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September 25, 2026Discovery MedicineOpen Access

Norepinephrine induces epicardial adipose inflammation and cellular injury via p38 MAPK and NF-κB pathway activation.

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Population

Adipogenically differentiated epicardial adipose-derived cells and H9c2 rat cardiomyoblasts

Comparison

Norepinephrine, atropine, or their combination… vs Control group and EAT-CM

Design

Preclinical

Key result

Norepinephrine activated the p38 MAPK and NF-κB signaling pathways, inducing inflammatory changes and cellular injury in epicardial adipose-derived cells, and was associated with calcium-handling protein changes and cellular injury in H9c2 cells.

Authors

FLFu LiPCPing ChenLMLina Ma

Discussion

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Overview

May suggest norepinephrine effects on epicardial cells; leaves open clinical relevance pending human validation.

Key Points

  • To determine how norepinephrine influences inflammatory responses and cellular injury in epicardial adipose-derived cells, and to evaluate subsequent calcium-handling alterations and damage in exposed H9c2 cardiomyoblasts.
  • Cultured adipogenically differentiated epicardial adipose-derived cells and treated them with norepinephrine, atropine, or combination treatments, with or without p38 MAPK (SB203580) or NF-κB (Bay 11-7082) inhibitors.
  • Evaluated inflammatory cytokines, apoptosis, autophagy proteins, and pathway signaling via ELISA, flow cytometry, immunofluorescence, and Western blotting.
  • Exposed H9c2 rat cardiomyoblasts to conditioned media from the treated adipose cultures to assess Fluo-4 calcium fluorescence intensity, calcium-handling proteins (SERCA2a, PLB, RyR2), Cx43, and cell apoptosis.
  • Norepinephrine significantly increased TNF-α, IL-6, leptin, apoptosis, and p38 MAPK/NF-κB pathway activation while decreasing adiponectin in epicardial adipose-derived cells (all p < 0.05).
  • Conditioned media from norepinephrine-treated adipose cells induced Fluo-4 fluorescence intensity increases, reduced SERCA2a and Cx43 expression, altered PLB and RyR2 phosphorylation, and elevated apoptosis in H9c2 cardiomyoblasts, with effects amplified by atropine.
  • Inhibition of p38 MAPK or NF-κB signaling significantly suppressed norepinephrine-induced inflammatory cytokine production and cellular damage in epicardial adipose-derived cells (all p < 0.05).

Structured PICO

P
Population
In vitro study using epicardial adipose-derived cells isolated from 6 7-week-old male Sprague-Dawley rats and H9c2 rat cardiomyoblasts.
I
Intervention
Norepinephrine, atropine, or their combination; and exposure of H9c2 cells to conditioned media from these treated cells
C
Comparator
Control group (untreated cells) and EAT-CM (conditioned media from untreated epicardial adipose-derived cells)
O
Outcome
Inflammatory responses, apoptosis, autophagy-related protein expression, and activation of p38 MAPK and NF-κB signaling pathways in epicardial cells; Fluo-4 fluorescence, calcium-handling protein expression, Cx43 expression, and apoptosis in H9c2 cellssurrogate

Main Result

p-value: p=<0.05

Norepinephrine induces inflammation and cellular injury in epicardial adipose-derived cells via p38 MAPK and NF-κB pathways, which in turn causes calcium-handling alterations and apoptosis in H9c2 cardiomyoblasts.

Limitations

  • Findings were based on in vitro models and require further validation in animal and clinical studies.
  • H9c2 cells are rat cardiomyoblasts rather than mature atrial cardiomyocytes, and electrophysiological function was not directly assessed.
  • Conditioned media from inhibitor-treated cells were not subsequently applied to H9c2 cells.
  • Observations across treatment groups may have been correlated within the same donor, and statistical analyses did not explicitly account for this within-donor correlation.
  • Conditioned-media samples were not normalized to the number of viable donor cells, and specific components responsible for the observed H9c2 cell responses remain uncertain.

Cite This Study

Li et al. (2026) studied Cellular injury and inflammation in epicardial adipose-derived cells (n=6). Norepinephrine vs. Control (0 μM norepinephrine) was evaluated on Inflammatory markers (TNF-α, IL-6, leptin, adiponectin) and cellular injury (p=<0.05). Norepinephrine activated the p38 MAPK and NF-κB signaling pathways, inducing inflammatory changes and cellular injury in epicardial adipose-derived cells, and was associated with calcium-handling protein changes and cellular injury in H9c2 cells.

synapsesocial.com/papers/6ab60fbe406bf401c14688a8https://doi.org/10.24976/discov.med.202638212.231
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