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Image Search Results
Journal: iScience
Article Title: Changes in the microglial phenotype drive neuroinflammation independent of systemic inflammation in the acute stage of heatstroke
doi: 10.1016/j.isci.2026.115254
Figure Lengend Snippet: Time course of functional damage to the intestinal barrier and blood-brain barrier during the acute stage of heatstroke The mice were exposed to 41.2 ± 0.5°C ambient temperature until their rectal temperature reached 42.4°C, and then they were allowed to recover at an ambient temperature of 25 ± 0.5°C for the indicated times. (A) The concentration of FD-4 in serum was measured after its oral administration. (B) Serum endotoxin levels. (C) EB was injected into the mice via the tail vein after the onset of heatstroke, and representative images of EB leakage was shown. (D) Quantitative analysis of EB concentrations in brain tissues. (E) Expression of MMP-2 in the cerebral cortex at 1 h, 6 h, and 24 h post heatstroke. (F) Expression of MMP-9 in the cerebral cortex at 1 h, 6 h, and 24 h post heatstroke. The data are expressed as the mean ± SEM of three independent experiments. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, vs. Con.
Article Snippet: The membrane was further incubated overnight at 4°C with primary antibodies against MMP9 (TA326652; ORIGENE, USA),
Techniques: Functional Assay, Concentration Assay, Injection, Expressing
Journal: BMC cancer
Article Title: Enhanced anti-cancer effect of AMTB hydrochloride via chitosan nanoparticles in pancreatic cancer.
doi: 10.1186/s12885-025-14356-w
Figure Lengend Snippet: Fig. 2 TRPM8 antagonist AMTB restricts pancreatic cancer cell migration and invasion. (A) Scratch assay showing reduced migration in AMTB-treated BxPC-3 and PANC-1 cells. (B) Transwell assay indicating decreased invasion in AMTB-treated cells. (C) Western blot analysis of EMT-related proteins and migration/invasion markers (MMP2, MMP9) in AMTB-treated cells. N = 3 (biological replicates)
Article Snippet: The relevant primary antibodies are as follows: GAPDH (5174 S, 1:1000, Cell signaling Technology [CST], Boston, USA), TRPM8 (ab85617, 1:1000, Abcam), E-cadherin (20874-1-AP, 1:20000, Proteintech, Wuhan, China), N-cadherin (AF4039, 1:500, Affinity Bioscience), Snail (CSB-PA004123, 1:1000, CUSABIO, Wuhan, China),
Techniques: Migration, Wound Healing Assay, Transwell Assay, Western Blot
Journal: Experimental and Therapeutic Medicine
Article Title: IL-32γ promotes integrin αvβ6 expression through the activation of NF-κB in HSCs
doi: 10.3892/etm.2017.4956
Figure Lengend Snippet: Effect of different concentrations (0, 5, 10 and 20 ng/ml) of IL-32γ on LX-2 activation phenotypes. (A) Growth curves of LX-2 demonstrated that upregulation of IL-32γ promoted proliferation of LX-2. (B) Reverse transcription-quantitative polymerase chain reaction assessing mRNA levels of α-SMA, (C) collagen I, (D) TIMP1, (E) MMP2 and (F) MMP9, representing the activation level of LX-2. (G) Western blot analysis was used to measure collagen I, MMP9, MMP2, α-SMA, TIMP1 and GAPDH expression in whole-cell extracts. Data are presented as the mean ± standard deviation of three experiments. *P<0.01 and **P<0.05 vs. 0 ng/ml IL-32γ. IL-32γ, interleukin-32γ; α-SMA, α-smooth muscle actin; TIMP1, tissue inhibitor of metalloproteinase 1; MMP, matrix metalloproteinases; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; RT-qPCR, reverse transcription-quantitative polymerase chain reaction.
Article Snippet: Primary antibodies were as follows: Anti-integrin αVβ6 (cat. no. ab97588; Abcam, Cambridge, MA, USA), anti-GAPDH (cat. no. KGAA002-2; Nanjing KeyGen Biotech Co., Ltd.), anti-α-SMA (cat. no. G6669; Sigma-Aldrich; Merck KGaA), collagen type I antibody (cat. no. 600-402-103;
Techniques: Activation Assay, Real-time Polymerase Chain Reaction, Western Blot, Expressing, Standard Deviation, Quantitative RT-PCR