Journal: International Dental Journal

Article Title: Obesity as a Determinant of Periodontal Therapy Outcomes: Insights on Oxidative and Endoplasmic Reticulum Stress Pathways

doi: 10.1016/j.identj.2026.109472

Figure Lengend Snippet: Oxidative stress markers in the study population, stratified by obesity presence, before and after non-surgical periodontal treatment. Total ROS (A and G), cytosolic superoxide (B and H) and mitochondrial superoxide (C and I) in leukocytes, and protein levels of SOD1 (D and J) in PBMCs normalized to the loading control actin with corresponding WB images (E), and serum total antioxidant capacity (F and K). Data are presented as box and whisker plots and were compared using two-factor analysis of variance (ANOVA) followed by post hoc tests. ** P < .01 when comparing baseline vs 12 wk. # P < .05 when comparing groups with vs without obesity. DCFH, diclorodihidrofluoresceína; dHE, dihydroethidium; MitoSOX, Mitochondrial Superoxide Indicator; ns, not significant; PBMCs, peripheral blood mononuclear cells; ROS, reactive oxygen species; SOD1, superoxide dismutase 1.

Article Snippet: Twenty-five micrograms of protein were separated by SDS-PAGE, transferred to nitrocellulose membranes, blocked, and incubated with the following specific antibodies: rabbit monoclonal anti-superoxide dismutase 1 (SOD1) (Cat# PA5-27240, RRID:AB_2544716), rabbit polyclonal anti-IRE1α (Cat# PA1-46027, RRID:AB_2262265), mouse monoclonal anti-CHOP (Cat# MA1-250, RRID:AB_2292611) from Thermo Fisher Scientific; rabbit polyclonal anti-GRP78 (Cat# ab21685, RRID:AB_2119834), mouse monoclonal anti-ATF6 (Cat# ab122897, RRID:AB_10899) from Abcam; rabbit polyclonal anti-eukaryotic initiation factor 2 phospho (p-eIF2α) (Innovative Research Cat# 44-728G, RRID:AB_15000); mouse monoclonal anti-actin (Cell Signaling Technology Cat# 3700, RRID:AB_2242334) or rabbit polyclonal anti-actin (Sigma-Aldrich Cat# A5060, RRID:AB_476738).

Techniques: Control, Whisker Assay

Journal: iScience

Article Title: NDUFA5 deficiency promotes renal inflammation in diabetic nephropathy via mitochondrial ROS signaling

doi: 10.1016/j.isci.2026.115555

Figure Lengend Snippet: Ndufa5 loss disrupts mitochondrial homeostasis and promotes oxidative stress (A) Transmission electron microscopy (TEM) images of renal mitochondria. cKO mice exhibit mitochondrial aberrations, including cristae loss, swelling, and reduced aspect ratio, compared to controls (scale bars, 5 μm). (B) ATP levels in renal tissues. NDUFA5 knockout leads to reduced ATP production, which is rescued by CV232-NDUFA5. (C and D) Assessment of oxidative stress markers. Glutathione (GSH) levels and Superoxide Dismutase (SOD) activity in kidney tissues. cKO mice show depleted GSH and reduced SOD activity. Data are represented as mean ± SD ( n = 5 mice per group). Statistical significance was determined by one-way ANOVA followed by Tukey’s post hoc test. The significance threshold was set at p < 0.05. Significance symbols: ns = non-significant, ∗∗ = p < 0.01 and ∗∗∗ = p < 0.001.

Article Snippet: Superoxide dismutase (SOD) assay kit and glutathione (GSH) assay kit were purchased from Jiancheng of China.

Techniques: Transmission Assay, Electron Microscopy, Knock-Out, Activity Assay

Journal: iScience

Article Title: NDUFA5 deficiency promotes renal inflammation in diabetic nephropathy via mitochondrial ROS signaling

doi: 10.1016/j.isci.2026.115555

Figure Lengend Snippet: Knockdown of Ndufa5 induces mitochondrial abnormality and ROS production in HK-2 cells (A) Western blot confirms the knockdown efficiency of NDUFA5 using siRNA. (B) Mitotracker Green staining shows mitochondrial morphology. Control cells display a tubular mitochondrial network, while Ndufa5 knockdown leads to fragmentation (scale bars, 10 μm). (C) ATP levels in HK-2 cells after Ndufa5 knockdown. (D) NDUFA5 knockdown significantly increases both mitochondrial superoxide (MitoSOX Red) and total cellular ROS (DCFH-DA) (scale bars, 25 μm). (E and F) NDUFA5 knockdown leads to a marked decrease in reduced GSH levels (E) and a significant inhibition of SOD activity (F). Ndufa5 knockdown triggers ROS overproduction. Data are represented as mean ± SD ( n = 3 independent experiments). Statistical significance was determined by a two-tailed Student’s t test for comparisons between two groups, or by one-way ANOVA followed by Tukey’s post hoc test for multiple group comparisons. The significance threshold was set at p < 0.05. Significance symbols: ns = non-significant, ∗∗ = p < 0.01 and ∗∗∗ = p < 0.001. Arrows in the figure point to representative positive signals.

Article Snippet: Superoxide dismutase (SOD) assay kit and glutathione (GSH) assay kit were purchased from Jiancheng of China.

Techniques: Knockdown, Western Blot, Staining, Control, Inhibition, Activity Assay, Two Tailed Test

Journal: iScience

Article Title: NDUFA5 deficiency promotes renal inflammation in diabetic nephropathy via mitochondrial ROS signaling

doi: 10.1016/j.isci.2026.115555

Figure Lengend Snippet: NDUFA5 overexpression attenuates HG-induced ROS and inflammatory response in HK-2 cells (A and B) Western blot analysis of NDUFA5 expression in (A) whole cell lysate (WCL) and (B) mitochondrial lysate, confirming overexpression efficiency. (C) NDUFA5 knockdown significantly increases both mitochondrial superoxide (MitoSOX Red) and total cellular ROS (DCFH-DA) (scale bars, 25 μm). (D and E) NDUFA5 knockdown leads to a marked decrease in reduced GSH levels (D) and a significant inhibition of SOD activity (E). NDUFA5 overexpression decreases HG-induced ROS production. Data are represented as mean ± SD ( n = 3 independent experiments). Statistical significance was determined by a two-tailed Student’s t test for comparisons between two groups, or one-way ANOVA followed by Tukey’s post hoc test for multiple group comparisons. The significance threshold was set at p < 0.05. Significance symbols: ns = non-significant, ∗ = p < 0.05, ∗∗ = p < 0.01, and ∗∗∗ = p < 0.001. Arrows in the figure point to representative positive signals.

Article Snippet: Superoxide dismutase (SOD) assay kit and glutathione (GSH) assay kit were purchased from Jiancheng of China.

Techniques: Over Expression, Western Blot, Expressing, Knockdown, Inhibition, Activity Assay, Two Tailed Test