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Patchouli Alcohol Protects the Heart against Diabetes-Related Cardiomyopathy through the JAK2/STAT3 Signaling Pathway.

Pharmaceuticals (Basel, Switzerland)
May 14, 2024
Lijun Ji et al. (9 authors)
Journal ArticleAnimal StudyMolecular Study
Extracted Claims (5)
InterventionDirectionEndpointPopulationDosageImpactClaim #
Patchouli alcohol (PatA) treatment
decrease
cardiac injury and dysfunction
diabetic mice
-
protects the heart against cardiomyopathy
#1
Patchouli alcohol (PatA) treatment
decrease
myocardial fibrosis
diabetic mice
-
controlling
#2
Patchouli alcohol (PatA) treatment
no change
hyperglycemia
diabetic mice
-
not by reducing
#3
Patchouli alcohol (PatA)
decrease
high glucose (HG) + palmitic acid (PA)-induced fibrotic and inflammatory responses
H9C2 cells
-
alleviates
#4
Patchouli alcohol (PatA)
decrease
HG + PA- or STZ-induced cardiomyopathy
-
-
mitigates the effects of
#5
Abstract

Diabetic cardiomyopathy (DCM) represents a common pathological state brought about by diabetes mellitus (DM). Patchouli alcohol (PatA) is known for its diverse advantageous effects, notably its anti-inflammatory properties and protective role against metabolic disorders. Despite this, the influence of PatA on DCM remains relatively unexplored. To explore the effect of PatA on diabetes-induced cardiac injury and dysfunction in mice, streptozotocin (STZ) was used to mimic type 1 diabetes in mice. Serological markers and echocardiography show that PatA treatment protects the heart against cardiomyopathy by controlling myocardial fibrosis but not by reducing hyperglycemia in diabetic mice. Discovery Studio 2017 software was used to perform reverse target screening of PatA, and we found that JAK2 may be a potential target of PatA. RNA-seq analysis of heart tissues revealed that PatA activity in the myocardium was primarily associated with the inflammatory fibrosis through the Janus tyrosine kinase 2 (JAK2)/signal transducer and activator of the transcription 3 (STAT3) pathway. In vitro, we also found that PatA alleviates high glucose (HG) + palmitic acid (PA)-induced fibrotic and inflammatory responses via inhibiting the JAK2/STAT3 signaling pathway in H9C2 cells. Our findings illustrate that PatA mitigates the effects of HG + PA- or STZ-induced cardiomyopathy by acting on the JAK2/STAT3 signaling pathway. These insights indicate that PatA could potentially serve as a therapeutic agent for DCM treatment.

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Citation Metrics
Total Citations3
Citations/Year3.0
Research Impact Scores
APT Score0.05
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