Journal: Virology Journal

Article Title: MG132-mediated inhibition of rabies virus replication via the Nrf2/SQSTM1/PINK1/Parkin autophagy pathway

doi: 10.1186/s12985-026-03164-8

Figure Lengend Snippet: MG132 inhibits CVS-11 and CTN replication by enhancing the Nrf2 pathway. ( A , E ) N2a cells were infected with CVS-11 (MOI = 1) or CTN (MOI = 1) and then treated with CDDO-Me (0.5 μM), MG132 (5 μM) respectively, or in combination for 48 h. Nrf2, SQSTM1 and RABV P protein levels were examined by western blot. ( C , G )N2a cells were pretreated with ATRA (10 μM) for 6 h and/or treated with MG132 (5 μM) during CVS-11 infection (MOI = 1) or CTN (MOI = 1) for 48 h. Nrf2, SQSTM1 and RABV P protein levels were determined by western blot. ( B , D , F , H ) Densitometric quantification of Nrf2, SQSTM1 and RABV P normalized to β-actin. ( I , J ) Viral titers in the culture supernatants were determined. Data represent the mean ± SD from three independent experiments performed in triplicate. Statistical analysis was carried out using one-way ANOVA with Dunnett’s post hoc test (*p < 0.05, **p < 0.01, ***p < 0.001

Article Snippet: MG132, ribavirin, T705, bardoxolone methyl (CDDO-Me), retinoic acid (ATRA), rapamycin (Rapa), 3-methyladenine (3-MA) and carbonyl cyanide m-chlorophenylhydrazone (CCCP) were purchased from Med-Chem-Express.

Techniques: Infection, Western Blot

Journal: Advances in redox research

Article Title: Inhibition of smooth muscle phenotypic modulation by bardoxolone methyl, omaveloxolone, and cinnamaldehyde is Nrf-2 dependent

doi: 10.1016/j.arres.2026.100158

Figure Lengend Snippet: Nrf2 activation inhibits vascular smooth muscle cell (VSMC) migration in a Nrf2-dependent manner. VSMC were synchronized overnight and then stimulated with 25 ng/mL PDGF-BB for 24 h in the presence or absence of Nrf2 activators: 200 nM bardoxolone (BAR), 400 nM omaveloxolone (OMV), or 100 μM cinnamaldehyde (CA). Nrf2 wild-type (WT), knock-out (KO), and Nrf2-rescued (RESC) VSMC were used. (A) Representative images depicting the initial scratch (0 h) and the same region 24 h later showing cell migration toward the wound area. (B) Quantification of cell migration based on the area occupied by cells within the scratch region after 24 h. (One-way ANOVA with post hoc Tukey’s correction for multiple comparisons; ns = not significant, * p < 0.05, ** p < 0.01, *** p < 0.001; data presented as mean ± SD.).

Article Snippet: Bardoxolone methyl (BAR) (HY-14909; MedChemExpress, NJ).

Techniques: Activation Assay, Migration, Knock-Out

Journal: Advances in redox research

Article Title: Inhibition of smooth muscle phenotypic modulation by bardoxolone methyl, omaveloxolone, and cinnamaldehyde is Nrf-2 dependent

doi: 10.1016/j.arres.2026.100158

Figure Lengend Snippet: Nrf2 activators upregulate downstream antioxidant enzymes only in Nrf2 wild-type (WT) and rescued vascular smooth muscle cells (VSMC). VSMC were synchronized overnight and then stimulated with 25 ng/mL PDGF-BB for 24 h in the presence or absence of Nrf2 activators: 200 nM bardoxolone methyl (BAR), 400 nM omaveloxolone (OMV), or 100 μM cinnamaldehyde (CA). Nrf2 WT, knock-out (KO), and Nrf2-rescued (RESC) VSMC were used (A) Western blot of HO-1 and NQO1 protein levels after 24 h, across genotypes and treatments.(B) Densitometric quantification of HO-1 and NQO1 expression normalized to loading control ( n = 3 biological replicates (One-way ANOVA with post hoc Tukey’s correction for multiple comparisons; ns = not significant, * p < 0.05, ** p < 0.01, *** p < 0.001; data presented as mean ± SD.).

Article Snippet: Bardoxolone methyl (BAR) (HY-14909; MedChemExpress, NJ).

Techniques: Knock-Out, Western Blot, Expressing, Control

Journal: Advances in redox research

Article Title: Inhibition of smooth muscle phenotypic modulation by bardoxolone methyl, omaveloxolone, and cinnamaldehyde is Nrf-2 dependent

doi: 10.1016/j.arres.2026.100158

Figure Lengend Snippet: Nrf2 activation inhibits proliferation only in Nrf2 wild-type (WT) and Nrf2-rescued (RESC) vascular smooth muscle cells (VSMC). VSMC were synchronized overnight and then stimulated with 25 ng/mL PDGF-BB for 24 h with or without Nrf2 activators: 200 nM bardoxolone methyl (BAR), 400 nM omaveloxolone (OMV), or 100 μM cinnamaldehyde (CA). Nrf2 WT, knock-out (KO), and Nrf2-rescued (RESC) VSMC were harvested for flow cytometry. (A, B) Quantification of viable and apoptotic/dead VSMC (n = 3 biological replicates, in triplicate). (C) Percentage of Ki67+ proliferating VSMC across genotypes and treatments ( n = 3; representative replicate shown). (One-way ANOVA with post hoc Tukey’s correction for multiple comparisons; ns = not significant, **** p < 0.0001; data presented as mean ± SD.).

Article Snippet: Bardoxolone methyl (BAR) (HY-14909; MedChemExpress, NJ).

Techniques: Activation Assay, Knock-Out, Flow Cytometry

Journal: Advances in redox research

Article Title: Inhibition of smooth muscle phenotypic modulation by bardoxolone methyl, omaveloxolone, and cinnamaldehyde is Nrf-2 dependent

doi: 10.1016/j.arres.2026.100158

Figure Lengend Snippet: Nrf2 activation preserves the contractile phenotype only in Nrf2 wild-type (WT) and rescued vascular smooth muscle cells (VSMC) under PDGF stimulation. Nrf2 WT, knock-out (KO), and Nrf2-rescued (RESC) VSMC were treated with with 30 mg/mL heparin for 5 days to induce a contractile phenotype, followed by 72 h stimulation with 25 ng/mL PDGF-BB in the presence or absence of Nrf2 activators: 200 nM bardoxolone methyl (BAR), 400 nM omaveloxolone (OMV), or 100 μM cinnamaldehyde (CA).(A) Representative western blots showing expression of contractile markers: calponin, transgelin (SM22α)(B) Densitometric quantification of marker expression across genotypes and treatments ( n = 3 biological replicates).(One-way ANOVA with post hoc Tukey’s correction for multiple comparisons; ns = not significant, * p < 0.05, ** p < 0.01, *** p < 0.001; data presented as mean ± SD.).

Article Snippet: Bardoxolone methyl (BAR) (HY-14909; MedChemExpress, NJ).

Techniques: Activation Assay, Knock-Out, Western Blot, Expressing, Marker

Journal: Advances in redox research

Article Title: Inhibition of smooth muscle phenotypic modulation by bardoxolone methyl, omaveloxolone, and cinnamaldehyde is Nrf-2 dependent

doi: 10.1016/j.arres.2026.100158

Figure Lengend Snippet: Bardoxolone methyl is more potent at inhibiting neointimal hyperplasia after balloon injury in rats. 100 nM bardoxolone methyl (BAR) in 100 μL Pluronic F-127 gel was applied periadventitially at the time of surgery. Arteries were harvested 14 days post-surgery and processed for imaging. (A) Representative longitudinal and cross-sections of uninjured and injured arteries, (green = autofluorescence, white = anti-CD31-AF647, L = lumen) (scale bars: A = 300 μm, B = 300 μm).(B) Quantitative measurements assessing intima-to-media ratio (I:M), and percent vessel occlusion, ( n = 5–7). Data analyzed by unpaired T-test, ** p < 0.01; data presented as mean ± SD.).

Article Snippet: Bardoxolone methyl (BAR) (HY-14909; MedChemExpress, NJ).

Techniques: Imaging