Journal: Neural Regeneration Research

Article Title: Overexpression of the inwardly rectifying potassium channel Kir4.1 or Kir4.1 Tyr 9 Asp in Müller cells exerts neuroprotective effects in an experimental glaucoma model

doi: 10.4103/NRR.NRR-D-24-00461

Figure Lengend Snippet: Kir4.1 overexpression and Kir4.1 Tyr 9 Asp overexpression in Müller cells suppress the MYD88/IRAK1/TRAF6/NF-κB p65 inflammatory signaling pathway. (A) Representative immunoblots showing changes in MYD88, IRAK1, TRAF6, and NF-κB p65 expression levels in microglia co-cultured with normal or activated Müller cells infected with LV-NC, Kir4.1, and Kir4.1 Tyr 9 Asp lentiviruses. (B, D, F, H) Bar charts summarizing the average densitometric quantification of immunoreactive bands for MYD88 (B), IRAK1 (D), TRAF6 (F), and NF-κB p65 (H) in microglia co-cultured with normal or activated Müller cells. n = 5 for each group. * P < 0.05, ** P < 0.01, vs. the + normal Müller cells group. Unpaired two-tailed t -test. (C, E, G, I) Bar charts summarizing the average densitometric quantification of immunoreactive bands for MYD88 (C), IRAK1 (E), TRAF6 (G), and NF-κB p65 (I) in microglia co-cultured with normal or activated Müller cells. n = 5 for each group. * P < 0.05, ** P < 0.01, vs. LV-NC + normal Müller cells group. One-way analysis of variance (Tukey–Kramer multiple comparisons test) was performed. eGFP: Enhanced green fluorescent protein; IRAK1: IL-1 receptor associated kinase 1; LV-NC: eGFP control lentiviruses; MYD88: myeloid differentiation primary response protein 88; NF-κB P65: nuclear factor kappa B P65; TRAF6: TNF receptor associated factor 6.

Article Snippet: Previous studies have demonstrated that Toll-like receptors play a role in microglial activation and the release of pro-inflammatory factors in the COH retina, a process mediated by the MYD88/IRAK1/TRAF6/NF-κB p65 signaling pathway (Takeda and Akira, 2004; Luo et al., 2010; Weber et al., 2010; Miao et al., 2023).

Techniques: Over Expression, Western Blot, Expressing, Cell Culture, Infection, Two Tailed Test, Control

Journal: Apoptosis

Article Title: Nicotine suppresses ferroptosis in colon cancer cells via HMOX1/NF-κB pathway to reduce oxaliplatin sensitivity

doi: 10.1007/s10495-026-02308-z

Figure Lengend Snippet: Nicotine reduces the sensitivity of colon cancer cells to oxaliplatin through modulation of the HMOX1/NF-κB signaling pathway. a-b The CCK-8 assay demonstrated that 10 µM oxaliplatin treatment for 24 h significantly inhibited the growth of LOVO and SW480 cells, while combined 1 µM nicotine treatment notably enhanced cell viability. Overexpression of HMOX1 reversed the 1 µM nicotine-induced increase in cell viability, and the 100 nM p-NF-κB pathway activator PMA treatment for 24 h partially restored this effect. c-d , k-l The scratch assay and quantitative analysis showed that HMOX1 overexpression reversed the 1 µM nicotine-induced increase in cell migration ability in LOVO and SW480 cells after 24 h of treatment, with 100 nM PMA treatment for 24 h partially restoring this effect. Scale bar = 20 μm. e-h The colony formation assay and quantitative analysis showed that HMOX1 overexpression reversed the 1 µM nicotine-induced enhancement of cell proliferation in LOVO and SW480 cells after 24 h, with 100 nM PMA treatment for 24 h partially restoring this effect. i-j , m-n The invasion assay and quantitative analysis showed that HMOX1 overexpression reversed the 1 µM nicotine-induced increase in cell invasion ability in LOVO and SW480 cells after 24 h of treatment, with 100 nM PMA treatment for 24 h partially restoring this effect. Scale bar = 20 μm. All data are expressed as mean ± standard deviation (independent triplicates). * p < 0.05; ** p < 0.01; *** p < 0.001; ns, no significant difference

Article Snippet: Iron death inducer RSL3 (Selleck, USA) and p-NF-κB signaling pathway activator PMA (Phorbol 12-myristate 13-acetate, Selleck, USA) were dissolved in DMSO to prepare stock solutions, stored at -20 °C in a dark environment, and diluted to working concentrations before use for cell treatment according to the experimental design.

Techniques: CCK-8 Assay, Over Expression, Wound Healing Assay, Migration, Colony Assay, Invasion Assay, Standard Deviation