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p10  (Actelion)

 
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    Actelion p10
    P10, supplied by Actelion, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/p10/p10/pm41932416-80-2-25
    Average 86 stars, based on 1 article reviews
    p10 - by Bioz Stars, 2026-09
    86/100 stars

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    Saline:

    Article Title: Altered bone structure in Niemann-Pick Type C1 mice, especially in females.
    Article Snippet: For the therapeutic treatment regime (Fig. 1), the animals were randomly divided into six groups: (1) Mice of group 1 (None) were not treated. (2) Mice of group 2 (Sham) were treated the same scheme as the mice of combination therapy (group 3, combi) group with injection of saline omitting the active substances. (3) Combi: On P7 and thereafter weekly, the mice received HPßCD/ALLO (25 mg/kg body weight ALLO dissolved in 40% HPßCD; Sigma-Aldrich, Munich, Germany). .. Additionally, from P10 to P23, the mice received daily injections of MIGLU (300 mg/kg, i.p.; Jo ur na l P re -p ro of Zavesca, Actelion Pharmaceuticals, San Francisco, CA, USA), dissolved in saline. .. From P23 until the end of the experiments, the mice received standard food (B1184-000, Ssniff, Soest, Germany) containing MIGLU at a daily dose of 1200 mg/kg body weight. (4) Mice of group 4 (HPßCD monotherapy, HPßCD) received weekly an intraperitoneal injection of HPßCD (4000 mg/kg body weight, Sigma-Aldrich) beginning at P7.



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    Image Search Results


    TUS inhibited the activation of NLRP3 inflammasome by activating Nrf2. (A) TUS at 2.5, 5, and 10 μM inhibited the activation of NLRP3 inflammasome. J774 A.1 cells were treated with 2.5, 5, and 10 μM TUS and induced by 200 ng/μL LPS and 3 μM nigericin, and the protein levels of IL-1β, Caspase-1, NLRP3, pro-caspase-1, and pro-IL-1β were detected. (B) TUS at 20 μM inhibited the activation of NLRP3 inflammasome induced by nigericin, MSU, and ATP. J774 A.1 cells were treated with 20 μM TUS and induced by 200 ng/μL LPS, nigericin, MSU, and ATP, and the protein levels of IL-1β, Caspase-1, NLRP3, pro-caspase-1, and pro-IL-1β were detected. (C) TUS inhibited the production and secretion of IL-1β. J774 A.1 cells were treated with 5, 10, and 20 μM TUS and induced by 200 ng/μL LPS and 3 μM nigericin, and the IL-1β levels were detected with ELISA kit. (D) TUS inhibited the protein–protein interaction b4etween NLRP3, ASC, and NEK7. (E) TUS inhibited ASC oligomerization. (F) The ROS scavenger NAC inhibited NLRP3 inflammasome activation. (G) The effect of TUS on NLRP3 inflammasome activation in WT and Nrf2-silenced J774 A.1 cells. (H) The effect of TUS on NLRP3 inflammasome activation in WT and C434A mutant J774 A.1 cells. The results were expressed as mean ± SD (n = 3). * p < 0.05, ** p < 0.01, *** p < 0.001 treated vs LPS + nigericin group.

    Journal: Journal of Advanced Research

    Article Title: Tussilagone attenuated cigarette smoke-induced chronic obstructive pulmonary disease through regulating Nrf2 and NF-κB/NLRP3 inflammasome via directly targeting cysteine 434 of KEAP1

    doi: 10.1016/j.jare.2025.07.019

    Figure Lengend Snippet: TUS inhibited the activation of NLRP3 inflammasome by activating Nrf2. (A) TUS at 2.5, 5, and 10 μM inhibited the activation of NLRP3 inflammasome. J774 A.1 cells were treated with 2.5, 5, and 10 μM TUS and induced by 200 ng/μL LPS and 3 μM nigericin, and the protein levels of IL-1β, Caspase-1, NLRP3, pro-caspase-1, and pro-IL-1β were detected. (B) TUS at 20 μM inhibited the activation of NLRP3 inflammasome induced by nigericin, MSU, and ATP. J774 A.1 cells were treated with 20 μM TUS and induced by 200 ng/μL LPS, nigericin, MSU, and ATP, and the protein levels of IL-1β, Caspase-1, NLRP3, pro-caspase-1, and pro-IL-1β were detected. (C) TUS inhibited the production and secretion of IL-1β. J774 A.1 cells were treated with 5, 10, and 20 μM TUS and induced by 200 ng/μL LPS and 3 μM nigericin, and the IL-1β levels were detected with ELISA kit. (D) TUS inhibited the protein–protein interaction b4etween NLRP3, ASC, and NEK7. (E) TUS inhibited ASC oligomerization. (F) The ROS scavenger NAC inhibited NLRP3 inflammasome activation. (G) The effect of TUS on NLRP3 inflammasome activation in WT and Nrf2-silenced J774 A.1 cells. (H) The effect of TUS on NLRP3 inflammasome activation in WT and C434A mutant J774 A.1 cells. The results were expressed as mean ± SD (n = 3). * p < 0.05, ** p < 0.01, *** p < 0.001 treated vs LPS + nigericin group.

    Article Snippet: The primary antibodies for KEAP1 (10503-2-AP, 1:5000), Nrf2 (16396-1-AP, 1:2000), glutamate-cystine ligase, modifier subunit (GCLM, 14241-1-AP, 1:2000), cyclooxygenase-2 (COX-2, 27308-1-AP, 1:1000), IL-1β (16806-1-AP, 1:500), β-actin (20536-1-AP, 1:30000), inducible Nitric Oxide Synthase (iNOS, 22226-1-AP, 1:2000), HA (51064-2-AP, 1:2000), inhibitor of NF-κB (IκB, 10268-1-AP, 1:2000), Caspase-1 (22915-1-AP, 1:2000), NLRP3 (27458-1-AP, 1:2000), α-tubulin (11224-1-AP, 1:10000), and the secondary antibodies HRP-conjugated goat anti-mouse IgG (66031-1-Ig, 1:10000) and HRP-conjugated goat anti-rabbit IgG (66031-2-Ig, 1:10000) were purchased from Proteintech Group (Wuhan, China).

    Techniques: Activation Assay, Enzyme-linked Immunosorbent Assay, Mutagenesis