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Related Experiment Video

Updated: May 23, 2026

Herbal Munziq Ameliorates Myocardial Ischemia-Reperfusion Injury by Inhibiting Inflammation
09:53

Herbal Munziq Ameliorates Myocardial Ischemia-Reperfusion Injury by Inhibiting Inflammation

Published on: January 10, 2025

Baicalein Protects H9c2 Cardiomyoblasts Against LPS-Induced Inflammatory Injury by Modulating the NF-κB/NLRP3

Yi Lu1, Zahra Zahid Piracha2,3, Umar Saeed4,5

  • 1Department of Rehabilitation, Sengong Hospital of Shaanxi Province, Xian, China.

Iranian Journal of Pharmaceutical Research : IJPR
|May 22, 2026
PubMed
Summary

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NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
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Baicalein protects heart cells from sepsis-induced damage by reducing inflammation and oxidative stress. This natural compound inhibits key inflammatory pathways, preserving mitochondrial function and cell viability.

Area of Science:

  • Cardiovascular Research
  • Molecular Biology
  • Pharmacology

Background:

  • Sepsis-induced cardiomyopathy involves inflammation and mitochondrial damage from endotoxins like lipopolysaccharide (LPS).
  • LPS activates TLR4/NF-κB and NLRP3 inflammasome pathways, leading to pro-inflammatory cytokine release and mitochondrial dysfunction.
  • Baicalein, a flavonoid, has known anti-inflammatory and antioxidant effects, but its impact on LPS-induced cardiac cell signaling requires further investigation.

Purpose of the Study:

  • To investigate baicalein's protective effects against LPS-induced inflammatory and mitochondrial injury in H9c2 cardiomyoblasts.
  • To determine if baicalein modulates NF-κB, NLRP3 inflammasome, caspase-1 activity, and oxidative stress.

Main Methods:

  • H9c2 cells were treated with baicalein followed by LPS exposure.
Keywords:
Antioxidant TherapyBaicaleinCardiomyocyte InflammationCaspase-1H9c2 CardiomyoblastsIL-18IL-1βLipopolysaccharideMitochondrial Membrane PotentialNF-κB SignalingNLRP3 InflammasomeOxidative StressReactive Oxygen SpeciesSepsis-associated Cardiomyopathy

Related Experiment Videos

Last Updated: May 23, 2026

Herbal Munziq Ameliorates Myocardial Ischemia-Reperfusion Injury by Inhibiting Inflammation
09:53

Herbal Munziq Ameliorates Myocardial Ischemia-Reperfusion Injury by Inhibiting Inflammation

Published on: January 10, 2025

  • Assessed cell viability (MTT), LDH release, and morphology.
  • Analyzed gene and protein expression of NLRP3 inflammasome components and NF-κB pathway.
  • Measured caspase-1 activity, IL-1β and IL-18 secretion, mitochondrial membrane potential, and reactive oxygen species (ROS).

    • Main Results:

    • LPS increased Nlrp3, Il1b transcription, NLRP3 protein, caspase-1 activity, and IL-1β/IL-18 secretion.
    • LPS induced mitochondrial depolarization, elevated ROS, reduced cell viability, and increased cytotoxicity.
    • Baicalein pretreatment suppressed NF-κB activation, inflammasome priming, caspase-1 activity, and cytokine secretion.
    • Baicalein preserved mitochondrial membrane potential, reduced ROS, and improved cell viability and morphology.

    Conclusions:

    • Baicalein protects H9c2 cardiomyoblasts from LPS-induced damage by inhibiting NF-κB and NLRP3 inflammasome signaling.
    • Baicalein stabilizes mitochondrial function and reduces oxidative stress, offering a potential therapeutic strategy for sepsis-related cardiac dysfunction.