mouse β endorphin elisa kit  (Cusabio)

Journal: Journal of Biomedical Science

Article Title: OPRM1/MRGPRX1 heterodimers drive opioid-induced itch through a peripheral mechanism

doi: 10.1186/s12929-026-01238-x

Figure Lengend Snippet: Endogenous µ-opioid agonists induce OPRM1/MRGPRX1-dependent calcium mobilization. A Schematic representation of a calcium imaging assay to verify whether endogenous opioids can induce intracellular calcium mobilization via OPRM1/MRGRPX1. B Time course of normalized fluorescence (F/F₀) in HEK293T cells co-expressing mouse Oprm1 and MrgprX1 (mOprm1/mMrgprX1) after treatment with 1 µM β-endorphin, in the absence or presence of 10 µM naltrexone. C Dose–response relationship showing ΔPeak F/F₀ in mOprm1/mMrgprX1 cells treated with increasing concentrations of β-endorphin (0.01–10 µM). Time-course calcium mobilization in mOprm1/mMrgprX1 cells treated with 1 µM endomorphin-1 ( D ) or endomorphin-2 ( E ), with or without naltrexone. F Calcium responses (F/F 0 ) in HEK293T cells co-expressing hOPRM1 and hMRGPRX1 (hOPRM1/hMRGPRX1) treated with 1 µM β-endorphin in the presence of naltrexone (10 µM) or berbamine (10 µM, an MRGPRX1 antagonist). G Quantification of peak responses (ΔPeak F/F 0 ) in hOPRM1/hMRGPRX1 cells treated with endomorphin-1 or endomorphin-2, with or without berbamine. ***p < 0.001 compared to control

Article Snippet: The levels of β-endorphin were measured using a mouse β-endorphin ELISA kit (catalog # CSB-E06827m; CUSABIO, Houston, USA), following the manufacturer’s protocols.

Techniques: Imaging, Fluorescence, Expressing, Control

Journal: Journal of Biomedical Science

Article Title: OPRM1/MRGPRX1 heterodimers drive opioid-induced itch through a peripheral mechanism

doi: 10.1186/s12929-026-01238-x

Figure Lengend Snippet: Peripheral OPRM1 mediates opioid-induced and atopic dermatitis–associated itch. A Schematic of intradermal DAMGO injection and subsequent scratching behavior assay. B Quantification of scratching bouts over 60 min in wild-type mice following intradermal injection of vehicle (Control, n = 6) or DAMGO (n = 7). C Schematic of investigation into the effect of MC903 treatment on OPRM1/MRGPRX1 heterodimers in sensory neurons. D Spontaneous scratching bouts measured over 30 min in control (n = 6) and MC903-treated mice (n = 8). E Time-course calcium mobilization (F/F₀) in dorsal root ganglion (DRG) neurons from wild-type (WT) and MC903-treated mice stimulated with 10 µM DAMGO. F Quantification of peak calcium responses (ΔPeak F/F₀) in DRG neurons from control and MC903-treated mice stimulated with DAMGO. Numbers shown inside the bars indicate the sample sizes (n). G DAMGO-evoked calcium signals in MC903 DRG neurons (n = 787) were significantly diminished by MrgprX1 siRNA (n = 580). KCl (100 mM) was applied to confirm neuronal viability. H Immunofluorescence micrographs of lumbar DRG sections from control (identical to Fig. A) and MC903-treated mice. OPRM1 (green), MRGPRX1 (red), and nuclei (DAPI, blue) merge to reveal colocalization. Scale bar = 50 µm. I – L Quantification of gene expression changes (fold change) in DRG neurons from MC903-treated mice for Oprm1 ( I ), Mrgprx1 ( J ), Trpv1 ( K ), and Trpa1 ( L ). M Schematic of assay to verify changes of β-endorphin levels in MC903-treated mice. Levels of β-endorphin in the skin ( N ) and serum ( O ) of control and MC903-treated mice. *p < 0.05, ***p < 0.001, ns = not significant

Article Snippet: The levels of β-endorphin were measured using a mouse β-endorphin ELISA kit (catalog # CSB-E06827m; CUSABIO, Houston, USA), following the manufacturer’s protocols.

Techniques: Injection, Behavioral Assay, Control, Immunofluorescence, Gene Expression