mediated Anxiety and Depression
Article Snippet: After deparaffinage, antigen retrieval was carried out in a retrieval box using the EDTA (pH 8.0) antigen retrieval solution (Servicebio Technology Co., Ltd., Wuhan, China). .. Then, fluorescence quencher was added, and BSA was also added dropwise for incubation; then, primary antibodies (anti-ionized calcium-binding adapter molecule-1 (anti-Iba-1; Servicebio Technology Co., Ltd., Wuhan, China); anti-rabbit-INOS (1 : 100, Proteintech Group, Inc., USA)) were added to incubate overnight at 4°C, followed by incubation with fluorescence secondary antibodies (goat anti-mouse (Alexa 488 conjugated, 1 : 100, Proteintech Group, Inc., USA); goat anti-rabbit (Alexa 594 conjugated, 1 : 100, Proteintech Group, Inc., USA)) in the dark at room temperature. .. Later, DAPI (Servicebio Technology Co., Ltd., Wuhan, China) was added to counterstain the cell nuclei, followed by mounting with the antifluorescence quenching mounting medium.

Immunostaining:

Western Blot:

Article Title: Antioxidant activity and protective effect of ethanolic extract from Phlomis umbrosa Turcz. roots on H2O2- and PM2.5-induced oxidative stress in respiratory cells
Article Snippet: PM2.5(평균직경 1.06 μm)는 Powder Technology Inc.(Arizona Test Dust, Arden Hills, MN, USA)로부터 구입 하였으며, dimethyl sulfoxide(DMSO)는 Daejung Chemicals & Metals Co.(Siheung, Korea)로부터 구입하였다. .. Western blot assay에 사용된 1차 항체인 anti-mouse TLR-4(sc-52962), MyD88(sc-74532), p-JNK(sc-6254), p-NF-κB(sc-136548), βactin(sc-69879)은 Santa Cruz Biotechnology Inc.(Dallas, TX, https://www.ekosfop.or.kr 719 USA)에서, anti-rabbit iNOS(18985-1-AP)는 Proteintech Group, Inc.(Rosemont, IL, USA)에서 구입하였다. .. 또한, 2차 항체인 horse radish peroxidase(HRP)가 결합된 anti-mouse IgG(AP124P)는 Merck (Darmstadt, Land Hessen, Germany)에서 구입하였고, anti-rabbit IgG(7074S)는 Cell Signaling Technology(Danvers, MA, USA)에서 구입하여 실험에 사용하였다.

Fluorescence:

Image Search Results

Establishment of the APAP-induced liver injury in mice and cell models. (A) Paraffin-embedded liver sections underwent H&E staining as well as TNF-α, IL-6 and IL-1β immunostaining; scale bars, 100 μ m. (B) Serum ALT and AST levels were measured in APAP-induced mice (n=6). (C) Representative western blots and densitometry analysis of TNF-α, IL-6 and IL-1β expression in liver extracts prepared from APAP-induced mouse liver tissues. (D) Representative western blots and densitometry analysis of SREBP-1, PPAR-α and Fasn expression in liver extracts prepared from APAP-induced mouse liver tissues. (E) Representative western blots and densitometry analysis of iNOS and NOX4 expression in liver extracts prepared from APAP-induced mouse liver tissues. (F) Representative western blots and densitometry analysis of TNF-α, IL-6 and IL-1β expression in APAP-induced AML-12 cells. (G) Representative western blots and densitometry analysis of SREBP-1, PPAR-α and Fasn expression in APAP-induced AML-12 cells. (H) Representative western blots and densitometry analysis of iNOS and NOX4 expression in APAP-induced AML-12 cells. Data are presented as the mean ± SD of at least three repeats and were compared using a one-way ANOVA followed by Bonferroni's correction. * P<0.05, ** P<0.01, **** P<0.0001. APAP, acetaminophen; H&E, hematoxylin and eosin; IHC, immunohistochemistry; ALT, alanine aminotransferase; AST, aspartate aminotransferase; SREBP-1, sterol regulatory element-binding protein 1; PPAR-α, peroxisome proliferator-activated receptor α; Fasn, fatty acid synthase; iNOS, inducible nitric oxide synthase; NOX4, NADPH oxidase 4.

Journal: International Journal of Molecular Medicine

Article Title: Hepatic p38γ exacerbates acetaminophen-induced acute liver injury via PI3K/Akt-dependent mechanisms

doi: 10.3892/ijmm.2026.5855

Figure Lengend Snippet: Establishment of the APAP-induced liver injury in mice and cell models. (A) Paraffin-embedded liver sections underwent H&E staining as well as TNF-α, IL-6 and IL-1β immunostaining; scale bars, 100 μ m. (B) Serum ALT and AST levels were measured in APAP-induced mice (n=6). (C) Representative western blots and densitometry analysis of TNF-α, IL-6 and IL-1β expression in liver extracts prepared from APAP-induced mouse liver tissues. (D) Representative western blots and densitometry analysis of SREBP-1, PPAR-α and Fasn expression in liver extracts prepared from APAP-induced mouse liver tissues. (E) Representative western blots and densitometry analysis of iNOS and NOX4 expression in liver extracts prepared from APAP-induced mouse liver tissues. (F) Representative western blots and densitometry analysis of TNF-α, IL-6 and IL-1β expression in APAP-induced AML-12 cells. (G) Representative western blots and densitometry analysis of SREBP-1, PPAR-α and Fasn expression in APAP-induced AML-12 cells. (H) Representative western blots and densitometry analysis of iNOS and NOX4 expression in APAP-induced AML-12 cells. Data are presented as the mean ± SD of at least three repeats and were compared using a one-way ANOVA followed by Bonferroni's correction. * P<0.05, ** P<0.01, **** P<0.0001. APAP, acetaminophen; H&E, hematoxylin and eosin; IHC, immunohistochemistry; ALT, alanine aminotransferase; AST, aspartate aminotransferase; SREBP-1, sterol regulatory element-binding protein 1; PPAR-α, peroxisome proliferator-activated receptor α; Fasn, fatty acid synthase; iNOS, inducible nitric oxide synthase; NOX4, NADPH oxidase 4.

Article Snippet: The anti-p38γ (cat. no. 20184-1-AP), anti-IL-6 (cat. no. 21865-1-AP), anti-IL-1β (cat. no. 16806-1-AP), anti-albumin (cat. no. 16475-1-AP), Akt (cat. no. 10176-2-AP), anti-phosphorylated (p-)Akt (cat. no. 66444-1-Ig), anti-TNF-α (cat. no. 17590-1-AP), anti-peroxisome proliferator-activated receptor (PPAR)-α (cat. no. 66826-1-Ig), anti-sterol regulatory element-binding protein (SREBP)-1 (cat. no. 14088-1-AP) and anti-Fasn (cat. no. 10624-2-AP) antibodies were purchased from Proteintech Group, Inc. Anti-NADPH oxidase 4 (NOX4) (cat. no. A11274) and anti-inducible nitric oxide synthase (iNOS) (cat. no. A14031) were purchased from ABclonal Biotech Co., Ltd. Anti-β-actin (cat. no. AF7018), anti-PI3K (cat. no. AF3241) and anti-p-PI3K (cat. no. AF6241) were purchased from Affinity Biosciences, Ltd. ELISA kits for IL-1β (cat. no. MLB00C-1), IL-6 (cat. no. M6000B-1) and TNF-α (cat. no. MTA00B-1) were purchased R&D Systems, Inc.

Techniques: Staining, Immunostaining, Western Blot, Expressing, Immunohistochemistry, Binding Assay

p38γ knockdown inhibits oxidative stress and lipid accumulation in APAP-induced AML-12 cells. Intracellular (A) MDA, (B) GSH and (C) SOD activities were assayed in AML-12 cells transfected with p38γ siRNA and pEGFP-C1-p38γ according to the manufacturer's instructions (n=3). (D) Representative images of Oil red O staining of AML12 cells transfected with p38γ siRNA and pEGFP-C1-p38γ; scale bar, 100 μ m. (E) Reactive oxygen species production was detected by DCF, DHE and MitoSOX assay after overexpression and knockdown of p38γ. Western blot analysis of PPAR-α, SREBP-1, Fasn, iNOS and NOX4 expression in AML-12 cells following p38γ (F) knockdown and (G) overexpression. Data are presented as the mean ± SD of at least three repeats and were compared using a one-way ANOVA followed by Bonferroni's correction. * P<0.05, ** P<0.01, *** P<0.001. APAP, acetaminophen; MDA, malondialdehyde; GSH, glutathione; SOD, superoxide dismutase; siRNA, small interfering RNA; NC, negative control; DCF, 2',7'-dichlorofluorescein; DHE, dihydroethidium; PPAR-α, peroxisome proliferator-activated receptor α; SREBP-1, sterol regulatory element-binding protein 1; Fasn, fatty acid synthase; iNOS, inducible nitric oxide synthase; NOX4, NADPH oxidase 4.

Journal: International Journal of Molecular Medicine

Article Title: Hepatic p38γ exacerbates acetaminophen-induced acute liver injury via PI3K/Akt-dependent mechanisms

doi: 10.3892/ijmm.2026.5855

Figure Lengend Snippet: p38γ knockdown inhibits oxidative stress and lipid accumulation in APAP-induced AML-12 cells. Intracellular (A) MDA, (B) GSH and (C) SOD activities were assayed in AML-12 cells transfected with p38γ siRNA and pEGFP-C1-p38γ according to the manufacturer's instructions (n=3). (D) Representative images of Oil red O staining of AML12 cells transfected with p38γ siRNA and pEGFP-C1-p38γ; scale bar, 100 μ m. (E) Reactive oxygen species production was detected by DCF, DHE and MitoSOX assay after overexpression and knockdown of p38γ. Western blot analysis of PPAR-α, SREBP-1, Fasn, iNOS and NOX4 expression in AML-12 cells following p38γ (F) knockdown and (G) overexpression. Data are presented as the mean ± SD of at least three repeats and were compared using a one-way ANOVA followed by Bonferroni's correction. * P<0.05, ** P<0.01, *** P<0.001. APAP, acetaminophen; MDA, malondialdehyde; GSH, glutathione; SOD, superoxide dismutase; siRNA, small interfering RNA; NC, negative control; DCF, 2',7'-dichlorofluorescein; DHE, dihydroethidium; PPAR-α, peroxisome proliferator-activated receptor α; SREBP-1, sterol regulatory element-binding protein 1; Fasn, fatty acid synthase; iNOS, inducible nitric oxide synthase; NOX4, NADPH oxidase 4.

Techniques: Knockdown, Transfection, Staining, Mitosox Assay, Over Expression, Western Blot, Expressing, Small Interfering RNA, Negative Control, Binding Assay

p38γ is a direct target of miR-125. (A) TargetScan was used to predict that p38γ possesses binding sites for miR-125. (B) A luciferase reporter assay was performed to detect luciferase activity in the mimics NC + MUT p38γ, miR-125 mimics + MUT p38γ, mimics NC + WT p38γ and miR-125 mimics + WT p38γ groups. (C) The mRNA levels of p38γ in cells were determined by RT-qPCR. (D) Western blot analysis of p38γ expression in AML-12 cells treated with miR-125 inhibitor or miR-125 mimics. (E) Western blot analysis of iNOS, NOX4, TNF-α, IL-6 and IL-1β expression in AML-12 cells. (F) The miR-125 expression was determined by RT-qPCR in liver injury tissues and primary hepatocytes. (G) miR-125 expression were determined by RT-qPCR in AML-12 cells. Data are presented as the mean ± SD of at least three repeats and were compared using a one-way ANOVA followed by Bonferroni's correction. * P<0.05, ** P<0.01, *** P<0.001. ns, not significant; miR-125, microRNA-125; NC, negative control; MUT, mutant; WT, wild type; RT-qPCR, reverse transcription quantitative PCR; iNOS, inducible nitric oxide synthase; NOX4, NADPH oxidase 4; UTR, untranslated region; APAP, acetaminophen.

Journal: International Journal of Molecular Medicine

Article Title: Hepatic p38γ exacerbates acetaminophen-induced acute liver injury via PI3K/Akt-dependent mechanisms

doi: 10.3892/ijmm.2026.5855

Figure Lengend Snippet: p38γ is a direct target of miR-125. (A) TargetScan was used to predict that p38γ possesses binding sites for miR-125. (B) A luciferase reporter assay was performed to detect luciferase activity in the mimics NC + MUT p38γ, miR-125 mimics + MUT p38γ, mimics NC + WT p38γ and miR-125 mimics + WT p38γ groups. (C) The mRNA levels of p38γ in cells were determined by RT-qPCR. (D) Western blot analysis of p38γ expression in AML-12 cells treated with miR-125 inhibitor or miR-125 mimics. (E) Western blot analysis of iNOS, NOX4, TNF-α, IL-6 and IL-1β expression in AML-12 cells. (F) The miR-125 expression was determined by RT-qPCR in liver injury tissues and primary hepatocytes. (G) miR-125 expression were determined by RT-qPCR in AML-12 cells. Data are presented as the mean ± SD of at least three repeats and were compared using a one-way ANOVA followed by Bonferroni's correction. * P<0.05, ** P<0.01, *** P<0.001. ns, not significant; miR-125, microRNA-125; NC, negative control; MUT, mutant; WT, wild type; RT-qPCR, reverse transcription quantitative PCR; iNOS, inducible nitric oxide synthase; NOX4, NADPH oxidase 4; UTR, untranslated region; APAP, acetaminophen.

Techniques: Binding Assay, Luciferase, Reporter Assay, Activity Assay, Quantitative RT-PCR, Western Blot, Expressing, Negative Control, Mutagenesis, Reverse Transcription, Real-time Polymerase Chain Reaction

miR-125 inhibits oxidative stress and lipid accumulation by targeting p38γ. Intracellular levels of (A) MDA and (C) GSH and (B) activity of SOD were assessed in AML-12 cells. (D) Representative images of Oil red O staining of AML12 cells; scale bar, 100 μ m. (E) Reactive oxygen species production was detected using DCF, DHE and MitoSOX assays following overexpression and knockdown of miR-125. Western blot analysis of PPAR-α, SREBP-1, Fasn, iNOS and NOX4 activity in AML-12 cells treated with (F) miR-125 inhibitor and (G) miR-125 mimics. Data are presented as the mean ± SD of at least three repeats and were compared using a one-way ANOVA followed by Bonferroni's correction. * P<0.05, ** P<0.01, *** P<0.001. APAP, acetaminophen; miR-125, microRNA-125; NC, negative control; siRNA, small interfering RNA; MDA, malondialdehyde; GSH, glutathione; SOD, superoxide dismutase; DCF, 2',7'-dichlorofluorescein; DHE, dihydroethidium; PPAR-α, peroxisome proliferator-activated receptor-α; SREBP-1, sterol regulatory element-binding protein 1; Fasn, fatty acid synthase; iNOS, inducible nitric oxide synthase; NOX4, NADPH oxidase 4.

Journal: International Journal of Molecular Medicine

Article Title: Hepatic p38γ exacerbates acetaminophen-induced acute liver injury via PI3K/Akt-dependent mechanisms

doi: 10.3892/ijmm.2026.5855

Figure Lengend Snippet: miR-125 inhibits oxidative stress and lipid accumulation by targeting p38γ. Intracellular levels of (A) MDA and (C) GSH and (B) activity of SOD were assessed in AML-12 cells. (D) Representative images of Oil red O staining of AML12 cells; scale bar, 100 μ m. (E) Reactive oxygen species production was detected using DCF, DHE and MitoSOX assays following overexpression and knockdown of miR-125. Western blot analysis of PPAR-α, SREBP-1, Fasn, iNOS and NOX4 activity in AML-12 cells treated with (F) miR-125 inhibitor and (G) miR-125 mimics. Data are presented as the mean ± SD of at least three repeats and were compared using a one-way ANOVA followed by Bonferroni's correction. * P<0.05, ** P<0.01, *** P<0.001. APAP, acetaminophen; miR-125, microRNA-125; NC, negative control; siRNA, small interfering RNA; MDA, malondialdehyde; GSH, glutathione; SOD, superoxide dismutase; DCF, 2',7'-dichlorofluorescein; DHE, dihydroethidium; PPAR-α, peroxisome proliferator-activated receptor-α; SREBP-1, sterol regulatory element-binding protein 1; Fasn, fatty acid synthase; iNOS, inducible nitric oxide synthase; NOX4, NADPH oxidase 4.

Techniques: Activity Assay, Staining, Over Expression, Knockdown, Western Blot, Negative Control, Small Interfering RNA, Binding Assay

miR-125 reverses APAP-induced liver injury by targeting p38γ via activation of the PI3K/AKT signaling. (A) Kyoto Encyclopedia of Genes and Genomes enrichment of the potential signaling pathways associated with significantly differentially expressed genes between the control and APAP-treated groups. Western blot analysis of p-PI3K and p-AKT expression in (B) liver injury tissues and (C) AML-12 cells. Western blot analysis of p-PI3K and p-AKT expression in AML-12 cells transfected with (D) p38γ siRNA and (E) pEGFP-C1-p38γ. Western blot analysis of p-PI3K and p-AKT expression in AML-12 cells following (F) overexpression and (G) knockdown of miR-125. (H) Chemical structure of the PI3K/AKT signaling pathway inhibitor, LY294002. (I) Western blot analysis of PPAR-α, SREBP-1, Fasn, iNOS and NOX4 activity in AML-12 cells following p38γ knockdown and treatment with LY294002. (J) Western blot analysis of PPAR-α, SREBP-1, Fasn, iNOS and NOX4 activity in AML-12 cells following p38γ overexpression and treatment with LY294002. Data are presented as the mean ± SD of at least three repeats and were compared using a one-way ANOVA followed by Bonferroni's correction. * P<0.05, ** P<0.01, *** P<0.001. APAP, acetaminophen; miR-125, microRNA-125; NC, negative control; siRNA, small interfering RNA; p-, phosphorylated; PPAR-α, peroxisome proliferator-activated receptor α; SREBP-1, sterol regulatory element-binding protein 1; Fasn, fatty acid synthase; iNOS, inducible nitric oxide synthase; NOX4, NADPH oxidase 4.

Journal: International Journal of Molecular Medicine

Article Title: Hepatic p38γ exacerbates acetaminophen-induced acute liver injury via PI3K/Akt-dependent mechanisms

doi: 10.3892/ijmm.2026.5855

Figure Lengend Snippet: miR-125 reverses APAP-induced liver injury by targeting p38γ via activation of the PI3K/AKT signaling. (A) Kyoto Encyclopedia of Genes and Genomes enrichment of the potential signaling pathways associated with significantly differentially expressed genes between the control and APAP-treated groups. Western blot analysis of p-PI3K and p-AKT expression in (B) liver injury tissues and (C) AML-12 cells. Western blot analysis of p-PI3K and p-AKT expression in AML-12 cells transfected with (D) p38γ siRNA and (E) pEGFP-C1-p38γ. Western blot analysis of p-PI3K and p-AKT expression in AML-12 cells following (F) overexpression and (G) knockdown of miR-125. (H) Chemical structure of the PI3K/AKT signaling pathway inhibitor, LY294002. (I) Western blot analysis of PPAR-α, SREBP-1, Fasn, iNOS and NOX4 activity in AML-12 cells following p38γ knockdown and treatment with LY294002. (J) Western blot analysis of PPAR-α, SREBP-1, Fasn, iNOS and NOX4 activity in AML-12 cells following p38γ overexpression and treatment with LY294002. Data are presented as the mean ± SD of at least three repeats and were compared using a one-way ANOVA followed by Bonferroni's correction. * P<0.05, ** P<0.01, *** P<0.001. APAP, acetaminophen; miR-125, microRNA-125; NC, negative control; siRNA, small interfering RNA; p-, phosphorylated; PPAR-α, peroxisome proliferator-activated receptor α; SREBP-1, sterol regulatory element-binding protein 1; Fasn, fatty acid synthase; iNOS, inducible nitric oxide synthase; NOX4, NADPH oxidase 4.

Techniques: Activation Assay, Protein-Protein interactions, Control, Western Blot, Expressing, Transfection, Over Expression, Knockdown, Activity Assay, Negative Control, Small Interfering RNA, Binding Assay

miR-125 reverses APAP-induced liver injury by targeting p38γ via activation of the PI3K/AKT signaling pathway. (A) Western blot analysis of PPAR-α, SREBP-1, Fasn, iNOS and NOX4 expression in AML-12 cells transfected with miR-125 inhibitor and treated with LY294002. (B) Western blot analysis of PPAR-α, SREBP-1, Fasn, iNOS and NOX4 expression in AML-12 cells transfected with miR-125 mimics and then treated with LY294002. Western blot analysis of TNF-α, IL-6 and IL-1β expression in AML-12 cells transfected with (C) p38γ siRNA and (D) pEGFP-C1-p38γ and then treated with LY294002. Western blot analysis of TNF-α, IL-6 and IL-1β expression in AML-12 cells transfected with (E) miR-125 inhibitor or (F) miR-125 mimics and then treated with LY294002. Data are presented as the mean ± SD of at least three repeats and were compared using a one-way ANOVA followed by Bonferroni's correction. * P<0.05, ** P<0.01. ns, not significant; APAP, acetaminophen; miR-125, microRNA-125; NC, negative control; siRNA, small interfering RNA; PPAR-α, peroxisome proliferator-activated receptor α; SREBP-1, sterol regulatory element-binding protein 1; Fasn, fatty acid synthase; iNOS, inducible nitric oxide synthase; NOX4, NADPH oxidase 4.

Journal: International Journal of Molecular Medicine

Article Title: Hepatic p38γ exacerbates acetaminophen-induced acute liver injury via PI3K/Akt-dependent mechanisms

doi: 10.3892/ijmm.2026.5855

Figure Lengend Snippet: miR-125 reverses APAP-induced liver injury by targeting p38γ via activation of the PI3K/AKT signaling pathway. (A) Western blot analysis of PPAR-α, SREBP-1, Fasn, iNOS and NOX4 expression in AML-12 cells transfected with miR-125 inhibitor and treated with LY294002. (B) Western blot analysis of PPAR-α, SREBP-1, Fasn, iNOS and NOX4 expression in AML-12 cells transfected with miR-125 mimics and then treated with LY294002. Western blot analysis of TNF-α, IL-6 and IL-1β expression in AML-12 cells transfected with (C) p38γ siRNA and (D) pEGFP-C1-p38γ and then treated with LY294002. Western blot analysis of TNF-α, IL-6 and IL-1β expression in AML-12 cells transfected with (E) miR-125 inhibitor or (F) miR-125 mimics and then treated with LY294002. Data are presented as the mean ± SD of at least three repeats and were compared using a one-way ANOVA followed by Bonferroni's correction. * P<0.05, ** P<0.01. ns, not significant; APAP, acetaminophen; miR-125, microRNA-125; NC, negative control; siRNA, small interfering RNA; PPAR-α, peroxisome proliferator-activated receptor α; SREBP-1, sterol regulatory element-binding protein 1; Fasn, fatty acid synthase; iNOS, inducible nitric oxide synthase; NOX4, NADPH oxidase 4.

Techniques: Activation Assay, Western Blot, Expressing, Transfection, Negative Control, Small Interfering RNA, Binding Assay

p38γ knockdown attenuates liver injury in APAP-treated mice. (A) Small animal imaging analysis. (B) Fluorescence imaging analysis showed that AAV9-shRNA-p38γ was specifically located in the mouse liver tissues. (C) Immunofluorescence staining of p38γ in APAP-induced mice liver injury tissues; scale bar, 100 μ m. (D) Western blot analysis of p38γ expression in mouse liver tissues. (E) The H&E staining of liver sections; scale bar, 100 and 40 μ m. (F) IHC analysis of TNF-α, IL-6 and IL-1β expression in liver extracts prepared from mice liver tissues. Serum levels of (G) AST and (H) ALT were measured (n=6). Serum levels of (I) GSH, (J) MDA and (K) SOD were measured (n=3). (L) Representative images of Oil red O staining of AML-12 cells; scale bar, 100 and 40 μ m. (M) DCF analysis of reactive oxygen species production; scale bar, 100 and 40 μ m. (N) Western blot analysis of TNF-α, IL-6 and IL-1β expression in mouse liver tissues. (O) Western blot analysis of PPAR-α, SREBP-1, Fasn, iNOS and NOX4 expression in mouse liver tissues. Data are presented as the mean ± SD of at least three repeats and were compared using a two-tailed unpaired Student's t-test. * P<0.05, ** P<0.01, *** P<0.001. APAP, acetaminophen; AAV, adeno-associated virus; shRNA, short hairpin RNA; H&E, hematoxylin and eosin; IHC, immunohistochemistry; AST, aspartate aminotransferase; ALT, alanine aminotransferase; GSH, glutathione; MDA, malondialdehyde; SOD, superoxide dismutase; DFH, dihydrofluorescein; DCF, 2',7'-dichlorofluorescein; PPAR-α, peroxisome proliferator-activated receptor alpha; SREBP-1, sterol regulatory element-binding protein 1; Fasn, fatty acid synthase; iNOS, inducible nitric oxide synthase; NOX4, NADPH oxidase 4.

Journal: International Journal of Molecular Medicine

Article Title: Hepatic p38γ exacerbates acetaminophen-induced acute liver injury via PI3K/Akt-dependent mechanisms

doi: 10.3892/ijmm.2026.5855

Figure Lengend Snippet: p38γ knockdown attenuates liver injury in APAP-treated mice. (A) Small animal imaging analysis. (B) Fluorescence imaging analysis showed that AAV9-shRNA-p38γ was specifically located in the mouse liver tissues. (C) Immunofluorescence staining of p38γ in APAP-induced mice liver injury tissues; scale bar, 100 μ m. (D) Western blot analysis of p38γ expression in mouse liver tissues. (E) The H&E staining of liver sections; scale bar, 100 and 40 μ m. (F) IHC analysis of TNF-α, IL-6 and IL-1β expression in liver extracts prepared from mice liver tissues. Serum levels of (G) AST and (H) ALT were measured (n=6). Serum levels of (I) GSH, (J) MDA and (K) SOD were measured (n=3). (L) Representative images of Oil red O staining of AML-12 cells; scale bar, 100 and 40 μ m. (M) DCF analysis of reactive oxygen species production; scale bar, 100 and 40 μ m. (N) Western blot analysis of TNF-α, IL-6 and IL-1β expression in mouse liver tissues. (O) Western blot analysis of PPAR-α, SREBP-1, Fasn, iNOS and NOX4 expression in mouse liver tissues. Data are presented as the mean ± SD of at least three repeats and were compared using a two-tailed unpaired Student's t-test. * P<0.05, ** P<0.01, *** P<0.001. APAP, acetaminophen; AAV, adeno-associated virus; shRNA, short hairpin RNA; H&E, hematoxylin and eosin; IHC, immunohistochemistry; AST, aspartate aminotransferase; ALT, alanine aminotransferase; GSH, glutathione; MDA, malondialdehyde; SOD, superoxide dismutase; DFH, dihydrofluorescein; DCF, 2',7'-dichlorofluorescein; PPAR-α, peroxisome proliferator-activated receptor alpha; SREBP-1, sterol regulatory element-binding protein 1; Fasn, fatty acid synthase; iNOS, inducible nitric oxide synthase; NOX4, NADPH oxidase 4.

Techniques: Knockdown, Imaging, Fluorescence, shRNA, Immunofluorescence, Staining, Western Blot, Expressing, Two Tailed Test, Virus, Immunohistochemistry, Binding Assay

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