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sodium l lactate  (MedChemExpress)


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    MedChemExpress sodium l lactate
    Sodium L Lactate, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 58 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/sodium+lactate/Lactic+acid/pm42436128-62-7-9
    Average 95 stars, based on 58 article reviews
    sodium l lactate - by Bioz Stars, 2026-09
    95/100 stars

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    Saline:

    Article Title: TDP-43 Dysfunction Causes Hyper-Lactate State, Increased AARS1 Expression and Enhanced Protein Lactylation.
    Article Snippet: TAR DNA-binding protein of 43 kDa (TDP-43) is a nuclear protein encoded by the TARDBP gene.. As an RNA-binding protein, it physiologically participates in key processes such as RNA transcription, alternative splicing, and the processing of microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), playing a crucial role in maintaining cellular RNA homeostasis(Zong, Xie et al. 2024).. Studies have shown that the hallmark pathological feature of TDP-43 involves nuclear depletion and cytoplasmic aggregation, which was first identified in amyotrophic lateral sclerosis Tianshuo Zhang, Kaixin Yan contributed equally to this article.

    Article Title: Integrative profiling of lactylation reveals prognostic biomarkers and an immunosuppressive niche in acute myeloid leukemia
    Article Snippet: All cells were cultured in RPMI-1640 medium (Gibco, Thermo Fisher Scientific, Waltham, MA, USA) supplemented with 10% fetal bovine serum (FBS, Gibco), 100 U/mL penicillin/streptomycin (Gibco), and 2 mM L-glutamine (Gibco) at 37 °C in a 5% CO 2 humidified incubator (Thermo Fisher Scientific). .. Sodium oxamate and sodium lactate (MCE; Monmouth Junction, NJ, USA) were dissolved in sterile phosphate-buffered saline (PBS) to prepare 20 mM stock solutions. .. Working concentrations (0.5–20 mM) were prepared fresh daily and filter-sterilized (0.22 μm, Millipore, MA, USA).

    Sterility:

    Article Title: Integrative profiling of lactylation reveals prognostic biomarkers and an immunosuppressive niche in acute myeloid leukemia
    Article Snippet: All cells were cultured in RPMI-1640 medium (Gibco, Thermo Fisher Scientific, Waltham, MA, USA) supplemented with 10% fetal bovine serum (FBS, Gibco), 100 U/mL penicillin/streptomycin (Gibco), and 2 mM L-glutamine (Gibco) at 37 °C in a 5% CO 2 humidified incubator (Thermo Fisher Scientific). .. Sodium oxamate and sodium lactate (MCE; Monmouth Junction, NJ, USA) were dissolved in sterile phosphate-buffered saline (PBS) to prepare 20 mM stock solutions. .. Working concentrations (0.5–20 mM) were prepared fresh daily and filter-sterilized (0.22 μm, Millipore, MA, USA).

    Control:

    Article Title: Histone H3K9 lactylation activates the TXNIP/NLRP3 pathway to drive macrophage inflammation after spinal cord injury
    Article Snippet: .. For treatments, cells were exposed to l -lactate (20 mM) (L6402, sigma), sodium lactate (20 mM) (867-56-1, MCE), 2-deoxy- d -glucose (2-DG, 10 mM) (HY-13966, MCE), Mito-TEMPO (50 μM) (HY-112879, MCE) or PBS (control) for 24 h. .. Intracellular lactate level was measured by using d -lactate, l -lactate, LDH (Elabscience) Colorimetric/Fluorometric assay kit according to manufacturer's protocol.



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    a Representative microscopy images showing hematoxylin and eosin (HE) and Masson’s trichrome staining of kidney biopsy samples from control (Con) and diabetic kidney disease (DKD) model mice (scale bar, 50 μm). HE staining of renal tissue from DKD model mice revealed marked glomerular enlargement and adaptive tubular hypertrophy. Moreover, Masson’s trichrome staining revealed greater fibrosis in the renal tissues of DKD model mice than in those of control mice (data are presented as the mean ± SD; n = 8 per group). b The levels of kidney metabolites in DKD model mice were normalized to those in control mice and are shown in heatmaps, with the color scale indicating relative differences ( n = 5 in the Con group and n = 4 in the DKD group). c Lactate levels were increased in DKD model mice compared with control mice (data are presented as the mean ± SD; n = 8 per group). d Quantitative PCR assays indicated that the mRNA levels of lactate <t>dehydrogenase</t> <t>A</t> <t>(LDHA)</t> were increased in the kidneys of DKD model mice (data are presented as the mean ± SD; n = 8 per group). e Western blotting revealed that the protein levels of H3K18la, H3K27la, and LDHA were increased in the kidneys of DKD model mice; however, H3K9la levels did not change significantly. f Representative images of immunohistochemistry (IHC) staining for LDHA, Kla, H3K18la, and H3K27la in renal biopsy samples from control group and DKD model mice (scale bar, 50 μm). The levels of LDHA, Kla, H3K18la, and H3K27la were increased in the kidneys of DKD model mice (data are presented as the mean ± SD; n = 8 per group). g Western blotting revealed that the protein levels of Kla were increased in the kidneys of DKD model mice. h Double immunofluorescence staining for Kla and histones H1 (H1), H2A, H2B, H3, or H4 verified the strong colocalization of Kla with H3 in the kidneys of DKD model mice, which indicated that histone lactylation modifications predominantly occur on H3 in DKD. i Representative images of HE staining, Masson’s trichrome staining, and IHC staining for LDHA, Kla, H3K18la, and H3K27la in renal biopsy specimens from patients with DKD in the present study (scale bar, 50 μm). HE staining indicated that glomerular sclerosis intensified progressively and that tubulointerstitial lesions transitioned from multifocal to diffuse involvement as the DKD stage progressed. Masson’s trichrome staining revealed an increase in collagen deposition and interstitial fibrosis as the DKD stage progressed. IHC data indicated that LDHA, Kla, H3K18la, and H3K27la levels in renal biopsy samples from patients with DKD gradually increased with increasing DKD stage (data are presented as the mean ± SD; n = 5 per group). DAPI, 4′,6-diamidino-2-phenylindole; ns, not significant. * P < 0.05 and ** P < 0.01.
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    a Representative microscopy images showing hematoxylin and eosin (HE) and Masson’s trichrome staining of kidney biopsy samples from control (Con) and diabetic kidney disease (DKD) model mice (scale bar, 50 μm). HE staining of renal tissue from DKD model mice revealed marked glomerular enlargement and adaptive tubular hypertrophy. Moreover, Masson’s trichrome staining revealed greater fibrosis in the renal tissues of DKD model mice than in those of control mice (data are presented as the mean ± SD; n = 8 per group). b The levels of kidney metabolites in DKD model mice were normalized to those in control mice and are shown in heatmaps, with the color scale indicating relative differences ( n = 5 in the Con group and n = 4 in the DKD group). c Lactate levels were increased in DKD model mice compared with control mice (data are presented as the mean ± SD; n = 8 per group). d Quantitative PCR assays indicated that the mRNA levels of lactate <t>dehydrogenase</t> <t>A</t> <t>(LDHA)</t> were increased in the kidneys of DKD model mice (data are presented as the mean ± SD; n = 8 per group). e Western blotting revealed that the protein levels of H3K18la, H3K27la, and LDHA were increased in the kidneys of DKD model mice; however, H3K9la levels did not change significantly. f Representative images of immunohistochemistry (IHC) staining for LDHA, Kla, H3K18la, and H3K27la in renal biopsy samples from control group and DKD model mice (scale bar, 50 μm). The levels of LDHA, Kla, H3K18la, and H3K27la were increased in the kidneys of DKD model mice (data are presented as the mean ± SD; n = 8 per group). g Western blotting revealed that the protein levels of Kla were increased in the kidneys of DKD model mice. h Double immunofluorescence staining for Kla and histones H1 (H1), H2A, H2B, H3, or H4 verified the strong colocalization of Kla with H3 in the kidneys of DKD model mice, which indicated that histone lactylation modifications predominantly occur on H3 in DKD. i Representative images of HE staining, Masson’s trichrome staining, and IHC staining for LDHA, Kla, H3K18la, and H3K27la in renal biopsy specimens from patients with DKD in the present study (scale bar, 50 μm). HE staining indicated that glomerular sclerosis intensified progressively and that tubulointerstitial lesions transitioned from multifocal to diffuse involvement as the DKD stage progressed. Masson’s trichrome staining revealed an increase in collagen deposition and interstitial fibrosis as the DKD stage progressed. IHC data indicated that LDHA, Kla, H3K18la, and H3K27la levels in renal biopsy samples from patients with DKD gradually increased with increasing DKD stage (data are presented as the mean ± SD; n = 5 per group). DAPI, 4′,6-diamidino-2-phenylindole; ns, not significant. * P < 0.05 and ** P < 0.01.
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    a Representative microscopy images showing hematoxylin and eosin (HE) and Masson’s trichrome staining of kidney biopsy samples from control (Con) and diabetic kidney disease (DKD) model mice (scale bar, 50 μm). HE staining of renal tissue from DKD model mice revealed marked glomerular enlargement and adaptive tubular hypertrophy. Moreover, Masson’s trichrome staining revealed greater fibrosis in the renal tissues of DKD model mice than in those of control mice (data are presented as the mean ± SD; n = 8 per group). b The levels of kidney metabolites in DKD model mice were normalized to those in control mice and are shown in heatmaps, with the color scale indicating relative differences ( n = 5 in the Con group and n = 4 in the DKD group). c Lactate levels were increased in DKD model mice compared with control mice (data are presented as the mean ± SD; n = 8 per group). d Quantitative PCR assays indicated that the mRNA levels of lactate <t>dehydrogenase</t> <t>A</t> <t>(LDHA)</t> were increased in the kidneys of DKD model mice (data are presented as the mean ± SD; n = 8 per group). e Western blotting revealed that the protein levels of H3K18la, H3K27la, and LDHA were increased in the kidneys of DKD model mice; however, H3K9la levels did not change significantly. f Representative images of immunohistochemistry (IHC) staining for LDHA, Kla, H3K18la, and H3K27la in renal biopsy samples from control group and DKD model mice (scale bar, 50 μm). The levels of LDHA, Kla, H3K18la, and H3K27la were increased in the kidneys of DKD model mice (data are presented as the mean ± SD; n = 8 per group). g Western blotting revealed that the protein levels of Kla were increased in the kidneys of DKD model mice. h Double immunofluorescence staining for Kla and histones H1 (H1), H2A, H2B, H3, or H4 verified the strong colocalization of Kla with H3 in the kidneys of DKD model mice, which indicated that histone lactylation modifications predominantly occur on H3 in DKD. i Representative images of HE staining, Masson’s trichrome staining, and IHC staining for LDHA, Kla, H3K18la, and H3K27la in renal biopsy specimens from patients with DKD in the present study (scale bar, 50 μm). HE staining indicated that glomerular sclerosis intensified progressively and that tubulointerstitial lesions transitioned from multifocal to diffuse involvement as the DKD stage progressed. Masson’s trichrome staining revealed an increase in collagen deposition and interstitial fibrosis as the DKD stage progressed. IHC data indicated that LDHA, Kla, H3K18la, and H3K27la levels in renal biopsy samples from patients with DKD gradually increased with increasing DKD stage (data are presented as the mean ± SD; n = 5 per group). DAPI, 4′,6-diamidino-2-phenylindole; ns, not significant. * P < 0.05 and ** P < 0.01.
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    a Representative microscopy images showing hematoxylin and eosin (HE) and Masson’s trichrome staining of kidney biopsy samples from control (Con) and diabetic kidney disease (DKD) model mice (scale bar, 50 μm). HE staining of renal tissue from DKD model mice revealed marked glomerular enlargement and adaptive tubular hypertrophy. Moreover, Masson’s trichrome staining revealed greater fibrosis in the renal tissues of DKD model mice than in those of control mice (data are presented as the mean ± SD; n = 8 per group). b The levels of kidney metabolites in DKD model mice were normalized to those in control mice and are shown in heatmaps, with the color scale indicating relative differences ( n = 5 in the Con group and n = 4 in the DKD group). c Lactate levels were increased in DKD model mice compared with control mice (data are presented as the mean ± SD; n = 8 per group). d Quantitative PCR assays indicated that the mRNA levels of lactate <t>dehydrogenase</t> <t>A</t> <t>(LDHA)</t> were increased in the kidneys of DKD model mice (data are presented as the mean ± SD; n = 8 per group). e Western blotting revealed that the protein levels of H3K18la, H3K27la, and LDHA were increased in the kidneys of DKD model mice; however, H3K9la levels did not change significantly. f Representative images of immunohistochemistry (IHC) staining for LDHA, Kla, H3K18la, and H3K27la in renal biopsy samples from control group and DKD model mice (scale bar, 50 μm). The levels of LDHA, Kla, H3K18la, and H3K27la were increased in the kidneys of DKD model mice (data are presented as the mean ± SD; n = 8 per group). g Western blotting revealed that the protein levels of Kla were increased in the kidneys of DKD model mice. h Double immunofluorescence staining for Kla and histones H1 (H1), H2A, H2B, H3, or H4 verified the strong colocalization of Kla with H3 in the kidneys of DKD model mice, which indicated that histone lactylation modifications predominantly occur on H3 in DKD. i Representative images of HE staining, Masson’s trichrome staining, and IHC staining for LDHA, Kla, H3K18la, and H3K27la in renal biopsy specimens from patients with DKD in the present study (scale bar, 50 μm). HE staining indicated that glomerular sclerosis intensified progressively and that tubulointerstitial lesions transitioned from multifocal to diffuse involvement as the DKD stage progressed. Masson’s trichrome staining revealed an increase in collagen deposition and interstitial fibrosis as the DKD stage progressed. IHC data indicated that LDHA, Kla, H3K18la, and H3K27la levels in renal biopsy samples from patients with DKD gradually increased with increasing DKD stage (data are presented as the mean ± SD; n = 5 per group). DAPI, 4′,6-diamidino-2-phenylindole; ns, not significant. * P < 0.05 and ** P < 0.01.
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    a Representative microscopy images showing hematoxylin and eosin (HE) and Masson’s trichrome staining of kidney biopsy samples from control (Con) and diabetic kidney disease (DKD) model mice (scale bar, 50 μm). HE staining of renal tissue from DKD model mice revealed marked glomerular enlargement and adaptive tubular hypertrophy. Moreover, Masson’s trichrome staining revealed greater fibrosis in the renal tissues of DKD model mice than in those of control mice (data are presented as the mean ± SD; n = 8 per group). b The levels of kidney metabolites in DKD model mice were normalized to those in control mice and are shown in heatmaps, with the color scale indicating relative differences ( n = 5 in the Con group and n = 4 in the DKD group). c Lactate levels were increased in DKD model mice compared with control mice (data are presented as the mean ± SD; n = 8 per group). d Quantitative PCR assays indicated that the mRNA levels of lactate <t>dehydrogenase</t> <t>A</t> <t>(LDHA)</t> were increased in the kidneys of DKD model mice (data are presented as the mean ± SD; n = 8 per group). e Western blotting revealed that the protein levels of H3K18la, H3K27la, and LDHA were increased in the kidneys of DKD model mice; however, H3K9la levels did not change significantly. f Representative images of immunohistochemistry (IHC) staining for LDHA, Kla, H3K18la, and H3K27la in renal biopsy samples from control group and DKD model mice (scale bar, 50 μm). The levels of LDHA, Kla, H3K18la, and H3K27la were increased in the kidneys of DKD model mice (data are presented as the mean ± SD; n = 8 per group). g Western blotting revealed that the protein levels of Kla were increased in the kidneys of DKD model mice. h Double immunofluorescence staining for Kla and histones H1 (H1), H2A, H2B, H3, or H4 verified the strong colocalization of Kla with H3 in the kidneys of DKD model mice, which indicated that histone lactylation modifications predominantly occur on H3 in DKD. i Representative images of HE staining, Masson’s trichrome staining, and IHC staining for LDHA, Kla, H3K18la, and H3K27la in renal biopsy specimens from patients with DKD in the present study (scale bar, 50 μm). HE staining indicated that glomerular sclerosis intensified progressively and that tubulointerstitial lesions transitioned from multifocal to diffuse involvement as the DKD stage progressed. Masson’s trichrome staining revealed an increase in collagen deposition and interstitial fibrosis as the DKD stage progressed. IHC data indicated that LDHA, Kla, H3K18la, and H3K27la levels in renal biopsy samples from patients with DKD gradually increased with increasing DKD stage (data are presented as the mean ± SD; n = 5 per group). DAPI, 4′,6-diamidino-2-phenylindole; ns, not significant. * P < 0.05 and ** P < 0.01.
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    a Representative microscopy images showing hematoxylin and eosin (HE) and Masson’s trichrome staining of kidney biopsy samples from control (Con) and diabetic kidney disease (DKD) model mice (scale bar, 50 μm). HE staining of renal tissue from DKD model mice revealed marked glomerular enlargement and adaptive tubular hypertrophy. Moreover, Masson’s trichrome staining revealed greater fibrosis in the renal tissues of DKD model mice than in those of control mice (data are presented as the mean ± SD; n = 8 per group). b The levels of kidney metabolites in DKD model mice were normalized to those in control mice and are shown in heatmaps, with the color scale indicating relative differences ( n = 5 in the Con group and n = 4 in the DKD group). c Lactate levels were increased in DKD model mice compared with control mice (data are presented as the mean ± SD; n = 8 per group). d Quantitative PCR assays indicated that the mRNA levels of lactate <t>dehydrogenase</t> <t>A</t> <t>(LDHA)</t> were increased in the kidneys of DKD model mice (data are presented as the mean ± SD; n = 8 per group). e Western blotting revealed that the protein levels of H3K18la, H3K27la, and LDHA were increased in the kidneys of DKD model mice; however, H3K9la levels did not change significantly. f Representative images of immunohistochemistry (IHC) staining for LDHA, Kla, H3K18la, and H3K27la in renal biopsy samples from control group and DKD model mice (scale bar, 50 μm). The levels of LDHA, Kla, H3K18la, and H3K27la were increased in the kidneys of DKD model mice (data are presented as the mean ± SD; n = 8 per group). g Western blotting revealed that the protein levels of Kla were increased in the kidneys of DKD model mice. h Double immunofluorescence staining for Kla and histones H1 (H1), H2A, H2B, H3, or H4 verified the strong colocalization of Kla with H3 in the kidneys of DKD model mice, which indicated that histone lactylation modifications predominantly occur on H3 in DKD. i Representative images of HE staining, Masson’s trichrome staining, and IHC staining for LDHA, Kla, H3K18la, and H3K27la in renal biopsy specimens from patients with DKD in the present study (scale bar, 50 μm). HE staining indicated that glomerular sclerosis intensified progressively and that tubulointerstitial lesions transitioned from multifocal to diffuse involvement as the DKD stage progressed. Masson’s trichrome staining revealed an increase in collagen deposition and interstitial fibrosis as the DKD stage progressed. IHC data indicated that LDHA, Kla, H3K18la, and H3K27la levels in renal biopsy samples from patients with DKD gradually increased with increasing DKD stage (data are presented as the mean ± SD; n = 5 per group). DAPI, 4′,6-diamidino-2-phenylindole; ns, not significant. * P < 0.05 and ** P < 0.01.
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    a Representative microscopy images showing hematoxylin and eosin (HE) and Masson’s trichrome staining of kidney biopsy samples from control (Con) and diabetic kidney disease (DKD) model mice (scale bar, 50 μm). HE staining of renal tissue from DKD model mice revealed marked glomerular enlargement and adaptive tubular hypertrophy. Moreover, Masson’s trichrome staining revealed greater fibrosis in the renal tissues of DKD model mice than in those of control mice (data are presented as the mean ± SD; n = 8 per group). b The levels of kidney metabolites in DKD model mice were normalized to those in control mice and are shown in heatmaps, with the color scale indicating relative differences ( n = 5 in the Con group and n = 4 in the DKD group). c Lactate levels were increased in DKD model mice compared with control mice (data are presented as the mean ± SD; n = 8 per group). d Quantitative PCR assays indicated that the mRNA levels of lactate <t>dehydrogenase</t> <t>A</t> <t>(LDHA)</t> were increased in the kidneys of DKD model mice (data are presented as the mean ± SD; n = 8 per group). e Western blotting revealed that the protein levels of H3K18la, H3K27la, and LDHA were increased in the kidneys of DKD model mice; however, H3K9la levels did not change significantly. f Representative images of immunohistochemistry (IHC) staining for LDHA, Kla, H3K18la, and H3K27la in renal biopsy samples from control group and DKD model mice (scale bar, 50 μm). The levels of LDHA, Kla, H3K18la, and H3K27la were increased in the kidneys of DKD model mice (data are presented as the mean ± SD; n = 8 per group). g Western blotting revealed that the protein levels of Kla were increased in the kidneys of DKD model mice. h Double immunofluorescence staining for Kla and histones H1 (H1), H2A, H2B, H3, or H4 verified the strong colocalization of Kla with H3 in the kidneys of DKD model mice, which indicated that histone lactylation modifications predominantly occur on H3 in DKD. i Representative images of HE staining, Masson’s trichrome staining, and IHC staining for LDHA, Kla, H3K18la, and H3K27la in renal biopsy specimens from patients with DKD in the present study (scale bar, 50 μm). HE staining indicated that glomerular sclerosis intensified progressively and that tubulointerstitial lesions transitioned from multifocal to diffuse involvement as the DKD stage progressed. Masson’s trichrome staining revealed an increase in collagen deposition and interstitial fibrosis as the DKD stage progressed. IHC data indicated that LDHA, Kla, H3K18la, and H3K27la levels in renal biopsy samples from patients with DKD gradually increased with increasing DKD stage (data are presented as the mean ± SD; n = 5 per group). DAPI, 4′,6-diamidino-2-phenylindole; ns, not significant. * P < 0.05 and ** P < 0.01.
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    Image Search Results


    a Representative microscopy images showing hematoxylin and eosin (HE) and Masson’s trichrome staining of kidney biopsy samples from control (Con) and diabetic kidney disease (DKD) model mice (scale bar, 50 μm). HE staining of renal tissue from DKD model mice revealed marked glomerular enlargement and adaptive tubular hypertrophy. Moreover, Masson’s trichrome staining revealed greater fibrosis in the renal tissues of DKD model mice than in those of control mice (data are presented as the mean ± SD; n = 8 per group). b The levels of kidney metabolites in DKD model mice were normalized to those in control mice and are shown in heatmaps, with the color scale indicating relative differences ( n = 5 in the Con group and n = 4 in the DKD group). c Lactate levels were increased in DKD model mice compared with control mice (data are presented as the mean ± SD; n = 8 per group). d Quantitative PCR assays indicated that the mRNA levels of lactate dehydrogenase A (LDHA) were increased in the kidneys of DKD model mice (data are presented as the mean ± SD; n = 8 per group). e Western blotting revealed that the protein levels of H3K18la, H3K27la, and LDHA were increased in the kidneys of DKD model mice; however, H3K9la levels did not change significantly. f Representative images of immunohistochemistry (IHC) staining for LDHA, Kla, H3K18la, and H3K27la in renal biopsy samples from control group and DKD model mice (scale bar, 50 μm). The levels of LDHA, Kla, H3K18la, and H3K27la were increased in the kidneys of DKD model mice (data are presented as the mean ± SD; n = 8 per group). g Western blotting revealed that the protein levels of Kla were increased in the kidneys of DKD model mice. h Double immunofluorescence staining for Kla and histones H1 (H1), H2A, H2B, H3, or H4 verified the strong colocalization of Kla with H3 in the kidneys of DKD model mice, which indicated that histone lactylation modifications predominantly occur on H3 in DKD. i Representative images of HE staining, Masson’s trichrome staining, and IHC staining for LDHA, Kla, H3K18la, and H3K27la in renal biopsy specimens from patients with DKD in the present study (scale bar, 50 μm). HE staining indicated that glomerular sclerosis intensified progressively and that tubulointerstitial lesions transitioned from multifocal to diffuse involvement as the DKD stage progressed. Masson’s trichrome staining revealed an increase in collagen deposition and interstitial fibrosis as the DKD stage progressed. IHC data indicated that LDHA, Kla, H3K18la, and H3K27la levels in renal biopsy samples from patients with DKD gradually increased with increasing DKD stage (data are presented as the mean ± SD; n = 5 per group). DAPI, 4′,6-diamidino-2-phenylindole; ns, not significant. * P < 0.05 and ** P < 0.01.

    Journal: Experimental & Molecular Medicine

    Article Title: Keratin 18 functions as a lactyltransferase to trigger necroptosis in diabetic kidney disease by modulating Fas transcription

    doi: 10.1038/s12276-026-01737-9

    Figure Lengend Snippet: a Representative microscopy images showing hematoxylin and eosin (HE) and Masson’s trichrome staining of kidney biopsy samples from control (Con) and diabetic kidney disease (DKD) model mice (scale bar, 50 μm). HE staining of renal tissue from DKD model mice revealed marked glomerular enlargement and adaptive tubular hypertrophy. Moreover, Masson’s trichrome staining revealed greater fibrosis in the renal tissues of DKD model mice than in those of control mice (data are presented as the mean ± SD; n = 8 per group). b The levels of kidney metabolites in DKD model mice were normalized to those in control mice and are shown in heatmaps, with the color scale indicating relative differences ( n = 5 in the Con group and n = 4 in the DKD group). c Lactate levels were increased in DKD model mice compared with control mice (data are presented as the mean ± SD; n = 8 per group). d Quantitative PCR assays indicated that the mRNA levels of lactate dehydrogenase A (LDHA) were increased in the kidneys of DKD model mice (data are presented as the mean ± SD; n = 8 per group). e Western blotting revealed that the protein levels of H3K18la, H3K27la, and LDHA were increased in the kidneys of DKD model mice; however, H3K9la levels did not change significantly. f Representative images of immunohistochemistry (IHC) staining for LDHA, Kla, H3K18la, and H3K27la in renal biopsy samples from control group and DKD model mice (scale bar, 50 μm). The levels of LDHA, Kla, H3K18la, and H3K27la were increased in the kidneys of DKD model mice (data are presented as the mean ± SD; n = 8 per group). g Western blotting revealed that the protein levels of Kla were increased in the kidneys of DKD model mice. h Double immunofluorescence staining for Kla and histones H1 (H1), H2A, H2B, H3, or H4 verified the strong colocalization of Kla with H3 in the kidneys of DKD model mice, which indicated that histone lactylation modifications predominantly occur on H3 in DKD. i Representative images of HE staining, Masson’s trichrome staining, and IHC staining for LDHA, Kla, H3K18la, and H3K27la in renal biopsy specimens from patients with DKD in the present study (scale bar, 50 μm). HE staining indicated that glomerular sclerosis intensified progressively and that tubulointerstitial lesions transitioned from multifocal to diffuse involvement as the DKD stage progressed. Masson’s trichrome staining revealed an increase in collagen deposition and interstitial fibrosis as the DKD stage progressed. IHC data indicated that LDHA, Kla, H3K18la, and H3K27la levels in renal biopsy samples from patients with DKD gradually increased with increasing DKD stage (data are presented as the mean ± SD; n = 5 per group). DAPI, 4′,6-diamidino-2-phenylindole; ns, not significant. * P < 0.05 and ** P < 0.01.

    Article Snippet: The lactate dehydrogenase A (LDHA) inhibitor OXA (HY-W013032A; MCE) was used in the cellular experiments.

    Techniques: Microscopy, Staining, Control, Real-time Polymerase Chain Reaction, Western Blot, Immunohistochemistry, Double Immunofluorescence Staining

    a Oxamate (OXA) treatment decreased lactate accumulation in the renal tissues of diabetic kidney disease (DKD) model mice (data are presented as the mean ± SD; n = 8 per group). b OXA treatment decreased lactate dehydrogenase A (LDHA) mRNA levels in the renal tissues of DKD model mice (data are presented as the mean ± SD; n = 8 per group). c OXA treatment decreased LDHA, H3K18la, and H3K27la levels in the renal tissues of DKD model mice. d OXA treatment reduced lysine lactylation (Kla) levels in the renal tissues of DKD model mice. e Representative images of hematoxylin and eosin (HE) staining, Masson’s trichrome staining and immunohistochemistry staining for LDHA, Kla, H3K18la, and H3K27la in the renal tissues of control (Con), oxamate (OXA), DKD, and DKD + OXA model mice (scale bar, 50 μm). OXA treatment attenuated renal injury and fibrosis and decreased LDHA, Kla, H3K18la, and H3K27la levels in the renal tissues of DKD model mice (data are presented as the mean ± SD; n = 8 per group). f OXA treatment decreased lactate accumulation in hyperglycemic HK-2 cells (data are presented as the mean ± SD; n = 5 per group). g OXA treatment decreased LDHA mRNA levels in hyperglycemic HK-2 cells (data are presented as the mean ± SD; n = 5 per group). h OXA treatment decreased LDHA, H3K18la, and H3K27la levels in hyperglycemic HK-2 cells. i OXA treatment reduced Kla levels in hyperglycemic HK-2 cells. j OXA treatment inhibited the death of hyperglycemic HK-2 cells. HG, high glucose. * P < 0.05 and ** P < 0.01.

    Journal: Experimental & Molecular Medicine

    Article Title: Keratin 18 functions as a lactyltransferase to trigger necroptosis in diabetic kidney disease by modulating Fas transcription

    doi: 10.1038/s12276-026-01737-9

    Figure Lengend Snippet: a Oxamate (OXA) treatment decreased lactate accumulation in the renal tissues of diabetic kidney disease (DKD) model mice (data are presented as the mean ± SD; n = 8 per group). b OXA treatment decreased lactate dehydrogenase A (LDHA) mRNA levels in the renal tissues of DKD model mice (data are presented as the mean ± SD; n = 8 per group). c OXA treatment decreased LDHA, H3K18la, and H3K27la levels in the renal tissues of DKD model mice. d OXA treatment reduced lysine lactylation (Kla) levels in the renal tissues of DKD model mice. e Representative images of hematoxylin and eosin (HE) staining, Masson’s trichrome staining and immunohistochemistry staining for LDHA, Kla, H3K18la, and H3K27la in the renal tissues of control (Con), oxamate (OXA), DKD, and DKD + OXA model mice (scale bar, 50 μm). OXA treatment attenuated renal injury and fibrosis and decreased LDHA, Kla, H3K18la, and H3K27la levels in the renal tissues of DKD model mice (data are presented as the mean ± SD; n = 8 per group). f OXA treatment decreased lactate accumulation in hyperglycemic HK-2 cells (data are presented as the mean ± SD; n = 5 per group). g OXA treatment decreased LDHA mRNA levels in hyperglycemic HK-2 cells (data are presented as the mean ± SD; n = 5 per group). h OXA treatment decreased LDHA, H3K18la, and H3K27la levels in hyperglycemic HK-2 cells. i OXA treatment reduced Kla levels in hyperglycemic HK-2 cells. j OXA treatment inhibited the death of hyperglycemic HK-2 cells. HG, high glucose. * P < 0.05 and ** P < 0.01.

    Article Snippet: The lactate dehydrogenase A (LDHA) inhibitor OXA (HY-W013032A; MCE) was used in the cellular experiments.

    Techniques: Staining, Immunohistochemistry, Control