antibodies against ampk alpha  (Proteintech)

Journal: Redox Biology

Article Title: CO-mediated restoration of mitochondrial redox homeostasis contributes to alleviating multiple programmed cell deaths in hepatic I/R injury

doi: 10.1016/j.redox.2026.104440

Figure Lengend Snippet: Schematic illustration of CPs@HA preparation and its proposed therapeutic mechanisms against HIRI: attenuation of oxidative stress and inflammation, restoration of mitochondrial homeostasis, and reduced ferroptosis, cuproptosis, and disulfidptosis. (1) CPs@HA restores mitochondrial homeostasis by activating the AMPK–SIRT1–PGC-1α axis and restoring Ca 2+ balance. This leads to inhibition of mtROS burst, preservation of ΔΨm, and recovery of respiratory chain complex and PDHC activities, as well as restoration of ATP synthesis and NADPH reducing capacity. (2) CO promotes ROS clearance via HO-1 upregulation and enhanced CAT/SOD/GPX activities, reducing oxidative stress. It also suppresses inflammation by inhibiting TLR, NOD-like receptor, NF-κB/MAPK/JAK-STAT, TNF, and IL-17 pathways. (3) CO is associated with attenuated ferroptosis via the SLC7A11–GSH–GPX4 axis, accompanied by reduced Fe 2+ accumulation and lipid peroxidation. (4) CO is associated with reduced cuproptosis through decreased Cu + accumulation, inhibited DLAT oligomerization, and improved TCA cycle function. (5) CO is associated with reduced disulfidptosis through promotion of G6PD-dependent NADPH production, enhanced cystine-to-cysteine and GSSG-to-GSH reduction, restored Cys/GSH balance, and alleviated disulfide stress.

Article Snippet: Antibodies against DLAT, G6PD, FLNA, p -AMPK α , AMPK α , SIRT1, PGC-1 α , CD86, HO-1, CD163, 8-OHdG, iNOS, and GPX4, as well as mouse IL-4, IL-10, and IL-6 ELISA kits, were purchased from Proteintech (USA).

Techniques: Inhibition, Preserving, Immune Cell, In Vivo, In Vitro, RNA Sequencing

Journal: Redox Biology

Article Title: CO-mediated restoration of mitochondrial redox homeostasis contributes to alleviating multiple programmed cell deaths in hepatic I/R injury

doi: 10.1016/j.redox.2026.104440

Figure Lengend Snippet: In vivo CPs@HA restores mitochondrial homeostasis by activating the AMPK–SIRT1–PGC-1α axis to alleviate Ca 2+ overload and mtROS burst during HIRI. (A, B) GSEA of the response to hypoxia and response to oxidative stress pathways in the HIRI and CPs@HA groups. (C) Changes in the expression of key mitochondrial genes in the two groups. (D) Ridge plot of GO enrichment analysis related to calcium homeostasis in the Normal and HIRI groups. (E) Ridge plot of GO enrichment analysis related to calcium homeostasis in the HIRI and CPs@HA groups. (F, G) Protein expression levels of p-AMPKα and AMPKα in liver tissues, and the corresponding densitometric quantification of the bands. (H, I) Protein expression levels of SIRT1 and PGC-1α in liver tissues, and the corresponding densitometric quantification of the bands. (J, K) Fluorescence imaging of mitochondrial Ca 2+ in liver tissues and the corresponding quantitative analysis of fluorescence intensity (scale bar = 100 μm). (L, M) Fluorescence imaging of mtROS in liver tissues and the corresponding quantitative analysis of fluorescence intensity (scale bar = 100 μm). Statistical analyses were performed by comparing the HIRI group with each of the other groups ( n = 3). * P < 0.05, ** P < 0.01, *** P < 0.001 vs. indicated. ns, not significant.

Article Snippet: Antibodies against DLAT, G6PD, FLNA, p -AMPK α , AMPK α , SIRT1, PGC-1 α , CD86, HO-1, CD163, 8-OHdG, iNOS, and GPX4, as well as mouse IL-4, IL-10, and IL-6 ELISA kits, were purchased from Proteintech (USA).

Techniques: In Vivo, Expressing, Analysis, Fluorescence, Imaging, Significance Assay