Journal: Immunology letters

Article Title: A lack of confirmation with alternative assays questions the validity of IL-17A expression in human neutrophils using immunohistochemistry.

doi: 10.1016/j.imlet.2014.10.025

Figure Lengend Snippet: Fig. 1. Detection of IL-17A in human neutrophils by IHC. (A) Cyanine3 labelled IL-17A+ cells infiltrate Wolbachia-containing nodules but not Wolbachia-depleted nodules. (B) Counterstaining

Article Snippet: Immunoprecipitation was carried out using 100 g mouse anti-human IL-17A antibody (41802, R&D Systems) and 60 g goat anti-human IL-17A antibody (AF-317-NA, R&D Systems) coupled to 1 mL HiTrap NHS-activated HP columns and AKTAprime Plus low-pressure affinity chromatography system (both from GE Healthcare) using the manufacturer’s protocol.

Techniques:

Journal: Immunology letters

Article Title: A lack of confirmation with alternative assays questions the validity of IL-17A expression in human neutrophils using immunohistochemistry.

doi: 10.1016/j.imlet.2014.10.025

Figure Lengend Snippet: Fig. 2. Determination of IL-17A expression by human neutrophils. (A) Western blotting of neutrophil (PMN) cell lysate using goat anti-IL-17A antibody and mouse anti- IL-17A antibody.

Article Snippet: Immunoprecipitation was carried out using 100 g mouse anti-human IL-17A antibody (41802, R&D Systems) and 60 g goat anti-human IL-17A antibody (AF-317-NA, R&D Systems) coupled to 1 mL HiTrap NHS-activated HP columns and AKTAprime Plus low-pressure affinity chromatography system (both from GE Healthcare) using the manufacturer’s protocol.

Techniques: Expressing, Western Blot

Journal: Chinese Medicine

Article Title: Sodium tanshinone IIA sulfonate alleviates osteoarthritis through targeting SIRT1

doi: 10.1186/s13020-025-01166-2

Figure Lengend Snippet: STS promoted SIRT1-mediated deacetylation of NF-κB p65, thereby inhibiting inflammation and ferroptosis in chondrocytes. A The nuclear protein levels of SIRT1, NF-κB p65, and acetylated NF-κB p65 (Lys310) immunoprecipitated from primary chondrocytes treated with or without STS. Right: Quantification of these proteins (n = 6/group). B The nuclear protein levels of SIRT1, NF-κB p65, and acetylated NF-κB p65 (Lys310) immunoprecipitated from primary chondrocytes treated with EX-527 and/or STS. Right: Quantification of these proteins (n = 6/group). C The nuclear protein levels of acetylated NF-κB p65 (Lys310) immunoprecipitated from primary chondrocytes treated with SRT2104 and/or STS. D Quantification of these proteins in group C (n = 6/group). E The protein levels of P300, SIRT1, NF-κB p65, and acetylated NF-κB p65 (Lys310) immunoprecipitated from primary chondrocytes treated with NF-κB p65 plasmid/ NF-κB p65 (K310R) plasmid and/or STS. Right: Quantification of these proteins (n = 6/group). F The relative mRNA expression of TNF-α, IL-6, and IL-17A in primary chondrocytes treated with EX-527 and/or STS (n = 6/group). G The relative mRNA expression of TNF-α, IL-6, and IL-17A in primary chondrocytes treated with SRT2104 and/or STS (n = 6/group). H The concentrations of Fe 2+ , ROS, LPO, MDA, GSH, 4-HNE, and GPX4 in the primary chondrocytes treated with Erastin and/or STS (n = 6/group). I The protein level of FTH1, GPX4, and ACSL4 from primary chondrocytes treated with Erastin and/or STS. Right: Quantification of these proteins (n = 6/group). J Representative images of mitochondrial morphology of the primary chondrocytes treated with Erastin and/or STS. Scale bar, 200 μm. K The concentrations of Fe 2+ , ROS, LPO, MDA, GSH, 4-HNE, and GPX4 in the primary chondrocytes treated with EX-527 and/or STS (n = 6/group). L The protein level of FTH1, GPX4, and ACSL4 from primary chondrocytes treated with EX-527 and/or STS. Right: Quantification of these proteins (n = 6/group). M Representative images of mitochondrial morphology of the primary chondrocytes treated with EX-527 and/or STS. Scale bar, 200 μm. N The concentrations of Fe 2+ , ROS, LPO, MDA, GSH, 4-HNE, and GPX4 in the primary chondrocytes treated with SRT2104 and/or STS (n = 6/group). O The protein levels of FTH1, GPX4, and ACSL4 from primary chondrocytes treated with SRT2104 and/or STS. Right: Quantification of these proteins (n = 6/group). P Representative images of mitochondrial morphology from the primary chondrocytes treated with SRT2104 and/or STS. Scale bar, 200 μm. Data are means ± SD, one-wayANOVA for three groups; N.S., no significant differences, *P < 0.05, **P < 0.01, ***P < 0.001

Article Snippet: The ELISA kits included SIRT1 (MEIMAIN, MM-44881M1), IL-6 (MEIMAIN, MM-0163M1), IL-17A (MEIMAIN, MM-0759M1), TNF-α (MEIMAIN, MM-0132M1), Lipid peroxide (LPO) (Shanghai Yuanxin Biotech Co., Ltd., YX-13615M), Malondialdehyde (MDA) (Shanghai Yuanxin Biotech Co., Ltd., YX-130401M), Glutathione (GSH) (Shanghai Yuanxin Biotech Co., Ltd., YX-071908M), 4-Hydroxy-2-nonenal (4-HNE) ELISA Kit instruction (Shanghai Yaji Biotechnology Co., Ltd., YS03024B), and GPX4 Activity Assay Kit (Elabscience, E-BC-K883-M).

Techniques: Immunoprecipitation, Plasmid Preparation, Expressing

Journal: Chinese Medicine

Article Title: Sodium tanshinone IIA sulfonate alleviates osteoarthritis through targeting SIRT1

doi: 10.1186/s13020-025-01166-2

Figure Lengend Snippet: STS promoted SIRT1 deacetylation of NF-κB p65, thereby inhibiting inflammation and ferroptosis to alleviate OA. A Nuclear protein level of NF-κB p65 (Lys310) immunoprecipitated from primary chondrocytes treated with IL-1β and/or STS. Right: Quantification of the nuclear protein levels of the SIRT1, NF-κB p65, and acetylated NF-κB p65 (Lys310) immunoprecipitated from primary chondrocytes treated with IL-1β and/or STS (n = 6/group). B The relative mRNA expression of TNF-α, IL-6, and IL-17A in primary chondrocytes treated in the presence of IL-1β with or without STS (n = 6/group). C Concentrations of Fe 2+ , ROS, LPO, MDA, GSH, 4-HNE, and GPX4 in the primary chondrocytes of each group (Control, IL-1β, IL-1β + STS) (n = 6/group). D Protein levels of FTH1, GPX4, and ACSL4 from primary chondrocytes treated with 1L-1β and/or STS. Right: Quantification of these proteins (n = 6/group). E Representative images of mitochondrial morphology from the primary chondrocytes treated with 1L-1β and/or STS. Scale bar, 200 μm. Data are means ± SD. One-wayANOVA for three groups; N.S., no significant differences, *P < 0.05, **P < 0.01, ***P < 0.001

Article Snippet: The ELISA kits included SIRT1 (MEIMAIN, MM-44881M1), IL-6 (MEIMAIN, MM-0163M1), IL-17A (MEIMAIN, MM-0759M1), TNF-α (MEIMAIN, MM-0132M1), Lipid peroxide (LPO) (Shanghai Yuanxin Biotech Co., Ltd., YX-13615M), Malondialdehyde (MDA) (Shanghai Yuanxin Biotech Co., Ltd., YX-130401M), Glutathione (GSH) (Shanghai Yuanxin Biotech Co., Ltd., YX-071908M), 4-Hydroxy-2-nonenal (4-HNE) ELISA Kit instruction (Shanghai Yaji Biotechnology Co., Ltd., YS03024B), and GPX4 Activity Assay Kit (Elabscience, E-BC-K883-M).

Techniques: Immunoprecipitation, Expressing, Control

Journal: Chinese Medicine

Article Title: Sodium tanshinone IIA sulfonate alleviates osteoarthritis through targeting SIRT1

doi: 10.1186/s13020-025-01166-2

Figure Lengend Snippet: STS promoted SIRT1-mediated deacetylation of NF-κB p65, thereby inhibiting inflammation and ferroptosis to alleviate OA progression in DMM-induced mice. The STS of 45 μg was used in the study. A Representative images of SIRT1 staining in tibial articular cartilage of mice for each group (Sham, DMM, DMM + STS). Bar = 50 μm. B Quantification of SIRT1 positive chondrocytes in the tibial articular cartilage of mice for each group (Sham, DMM, DMM + STS) (n = 3/group). C Representative images of NF-κB p65 (Lys310) staining in tibial cartilage of DMM-induced mice treated with or without STS. Bar = 20 μm. D Quantification of NF-κB p65 (Lys310) positive chondrocytes in the mice tibial cartilage of each group (n = 3/group). E–H The serum expression of IL-1β, TNF-α, IL-6, and IL-17A in the mice of each group (Sham, DMM, DMM + STS) (n = 10/group). I Representative images of ACSL4 staining in the tibial articular cartilage of DMM-induced mice treated with or without STS. Bar = 20 μm. J Quantification of ACSL4 expression in the tibial articular cartilage of mice in each group (n = 3/group). K The protein levels of FTH1, GPX4, and ACSL4 from tibial articular cartilage of DMM-induced mice treated with or without STS. L Quantification of these proteins (n = 6/group). Data are means ± SD, One-wayANOVA; *P < 0.05, **P < 0.01, ***P < 0.001

Article Snippet: The ELISA kits included SIRT1 (MEIMAIN, MM-44881M1), IL-6 (MEIMAIN, MM-0163M1), IL-17A (MEIMAIN, MM-0759M1), TNF-α (MEIMAIN, MM-0132M1), Lipid peroxide (LPO) (Shanghai Yuanxin Biotech Co., Ltd., YX-13615M), Malondialdehyde (MDA) (Shanghai Yuanxin Biotech Co., Ltd., YX-130401M), Glutathione (GSH) (Shanghai Yuanxin Biotech Co., Ltd., YX-071908M), 4-Hydroxy-2-nonenal (4-HNE) ELISA Kit instruction (Shanghai Yaji Biotechnology Co., Ltd., YS03024B), and GPX4 Activity Assay Kit (Elabscience, E-BC-K883-M).

Techniques: Staining, Expressing

Journal: Chinese Medicine

Article Title: Sodium tanshinone IIA sulfonate alleviates osteoarthritis through targeting SIRT1

doi: 10.1186/s13020-025-01166-2

Figure Lengend Snippet: STS failed to alleviate the levels of NF-κB (Lys310), inflammation, and ferroptosis in Sirt1 cKO mice. STS at a concentration of 45 μg or 100 μM was used in the study. A Representative images of NF- κ B (Lys310) staining in the tibial articular cartilage of mice for each group (DMM + Control, DMM + Sirt1 cKO, DMM + Sirt1 cKO + STS). Bar = 50 μm. B Quantification of NF- κ B (Lys310) positive staining cells in each group (n = 3/group). C–E The relative mRNA expression of TNF-α, IL-6, and IL-17A in the IL-1β-induced primary chondrocytes of each group (IL-1β + Control, IL-1β + Sirt1 KO, IL-1β + Sirt1 KO + STS) (n = 6/group). F Representative images of ACSL4 staining in the tibial articular cartilage of mice for each group (DMM + Control, DMM + Sirt1 cKO, DMM + Sirt1 cKO + STS). Bar = 20 μm. G Quantification of ACSL4 positive cells in each group (n = 3/group). H Protein levels of FTH1, GPX4, and ACSL4 from tibial cartilage of mice for each group (DMM + Control, DMM + Sirt1 cKO, DMM + Sirt1 cKO + STS). I Quantification of these proteins (n = 6/group). Data are presented as the mean ± SD, one-wayANOVA; N.S., no significant differences, *P < 0.05, **P < 0.01, ***P < 0.001

Article Snippet: The ELISA kits included SIRT1 (MEIMAIN, MM-44881M1), IL-6 (MEIMAIN, MM-0163M1), IL-17A (MEIMAIN, MM-0759M1), TNF-α (MEIMAIN, MM-0132M1), Lipid peroxide (LPO) (Shanghai Yuanxin Biotech Co., Ltd., YX-13615M), Malondialdehyde (MDA) (Shanghai Yuanxin Biotech Co., Ltd., YX-130401M), Glutathione (GSH) (Shanghai Yuanxin Biotech Co., Ltd., YX-071908M), 4-Hydroxy-2-nonenal (4-HNE) ELISA Kit instruction (Shanghai Yaji Biotechnology Co., Ltd., YS03024B), and GPX4 Activity Assay Kit (Elabscience, E-BC-K883-M).

Techniques: Concentration Assay, Staining, Control, Expressing

Journal: Frontiers in Pharmacology

Article Title: Licoisoflavone B alleviates psoriasis via SCD1-targeted lipid metabolism reprogramming and suppression of Th17/IL-17–mediated inflammation

doi: 10.3389/fphar.2026.1754729

Figure Lengend Snippet: Integrated workflow for target prediction and experimental validation of Lico B in psoriasis. Bioinformatic analyses, including WGCNA module construction, gene–trait correlation analysis, multi-database target intersection (GEO, GeneCards, TTD), molecular docking, and SPR analysis were used to identify candidate targets of Lico B. Subsequent in vitro and in vivo experiments—comprising Western blotting, qPCR, immunofluorescence staining, and flow cytometry in IL-17–stimulated keratinocytes and IMQ-induced psoriatic mice—were conducted to validate the therapeutic mechanisms of Lico B.

Article Snippet: The IL-17 group was treated with 100 ng/mL IL-17 (Proteintech; HZ-1113); the Lico B group received 9 μM Lico B (MCE; HY-N3388); the IL-17 + Lico B group was co-treated with IL-17 and Lico B; and the control group was treated with PBS.

Techniques: Biomarker Discovery, In Vitro, In Vivo, Western Blot, Immunofluorescence, Staining, Flow Cytometry

Journal: Frontiers in Pharmacology

Article Title: Licoisoflavone B alleviates psoriasis via SCD1-targeted lipid metabolism reprogramming and suppression of Th17/IL-17–mediated inflammation

doi: 10.3389/fphar.2026.1754729

Figure Lengend Snippet: Schematic illustration of lico B treatment in psoriasis. Lico B modulates lipid metabolic pathways by suppressing SCD1-dependent metabolic reprogramming and reducing lipid droplet accumulation in keratinocyte, while simultaneously attenuating the TH17/IL-17 axis. Through concurrent regulation of keratinocyte metabolism and inflammatory cytokine production, Lico B ameliorate psoriatic skin pathology.

Article Snippet: The IL-17 group was treated with 100 ng/mL IL-17 (Proteintech; HZ-1113); the Lico B group received 9 μM Lico B (MCE; HY-N3388); the IL-17 + Lico B group was co-treated with IL-17 and Lico B; and the control group was treated with PBS.

Techniques: