Journal: Frontiers in Medicine

Article Title: Extracellular vesicles from Li-Qi-Yang-Yin formula attenuate LPS-stimulated inflammatory injury in human colonic epithelial cells in vitro by delivering bioactive metabolites and suppressing the oxidative stress–inflammation axis

doi: 10.3389/fmed.2026.1751807

Figure Lengend Snippet: Anti-inflammatory effects of LEVs and LEVs-F in LPS-stimulated NCM460 Cells. (A) Experimental design for LEVs or LEVs-F and LPS co-treatment. (B) Cell viability assessment following 12 h exposure to LPS (0–40 μg/mL, n = 6). (C) Cell viability assessment following 24 h exposure to LEVs-F (0–250 μg/mL, n = 6). (D) Measurement of intracellular and extracellular NO ( n = 6). (E–G) Levels of IL-6, IL-10, and TNF-α under LEVs intervention ( n = 6). Data were expressed as mean ± SD, * P < 0.05, ** P < 0.01 and *** P < 0.001.

Article Snippet: Intracellular levels of NO (A013-2-1, Jiancheng Bioengineering Institute, China), Interleukin-6 (IL-6, EK106, Multi Sciences, China), IL-10 (EK110, Multi Sciences, China), and tumor necrosis factor-α (TNF-α, EK182, Multi Sciences, China), as well as extracellular NO levels in the medium, were assayed using NO assay kits and ELISA kits for each cytokine, respectively, in accordance with the manufacturer’s protocols.

Techniques:

Journal: Frontiers in Immunology

Article Title: Aqueous Artemisia argyi extract mitigates acute lung injury in association with coordinated alterations in gut microbiota, metabolic homeostasis, and pulmonary inflammatory gene expression

doi: 10.3389/fimmu.2026.1770675

Figure Lengend Snippet: AEAA pretreatment is associated with reduced pathological features of LPS-induced acute lung injury in mice. (A) Experimental design of the LPS-induced acute lung injury (ALI) model. (B) Histopathological evaluation of lung tissues. Representative H&E-stained sections from different treatment groups at 20× and 40× magnification show alveolar wall thickening, inflammatory cell infiltration, hemorrhage, and edema in LPS-treated mice. AEAA treatment dose-dependently ameliorated these pathological alterations (red boxed areas). (C) Wet-to-dry (W/D) lung weight ratio. (D) Lung injury score. (E–G) Pro-inflammatory cytokines in serum and BALF.IL-1β (E) , IL-6 (F) , and IL-10 (G) levels in serum and BALF. (H) TNF-α levels in serum and BALF. (I) Myeloperoxidase (MPO) activity. Data are presented as mean ± SEM. n = 5 per group. Statistical analysis was performed using one-way ANOVA followed by post hoc tests. * P < 0.05 , ** P < 0.01 , *** P < 0.001 , **** P < 0.0001 .

Article Snippet: Enzyme-linked immunosorbent assay (ELISA) kits for mouse IL-1β (Cat. #EK201B), IL-6 (Cat. #EK206), IL-10 (Cat. #EK210), TNF-α (Cat. #EK282), and myeloperoxidase (MPO) (Cat. #EK2133) were obtained from Multisciences (Lianke) Biotech Co., Ltd. (Hangzhou, China).

Techniques: Staining, Activity Assay

Journal: bioRxiv

Article Title: In vivo expansion of gene-targeted hepatocytes through transient inhibition of an essential gene

doi: 10.1101/2023.07.26.550728

Figure Lengend Snippet: a , Eight-week-old C57BL/6J mice were injected with 5×10 11 GC of AAV-CRISPR and 1×10 11 GC of an AAV-Donor containing the promoterless coding sequences of human FAH (selectable marker) and FIX or 6×10 11 GC of AAV-GFP as control. Mice were injected with Fah -siRNA (3 mg/kg or saline as control) every 4 weeks until 12 weeks post-AAV injection. Blood was collected at time 0 and every two to four weeks and mice were sacrificed at 52 weeks post AAV-injection. Created with BioRender.com. b , Human FIX ELISA in plasma samples. c , Representative immunohistochemistry staining of 2A-tagged FAH (FAH-2A), hematoxylin and eosin (H&E) and Fah in the liver. Scale bar is 100 µm. Data are expressed as mean ± s.d. (n= 3 Control and 9 Unselected and Repair Drive mice) with significance determined by two-way ANOVA followed by Tukey test. **** p<0.0001 Repair Drive vs. Control and Unselected mice.

Article Snippet: Human FIX was measured in 1:16.7 diluted plasma by using Factor IX Human SimpleStep ELISA Kit (ab188393, Abcam), following the manufacturer’s protocol.

Techniques: Injection, CRISPR, Marker, Control, Saline, Enzyme-linked Immunosorbent Assay, Clinical Proteomics, Immunohistochemistry, Staining