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Santa Cruz Biotechnology sirna products
Sirna Products, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 96/100, based on 668 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/nrf2+sirna/Nrf2+siRNA/us12560609-327-24-34
Average 96 stars, based on 668 article reviews

sirna products - by Bioz Stars, 2026-09

96/100 stars

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Negative Control:

Article Title: Drynachromoside A from Drynaria fortunei attenuates oxidative stress and fibrosis of diabetic nephropathy via activating Nrf2 in vitro and in vivo
Article Snippet: ML385 (Cat. no. MB2620), a Nrf2 inhibitor, was obtained from Meilun Biotechnology (Dalian, China). .. Negative control siRNA (NC-siRNA) (Cat. no. sc-37007) and Nrf2-siRNA (Cat. no. sc-37030) together with protein A-agarose (Cat. no. sc-2001) were supplied by Santa Cruz Biotechnology (Dallas, TX, USA). ..

Article Title: Drynachromoside A from Drynaria fortunei attenuates oxidative stress and fibrosis of diabetic nephropathy via activating Nrf2 in vitro and in vivo .
Article Snippet: ML385 (Cat. no. MB2620), a Nrf2 inhibitor, was obtained from Meilun Biotechnology (Dalian, China). .. Negative control siRNA (NCsiRNA) (Cat. no. sc-37007) and Nrf2-siRNA (Cat. no. sc-37030) together with protein A-agarose (Cat. no. sc2001) were supplied by Santa Cruz Biotechnology (Dallas, TX, USA). ..

Transfection:

Article Title: Citrinin delays muscle aging and extends lifespan in C. elegans and prevents senescence in C2C12 through SKN-1/Nrf2 activation.
Article Snippet: Sarcopenia, a condition characterized by the loss of muscle mass and function with aging, is linked to various health issues including diabetes and increased risk of falls and fractures.. Currently, there is no FDA-approved treatment exists for sarcopenia.. Citrinin, a natural compound present in daily dietary sources such as grains, has not been well characterized for its biological effects on muscle aging.

Article Title: Targeting of a novel interplay between MET tyrosine kinase and NRF2 enhances sensitivity to Paclitaxel in triple negative breast cancer
Article Snippet: .. For transient silencing of MET expression (MGT-13 and BT-549) and NRF2 expression (MGT-13), cells were seeded the day before and transfected for 24 h with LipofectamineTM RNAiMAX Transfection Reagent (Invitrogen) by using murine and human MET siRNA (Santa Cruz Biotechnology; sc-35924, sc-29397) or NRF2 siRNA (Santa Cruz Biotechnology; sc-37049) according to the manufacturer’s instructions. .. For transient transfection, MGT-13 cells were seeded the day before and transfected for 24 h with LipofectamineTM 2000 Transfection Reagent (Invitrogen) by using empty pSGT, SRC Y527F and SRC K295M vectors according to the manufacturer’s instructions as previously described [ ].

Article Title: Dietary Quercetin-3-Glucuronide Mitigates Oxidative Stress, Inflammation, and Fibroblast Transition by Regulating Nrf2 and Autophagy in Pulmonary Fibrosis.
Article Snippet: Transient transfection was performed as previously described16 using the TransIT-X2 Dynamic Delivery System (Mirus Bio LLC, Madison, WI), a polymer-based transfection reagent. .. MRC-5 cells were transfected with Nrf2 siRNA (sc-37030), purchased from Santa Cruz Biotechnology (Santa Cruz, CA), in serum-free medium containing TransIT-X2 reagent for 12 h. Following transfection, the medium was replaced with complete medium containing double the concentration of FBS (20%), and cells were incubated for an additional 24 h. 2.3.4. ..

Article Title: CO-PERK-IRG1 axis attenuates oxidative stress and ferroptosis in hepatic ischemia-reperfusion injury.
Article Snippet: Hepatic ischemia-reperfusion injury (IRI) can arise as the consequence of surgical procedures, including liver transplant.. Hepatic IRI is characterized by oxidative stress, inflammation, and activation of multiple regulated cell death pathways (RCD).. Among RCD, ferroptosis is driven by enhanced lipid peroxidation and reactive oxygen species (ROS) formation.

Article Title: Targeting of a novel interplay between MET tyrosine kinase and NRF2 enhances sensitivity to Paclitaxel in triple negative breast cancer.
Article Snippet: .. For transient silencing of MET expression (MGT-13 and BT-549), and NRF2 expression (MGT-13), cells were seeded the day before and transfected for 24h with LipofectamineTM RNAiMAX Transfection Reagent (Invitrogen) by using murine and human MET siRNA (Santa Cruz Biotechnology; sc-35924, sc-29397) or NRF2 siRNA (Santa Cruz Biotechnology; sc-37049) according to the manufacturer’s instructions. .. For transient transfection, MGT-13 cells were seeded the day before and transfected for 24h with LipofectamineTM 2000 Transfection Reagent (Invitrogen) by using empty pSGT, SRCY527F and SRCK295M vectors according to the manufacturer’s instructions as previously described (30).

Article Title: Pharmacological inhibition of STING-mediated GPX4 autophagic degradation by 4-octyl itaconate ameliorates sepsis-induced acute kidney injury.
Article Snippet: Extended author information available on the last page of the article Abstract The precise pathogenic mechanisms underlying sepsis-induced acute kidney injury (AKI) remain elusive.. Emerging evidence suggests a link between tubular ferroptosis and the pathogenesis of AKI, though the regulatory pathways are not fully understood.. Stimulator of interferon genes (STING), previously recognized as a pivotal mediator of innate immunity via DNA-sensing pathways, is increasingly associated with lipid peroxidation, a hallmark of ferroptosis, and 4-octyl itaconate (4-OI) has been shown to inhibit STING activation, exerting anti-inflammatory effects.

Expressing:

Concentration Assay:

Incubation:

Knockdown:

Control:

Image Search Results

Regulation of lipid peroxidation is extrinsically regulated by the SLC7A11 pathway in CD4 + T cells (A) Statistical analysis of SLC7A11 protein expression assessed by flow cytometry (shown as mean fluorescent intensity (MFI). CD4 + T cells were either left unstimulated (control) or measured at a distinct time point after stimulation with anti-CD3/CD28 antibodies. N = 3, 3 independently performed experiments, a one-way ANOVA multiple comparison test was performed. The calculated power of this experiment is 0.84. (B) ΔCT of SLC7A11 mRNA expression in human CD4 + T cells with and without anti-CD3/CD28 stimulation. N = 13, 4 independently performed experiments. (C) Gene expression in CD4 + T cells from WT and VAV cre Keap fl/fl (Keap1-KO) mice was assessed by microarray analysis. Colors indicate significant upregulation (red), or downregulation (green) compared to WT. (D) ΔCT of SLC7A11 mRNA expression in CD4 + T cells of WT and Keap1-KO mice, either left unstimulated or stimulated with anti-CD3/CD28 antibodies, 4 independently performed experiments. The calculated power of this experiment is 0.99 for the stimulated and unstimulated groups. (E) N-fold SLC7A11 expression in human CD4 T cells, either transfected with a control siRNA (Ctrl) or NRF2 siRNA. 3 independently performed experiments were performed. (F) N-fold SLC7A11 mRNA expression in human CD4 T cells treated with 4-OI or vehicle (Ctrl) N = 6, 4 independently performed experiments. A paired Student's t-test was performed comparing the groups of B–F. Data are presented as mean, error bars present ± SEM for all the presented graphs in this figure. Values were considered significant if ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001. N represents the number of biological replicates.

Journal: iScience

Article Title: Inflammatory CD4 + T cells can waive NRF2-dependent SLC7A11-mediated cystine uptake by using ASCT1

doi: 10.1016/j.isci.2026.115680

Figure Lengend Snippet: Regulation of lipid peroxidation is extrinsically regulated by the SLC7A11 pathway in CD4 + T cells (A) Statistical analysis of SLC7A11 protein expression assessed by flow cytometry (shown as mean fluorescent intensity (MFI). CD4 + T cells were either left unstimulated (control) or measured at a distinct time point after stimulation with anti-CD3/CD28 antibodies. N = 3, 3 independently performed experiments, a one-way ANOVA multiple comparison test was performed. The calculated power of this experiment is 0.84. (B) ΔCT of SLC7A11 mRNA expression in human CD4 + T cells with and without anti-CD3/CD28 stimulation. N = 13, 4 independently performed experiments. (C) Gene expression in CD4 + T cells from WT and VAV cre Keap fl/fl (Keap1-KO) mice was assessed by microarray analysis. Colors indicate significant upregulation (red), or downregulation (green) compared to WT. (D) ΔCT of SLC7A11 mRNA expression in CD4 + T cells of WT and Keap1-KO mice, either left unstimulated or stimulated with anti-CD3/CD28 antibodies, 4 independently performed experiments. The calculated power of this experiment is 0.99 for the stimulated and unstimulated groups. (E) N-fold SLC7A11 expression in human CD4 T cells, either transfected with a control siRNA (Ctrl) or NRF2 siRNA. 3 independently performed experiments were performed. (F) N-fold SLC7A11 mRNA expression in human CD4 T cells treated with 4-OI or vehicle (Ctrl) N = 6, 4 independently performed experiments. A paired Student's t-test was performed comparing the groups of B–F. Data are presented as mean, error bars present ± SEM for all the presented graphs in this figure. Values were considered significant if ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001. N represents the number of biological replicates.

Article Snippet: To this, 10 nM NRF2 siRNA (OriGene, Germany; catalogue number SR321100) or a control was added, and transfection was performed according to the manufacturer’s instructions (Neon transfection, ThermoFisher Scientific; MPK10025).

Techniques: Expressing, Flow Cytometry, Control, Comparison, Gene Expression, Microarray, Transfection

SAS and erastin treatment reduce cystine uptake but not GSH content and cell viability in anti-CD3/CD28 stimulated CD4 + T cells (A) Flow cytometric analysis of cystine uptake measured by BioTracker Cystine-FITC in stimulated CD4 + T cells in the presence of SAS and erastin. Exemplary histogram, showing the cystine uptake after 0 min (blue) and after 30 min (red) of incubation, while the difference presented as ΔMFI was used to describe the cystine uptake. N = 4, 3 independently performed experiments. The calculated power of this experiment is 0.99. (B) Statistical analysis of cystine uptake (represented as MFI) of mouse WT and NRF2-KO CD4 + T cells with and without the addition of SAS and erastin. N = 6, 4 independently performed experiments. (C) Representative histograms of B showing the uptake after 0 min (blue) and 30 min (red), while the difference presented as ΔMFI was used to describe the cystine uptake. (D) Flow cytometric analysis of reactive oxygen species (ROS) (presented as MFI) of CD4 + T cells without and with the addition of SAS and erastin. Histograms of the measurements are shown on the right. The calculated power of this experiment is 0.986. (E) Flow cytometric analysis of intracellular GSH content (presented as ΔMFI) of CD4 + T cells with and without SAS and erastin. Histograms depict an overlay of the FMO (blue) and the GSH staining (red). GSH was determined by the GSH/GSSG Luminescence measurement of CD4 MACS HC PBMCs. The kit provides direct analysis of the supernatants' GSH and GSSG contents, which enables the calculation of the ratios. (F) Lipoperoxidation measurement using BODIPY 581/591 C11 (presented as MFI of the FITC signal) of CD4 + T cells without and with inhibition by SAS and erastin. Histograms of the two signals, i.e., PE and FITC, from BODIPY are shown on the right. The calculated power of this experiment is 0.94. (G) Flow cytometric analysis of Mitotracker (represented as MFI, mitochondrial mass) of CD4 + T cells and TMRM (represented by MFI, mitochondrial membrane potential) of Mitotracker positive cells is shown without and with the addition of SAS and erastin. The calculated power of this experiment is 0.99 for the mitochondrial mass and 1 for the mitochondrial membrane potential. (H) Fluorescent live/dead staining was evaluated by flow cytometry using the combinatory staining of Annexin V and fixable viability dye (FVD) without and with the addition of SAS and erastin. N = 3, 3 independent experiments were performed for the graphs (D) to (G). The statistical evaluation of all the represented graphs was performed using one-way ANOVA multiple comparison. (Data are presented as mean, error bars present ± SEM for all the presented graphs in this figure. Values were considered significant if ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001. N represents the number of biological replicates.

Journal: iScience

Article Title: Inflammatory CD4 + T cells can waive NRF2-dependent SLC7A11-mediated cystine uptake by using ASCT1

doi: 10.1016/j.isci.2026.115680

Figure Lengend Snippet: SAS and erastin treatment reduce cystine uptake but not GSH content and cell viability in anti-CD3/CD28 stimulated CD4 + T cells (A) Flow cytometric analysis of cystine uptake measured by BioTracker Cystine-FITC in stimulated CD4 + T cells in the presence of SAS and erastin. Exemplary histogram, showing the cystine uptake after 0 min (blue) and after 30 min (red) of incubation, while the difference presented as ΔMFI was used to describe the cystine uptake. N = 4, 3 independently performed experiments. The calculated power of this experiment is 0.99. (B) Statistical analysis of cystine uptake (represented as MFI) of mouse WT and NRF2-KO CD4 + T cells with and without the addition of SAS and erastin. N = 6, 4 independently performed experiments. (C) Representative histograms of B showing the uptake after 0 min (blue) and 30 min (red), while the difference presented as ΔMFI was used to describe the cystine uptake. (D) Flow cytometric analysis of reactive oxygen species (ROS) (presented as MFI) of CD4 + T cells without and with the addition of SAS and erastin. Histograms of the measurements are shown on the right. The calculated power of this experiment is 0.986. (E) Flow cytometric analysis of intracellular GSH content (presented as ΔMFI) of CD4 + T cells with and without SAS and erastin. Histograms depict an overlay of the FMO (blue) and the GSH staining (red). GSH was determined by the GSH/GSSG Luminescence measurement of CD4 MACS HC PBMCs. The kit provides direct analysis of the supernatants' GSH and GSSG contents, which enables the calculation of the ratios. (F) Lipoperoxidation measurement using BODIPY 581/591 C11 (presented as MFI of the FITC signal) of CD4 + T cells without and with inhibition by SAS and erastin. Histograms of the two signals, i.e., PE and FITC, from BODIPY are shown on the right. The calculated power of this experiment is 0.94. (G) Flow cytometric analysis of Mitotracker (represented as MFI, mitochondrial mass) of CD4 + T cells and TMRM (represented by MFI, mitochondrial membrane potential) of Mitotracker positive cells is shown without and with the addition of SAS and erastin. The calculated power of this experiment is 0.99 for the mitochondrial mass and 1 for the mitochondrial membrane potential. (H) Fluorescent live/dead staining was evaluated by flow cytometry using the combinatory staining of Annexin V and fixable viability dye (FVD) without and with the addition of SAS and erastin. N = 3, 3 independent experiments were performed for the graphs (D) to (G). The statistical evaluation of all the represented graphs was performed using one-way ANOVA multiple comparison. (Data are presented as mean, error bars present ± SEM for all the presented graphs in this figure. Values were considered significant if ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001. N represents the number of biological replicates.

Techniques: Incubation, Staining, Inhibition, Membrane, Flow Cytometry, Comparison

Characterization of an altered NRF2/cystine pathway in patients with JIA (A) Flow cytometric analysis of SLC7A11 expression in stimulated SF and PB CD4 + T cells. Statistical analysis was performed with N = 7 donors, 7 independently performed experiments. (B) Flow cytometric evaluation of cystine uptake (shown as MFI) by anti-CD3/CD28 stimulated CD4 + SF T cells. N = 6, 6 independently performed experiments. (C) Flow cytometric analysis of intracellular glutathione content (presented as ΔMFI) of stimulated SF and PB CD4 + T cells. N = 9, 9 independently performed experiments. (D) Statistical analysis of MFI of ROS in stimulated SF and PB CD4 + T cells ( N = 4), 4 independently performed experiments. The calculated power of this experiment is 0.85. (E) Lipid peroxidation as assessed by flow cytometric measurement of anti-CD3/CD28 stimulated CD4 + T cells derived from PBMCs and SFMCs. N = 11. (F) Gene set enrichment analysis (GSEA) was performed on differentially expressed genes from SF-derived CD4 + T cells of patients with active JIA compared to PBMC-derived CD4 + T cells from healthy controls. The enrichment plots shown represent driver ferroptosis-related gene sets from KEGG, WikiPathways, and FerrDb V2. ( N = 4). (G) Heat maps showing normalized counts of selected RNAs determined by RNA-seq in JIA CD4 + T cells compared to HC CD4 + T cells. N = 4 in each group. (H) SFMCs and PBMCs were analyzed for ASCT1 expression by quantitative RT-PCR. The calculated power of this experiment is 0.99. (I) Flow cytometric analysis of CD36 expression of stimulated SF and PB CD4 + T cells. N = 5, 5 independently performed experiments. (J) Representative histograms showing BODIPY Ferroptosis staining of anti-CD3/CD28 stimulated HC PBMCs in the absence and presence of ASCT1/2 inhibition by 4-Hydroxy-L-phenylglycin (HPG) and SAS. N = 3, 3 independent experiments. The statistical evaluation of (A), (C), (E), (H), and (I) from the represented graphs was performed using a paired Student’s t-test. One-way ANOVA multiple comparison was used for (B) and (D) of the represented graphs. Data are presented as mean, error bars present ± SEM for all the presented graphs in this figure. Values were considered significant if ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001. N represents the number of biological replicates.

Journal: iScience

Article Title: Inflammatory CD4 + T cells can waive NRF2-dependent SLC7A11-mediated cystine uptake by using ASCT1

doi: 10.1016/j.isci.2026.115680

Figure Lengend Snippet: Characterization of an altered NRF2/cystine pathway in patients with JIA (A) Flow cytometric analysis of SLC7A11 expression in stimulated SF and PB CD4 + T cells. Statistical analysis was performed with N = 7 donors, 7 independently performed experiments. (B) Flow cytometric evaluation of cystine uptake (shown as MFI) by anti-CD3/CD28 stimulated CD4 + SF T cells. N = 6, 6 independently performed experiments. (C) Flow cytometric analysis of intracellular glutathione content (presented as ΔMFI) of stimulated SF and PB CD4 + T cells. N = 9, 9 independently performed experiments. (D) Statistical analysis of MFI of ROS in stimulated SF and PB CD4 + T cells ( N = 4), 4 independently performed experiments. The calculated power of this experiment is 0.85. (E) Lipid peroxidation as assessed by flow cytometric measurement of anti-CD3/CD28 stimulated CD4 + T cells derived from PBMCs and SFMCs. N = 11. (F) Gene set enrichment analysis (GSEA) was performed on differentially expressed genes from SF-derived CD4 + T cells of patients with active JIA compared to PBMC-derived CD4 + T cells from healthy controls. The enrichment plots shown represent driver ferroptosis-related gene sets from KEGG, WikiPathways, and FerrDb V2. ( N = 4). (G) Heat maps showing normalized counts of selected RNAs determined by RNA-seq in JIA CD4 + T cells compared to HC CD4 + T cells. N = 4 in each group. (H) SFMCs and PBMCs were analyzed for ASCT1 expression by quantitative RT-PCR. The calculated power of this experiment is 0.99. (I) Flow cytometric analysis of CD36 expression of stimulated SF and PB CD4 + T cells. N = 5, 5 independently performed experiments. (J) Representative histograms showing BODIPY Ferroptosis staining of anti-CD3/CD28 stimulated HC PBMCs in the absence and presence of ASCT1/2 inhibition by 4-Hydroxy-L-phenylglycin (HPG) and SAS. N = 3, 3 independent experiments. The statistical evaluation of (A), (C), (E), (H), and (I) from the represented graphs was performed using a paired Student’s t-test. One-way ANOVA multiple comparison was used for (B) and (D) of the represented graphs. Data are presented as mean, error bars present ± SEM for all the presented graphs in this figure. Values were considered significant if ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001. N represents the number of biological replicates.

Techniques: Expressing, Derivative Assay, RNA Sequencing, Quantitative RT-PCR, Staining, Inhibition, Comparison

Carnosic acid inhibits activation of the Nrf2/NF-kB axis. (A–D) Following stimulation with LPS and carnosic acid, the protein levels of Nrf2, HO-1, p-p65 NF-kB and p65 NF-kB in macrophages were analyzed by western. The corresponding bands were quantified by Image J software. (E) The protein levels of nuclear Nrf2 and p65 in cells under LPS and carnosic acid conditions. *** P < 0.001 vs. control group, ### P < 0.001 vs. LPS groups.

Journal: Frontiers in Immunology

Article Title: Administration with carnosic acid alleviates the development of osteoarthritis by attenuating macrophage polarization-mediated inflammation and cartilage oxidative damage and degradation via regulating Nrf2/NF-kB axis

doi: 10.3389/fimmu.2026.1710302

Figure Lengend Snippet: Carnosic acid inhibits activation of the Nrf2/NF-kB axis. (A–D) Following stimulation with LPS and carnosic acid, the protein levels of Nrf2, HO-1, p-p65 NF-kB and p65 NF-kB in macrophages were analyzed by western. The corresponding bands were quantified by Image J software. (E) The protein levels of nuclear Nrf2 and p65 in cells under LPS and carnosic acid conditions. *** P < 0.001 vs. control group, ### P < 0.001 vs. LPS groups.

Article Snippet: The siRNA sequences targeting Nrf2 (cat. sc-37049) and si-NC (cat. sc- 37007) were synthesized from Santa Cruz Biotechnology, Inc. (Santa Cruz, CA, USA).

Techniques: Activation Assay, Western Blot, Software, Control

The Nrf2/NF-kB axis is responsible for carnosic acid-mediated chondroprotective efficacy from macrophage M1 polarization condition. (A) After transfection with si-Nrf2, the mRNA levels of Nrf2 were determined by qRT-PCR. (B) The effects of si-Nrf2 transfection on the activation of the Nrf2/NF-kB axis in macrophages. (C–E) Macrophages were transfected with si-Nrf2 under LPS and carnosic acid conditions. Then, the % of CD86 + M1 macrophages (C) , mRNA levels of CD86, iNOS, (D) and IL-1β (E) were assessed. (F–L) After incubation with CM from macrophages under si-Nrf2, LPS and carnosic acid conditions, the viability (F) and apoptosis (G) of chondrocytes were detected. Then, the levels of ROS (H) , SOD (I) , IL-6 and TNF-α (J) , mRNA expression of aggrecan, collagen II (K) , levels of MMPs (L) were further determined. *** P < 0.001 vs. control group, ### P < 0.001 vs. LPS groups, ☆☆ P < 0.01, ☆☆☆ P < 0.001 vs. LPS and CA groups.

Journal: Frontiers in Immunology

doi: 10.3389/fimmu.2026.1710302

Figure Lengend Snippet: The Nrf2/NF-kB axis is responsible for carnosic acid-mediated chondroprotective efficacy from macrophage M1 polarization condition. (A) After transfection with si-Nrf2, the mRNA levels of Nrf2 were determined by qRT-PCR. (B) The effects of si-Nrf2 transfection on the activation of the Nrf2/NF-kB axis in macrophages. (C–E) Macrophages were transfected with si-Nrf2 under LPS and carnosic acid conditions. Then, the % of CD86 + M1 macrophages (C) , mRNA levels of CD86, iNOS, (D) and IL-1β (E) were assessed. (F–L) After incubation with CM from macrophages under si-Nrf2, LPS and carnosic acid conditions, the viability (F) and apoptosis (G) of chondrocytes were detected. Then, the levels of ROS (H) , SOD (I) , IL-6 and TNF-α (J) , mRNA expression of aggrecan, collagen II (K) , levels of MMPs (L) were further determined. *** P < 0.001 vs. control group, ### P < 0.001 vs. LPS groups, ☆☆ P < 0.01, ☆☆☆ P < 0.001 vs. LPS and CA groups.

Article Snippet: The siRNA sequences targeting Nrf2 (cat. sc-37049) and si-NC (cat. sc- 37007) were synthesized from Santa Cruz Biotechnology, Inc. (Santa Cruz, CA, USA).

Techniques: Transfection, Quantitative RT-PCR, Activation Assay, Incubation, Expressing, Control

Carnosic acid suppresses macrophage M1-like polarization, inflammation and Nrf2/NF-kB axis in OA mice. (A, B) OA mice were administrated with the indicated concentration with carnosic acid. Eight weeks later, the % of CD86 + F4/80 + M1 macrophages (A) and CD206 + F4/80 + M2 macrophages in synovium were analyzed by flow cytometry. (C–E) The effects on cytokine levels of IL-6 (C) , TNF-α (D) , IL-1β (E) were analyzed. (F, G) The activation of Nrf2/NF-kB axis was detected in articular cartilage tissues. *** P < 0.001 vs. sham group. ## P < 0.01, ### P < 0.001 vs. OA groups.

Journal: Frontiers in Immunology

doi: 10.3389/fimmu.2026.1710302

Figure Lengend Snippet: Carnosic acid suppresses macrophage M1-like polarization, inflammation and Nrf2/NF-kB axis in OA mice. (A, B) OA mice were administrated with the indicated concentration with carnosic acid. Eight weeks later, the % of CD86 + F4/80 + M1 macrophages (A) and CD206 + F4/80 + M2 macrophages in synovium were analyzed by flow cytometry. (C–E) The effects on cytokine levels of IL-6 (C) , TNF-α (D) , IL-1β (E) were analyzed. (F, G) The activation of Nrf2/NF-kB axis was detected in articular cartilage tissues. *** P < 0.001 vs. sham group. ## P < 0.01, ### P < 0.001 vs. OA groups.

Article Snippet: The siRNA sequences targeting Nrf2 (cat. sc-37049) and si-NC (cat. sc- 37007) were synthesized from Santa Cruz Biotechnology, Inc. (Santa Cruz, CA, USA).

Techniques: Concentration Assay, Flow Cytometry, Activation Assay

ALA promotes CMA via facilitating NRF2 expression in HGHF-induced cells. ( A ) In NCTC 1469 cells, ALA restored NRF2 expression that was has been by HGHF treatment. ( B ) siRNA-NRF2-668 markedly downregulated NRF2 mRNA expression. ( C , D ) Protein expression of NRF2 after transfection. ( D – H ) NRF2 knockdown reduced LAMP2A and HSC70 levels while elevating PLIN2 expression in cells treated with HGHF and ALA. * p < 0.05.

Journal: Nutrients

Article Title: α-Lipoic Acid Alleviates Non-Alcoholic Fatty Liver Disease by Elevating Chaperone-Mediated Autophagy and Increasing β-Oxidation via AMPK-TFEB Axis

doi: 10.3390/nu18030402

Figure Lengend Snippet: ALA promotes CMA via facilitating NRF2 expression in HGHF-induced cells. ( A ) In NCTC 1469 cells, ALA restored NRF2 expression that was has been by HGHF treatment. ( B ) siRNA-NRF2-668 markedly downregulated NRF2 mRNA expression. ( C , D ) Protein expression of NRF2 after transfection. ( D – H ) NRF2 knockdown reduced LAMP2A and HSC70 levels while elevating PLIN2 expression in cells treated with HGHF and ALA. * p < 0.05.

Article Snippet: SiRNAs targeting mouse NRF2 (siRNA-334: sense, GGAUGAAGAAACAGGAGAATT, and antisense, UUCUCCUGUUUCUUCAUCCTT; siRNA-668: sense, GAAUUACAGUGUCUUAAUATT, and antisense, UAUUAAGACACUGUAAUUCTT; siRNA-1720: sense, CGACAGAAACCUCCAUCUATT, an-d antisense, UAGAUGGAGGUUUCUGUCGTT) and non-targeting control siRNA were obtained from Sangon Biotech.

Techniques: Expressing, Transfection, Knockdown

ALA promotes TFEB, NRF2, and CMA in HGHF-induced cells via activating AMPK (Thr172) phosphorylation. ( A ) ALA restored AMPK phosphorylation levels that had been reduced by HGHF treatment. ( B ) Impact of varying CpdC concentrations on AMPK phosphorylation in cells. ( C – H ) CpdC reversed the effect of ALA on induction in the HGHF group. * p < 0.05.

Journal: Nutrients

Article Title: α-Lipoic Acid Alleviates Non-Alcoholic Fatty Liver Disease by Elevating Chaperone-Mediated Autophagy and Increasing β-Oxidation via AMPK-TFEB Axis

doi: 10.3390/nu18030402

Figure Lengend Snippet: ALA promotes TFEB, NRF2, and CMA in HGHF-induced cells via activating AMPK (Thr172) phosphorylation. ( A ) ALA restored AMPK phosphorylation levels that had been reduced by HGHF treatment. ( B ) Impact of varying CpdC concentrations on AMPK phosphorylation in cells. ( C – H ) CpdC reversed the effect of ALA on induction in the HGHF group. * p < 0.05.

Techniques: Phospho-proteomics

ALA raises CMA activity via activating the AMPK-TFEB/NRF2 axis in cells. ( A – F ) Representative images showing mCherry fluorescent puncta for each treatment group (scale bar = 20 μm). * p < 0.05.

Journal: Nutrients

Article Title: α-Lipoic Acid Alleviates Non-Alcoholic Fatty Liver Disease by Elevating Chaperone-Mediated Autophagy and Increasing β-Oxidation via AMPK-TFEB Axis

doi: 10.3390/nu18030402

Figure Lengend Snippet: ALA raises CMA activity via activating the AMPK-TFEB/NRF2 axis in cells. ( A – F ) Representative images showing mCherry fluorescent puncta for each treatment group (scale bar = 20 μm). * p < 0.05.

Techniques: Activity Assay

ALA improves AMPK-TFEB/NRF2 axis-mediated CMA, β-oxidation, and antioxidant levels in HFD mice. ( A ) Effects of HFD and ALA treatment on relevant proteins in AMPK-TFEB/NRF2. Quantitative analysis of p -AMPK ( B ), TFEB, NRF2 ( C , D ) PGC1α, PPARα ( E , F ) and LAMP2A, HSC70, and PLIN2 ( G – I ). Quantitative analysis results. * p < 0.05.

Journal: Nutrients

Article Title: α-Lipoic Acid Alleviates Non-Alcoholic Fatty Liver Disease by Elevating Chaperone-Mediated Autophagy and Increasing β-Oxidation via AMPK-TFEB Axis

doi: 10.3390/nu18030402

Figure Lengend Snippet: ALA improves AMPK-TFEB/NRF2 axis-mediated CMA, β-oxidation, and antioxidant levels in HFD mice. ( A ) Effects of HFD and ALA treatment on relevant proteins in AMPK-TFEB/NRF2. Quantitative analysis of p -AMPK ( B ), TFEB, NRF2 ( C , D ) PGC1α, PPARα ( E , F ) and LAMP2A, HSC70, and PLIN2 ( G – I ). Quantitative analysis results. * p < 0.05.

Techniques:

A schematic diagram showing that ALA alleviates NAFLD by modulating AMPK-TFEB/NRF2 mediated activation of β-oxidation and CMA and oxidative stress suppression.

Journal: Nutrients

Article Title: α-Lipoic Acid Alleviates Non-Alcoholic Fatty Liver Disease by Elevating Chaperone-Mediated Autophagy and Increasing β-Oxidation via AMPK-TFEB Axis

doi: 10.3390/nu18030402

Figure Lengend Snippet: A schematic diagram showing that ALA alleviates NAFLD by modulating AMPK-TFEB/NRF2 mediated activation of β-oxidation and CMA and oxidative stress suppression.

Techniques: Activation Assay

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sirna products (Santa Cruz Biotechnology)

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