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Nattokinase suppresses COX-2 and MMP-1 via <t>Nrf2/HO-1</t> activation. Cells were pretreated with ML385 or Heme Oxygenase-1-IN-1 hydrochloride (HO-1i) for 1 h, with or without nattokinase, followed by PM exposure. (A) COX-2 protein expression, (B) PGE 2 release, and (C) MMP-1 release were examined. Cells were treated for different time points, and (D) HO-1 mRNA levels and (E) ARE-luciferase activity were examined. Data are presented as mean ± SD from at least three independent experiments. # P < 0.01 compared with cells treated with PM plus nattokinase (A–C). ∗ P < 0.05, # P < 0.01 compared with the control group (D and E). COX-2: cyclooxygenase-2; MMP-1: matrix metalloproteinase-1; Nrf2: nuclear factor erythroid 2-related factor 2; HO-1: heme oxygenase-1; PM: particulate matter; PGE 2 : prostaglandin E 2 ; HO-1i: heme oxygenase-1 inhibitor; ARE: antioxidant response element.
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Nattokinase suppresses COX-2 and MMP-1 via Nrf2/HO-1 activation. Cells were pretreated with ML385 or Heme Oxygenase-1-IN-1 hydrochloride (HO-1i) for 1 h, with or without nattokinase, followed by PM exposure. (A) COX-2 protein expression, (B) PGE 2 release, and (C) MMP-1 release were examined. Cells were treated for different time points, and (D) HO-1 mRNA levels and (E) ARE-luciferase activity were examined. Data are presented as mean ± SD from at least three independent experiments. # P < 0.01 compared with cells treated with PM plus nattokinase (A–C). ∗ P < 0.05, # P < 0.01 compared with the control group (D and E). COX-2: cyclooxygenase-2; MMP-1: matrix metalloproteinase-1; Nrf2: nuclear factor erythroid 2-related factor 2; HO-1: heme oxygenase-1; PM: particulate matter; PGE 2 : prostaglandin E 2 ; HO-1i: heme oxygenase-1 inhibitor; ARE: antioxidant response element.

Journal: Journal of Dental Sciences

Article Title: Nuclear factor erythroid 2-related factor 2/heme oxygenase-1 activation by nattokinase reduces pro-inflammatory and matrix-degrading mediators in human gingival fibroblasts

doi: 10.1016/j.jds.2025.10.022

Figure Lengend Snippet: Nattokinase suppresses COX-2 and MMP-1 via Nrf2/HO-1 activation. Cells were pretreated with ML385 or Heme Oxygenase-1-IN-1 hydrochloride (HO-1i) for 1 h, with or without nattokinase, followed by PM exposure. (A) COX-2 protein expression, (B) PGE 2 release, and (C) MMP-1 release were examined. Cells were treated for different time points, and (D) HO-1 mRNA levels and (E) ARE-luciferase activity were examined. Data are presented as mean ± SD from at least three independent experiments. # P < 0.01 compared with cells treated with PM plus nattokinase (A–C). ∗ P < 0.05, # P < 0.01 compared with the control group (D and E). COX-2: cyclooxygenase-2; MMP-1: matrix metalloproteinase-1; Nrf2: nuclear factor erythroid 2-related factor 2; HO-1: heme oxygenase-1; PM: particulate matter; PGE 2 : prostaglandin E 2 ; HO-1i: heme oxygenase-1 inhibitor; ARE: antioxidant response element.

Article Snippet: The transcriptional activity of Nrf2 was assessed using the antioxidant response element (ARE) Reporter Kit for Nrf2 (BPS Bioscience, Cat. #60514).

Techniques: Activation Assay, Expressing, Luciferase, Activity Assay, Control

Schematic illustration of the proposed mechanism. PM stimulation activates multiple signaling pathways, including ROS generation, NADPH oxidase activation, and PI3K/Akt as well as MAPK cascades, leading to the upregulation of COX-2 expression and PGE 2 release, which in turn promote MMP-1 mRNA expression and protein release. Pretreatment with nattokinase attenuates these PM-induced responses through the induction of the Nrf2/HO-1 signaling pathway, thereby suppressing downstream inflammatory and matrix-degrading processes.

Journal: Journal of Dental Sciences

Article Title: Nuclear factor erythroid 2-related factor 2/heme oxygenase-1 activation by nattokinase reduces pro-inflammatory and matrix-degrading mediators in human gingival fibroblasts

doi: 10.1016/j.jds.2025.10.022

Figure Lengend Snippet: Schematic illustration of the proposed mechanism. PM stimulation activates multiple signaling pathways, including ROS generation, NADPH oxidase activation, and PI3K/Akt as well as MAPK cascades, leading to the upregulation of COX-2 expression and PGE 2 release, which in turn promote MMP-1 mRNA expression and protein release. Pretreatment with nattokinase attenuates these PM-induced responses through the induction of the Nrf2/HO-1 signaling pathway, thereby suppressing downstream inflammatory and matrix-degrading processes.

Article Snippet: The transcriptional activity of Nrf2 was assessed using the antioxidant response element (ARE) Reporter Kit for Nrf2 (BPS Bioscience, Cat. #60514).

Techniques: Protein-Protein interactions, Activation Assay, Expressing