Related Experiment Video

Updated: Apr 28, 2026

Screening Assays to Characterize Novel Endothelial Regulators Involved in the Inflammatory Response
12:50

Screening Assays to Characterize Novel Endothelial Regulators Involved in the Inflammatory Response

Published on: September 15, 2017

6.0K

Kaempferol attenuates LPS-induced inflammatory responses in H9c2 cells through involvement of the IL-6/JAK2/STAT3

Hongyi Yue1,2, Yunfei Jia1,3, Ruohao Sun1

  • 1Clinical Medical Research Center for Plateau Gastroenterological disease of Xizang Autonomous Region, and School of Medicine, Xizang Minzu University, Xianyang, 712082, China.

Molecular Biology Reports
|April 27, 2026
PubMed

Insights

Kaempferol (Kae) protects against inflammation in heart cells by regulating the IL-6/JAK2/STAT3 pathway. This flavonoid compound shows promise for treating cardiovascular diseases and myocardial damage.

Area of Science:

  • Cardiovascular Research
  • Molecular Biology
  • Pharmacology

Background:

  • Kaempferol (Kae), a flavonoid, shows potential in cardiovascular disease prevention and myocardial damage amelioration.
  • Its precise mechanisms of action require further investigation.
  • This study focuses on Kae's protective effects against inflammation in cardiomyocytes.

Purpose of the Study:

  • To investigate the protective effects of Kae pretreatment against lipopolysaccharide (LPS)-induced inflammatory responses in H9c2 cardiomyocytes.
  • To elucidate the role of the interleukin-6 (IL-6)/Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling pathway.
  • To establish a theoretical basis for Kae's clinical application in cardiovascular conditions.

Main Methods:

  • Network pharmacology and molecular docking were used to identify potential therapeutic targets.
  • In vivo studies utilized histopathological analysis (H&E staining) to assess Kae's efficacy.
  • An in vitro model of LPS-induced inflammation in H9c2 cardiomyocytes was established to explore underlying mechanisms.

Main Results:

  • Network pharmacology suggested Kae modulates the IL-6/JAK2/STAT3 pathway for anti-inflammatory effects.
  • In vivo, Kae ameliorated cardiac histopathology and reduced inflammatory cytokine levels (TNF-α, IL-6, IL-1β).
  • In vitro, Kae pretreatment significantly decreased LPS-induced inflammatory markers, downregulated p-JAK2 and p-STAT3, and improved antioxidant status.

Conclusions:

  • Kae pretreatment confers protection against LPS-induced inflammation in H9c2 cells.
  • The protective mechanism is associated with the regulation of the IL-6/JAK2/STAT3 signaling pathway.
  • Kae demonstrates potential as a therapeutic agent for inflammatory cardiovascular conditions.
Abstract

Keywords:
Cytokine stormKaempferolLipopolysaccharideOxidative stressSignaling pathway

More Related Videos

Isolation Protocol of Mouse Monocyte-derived Dendritic Cells and Their Subsequent In Vitro Activation with Tumor Immune Complexes11:48

Isolation Protocol of Mouse Monocyte-derived Dendritic Cells and Their Subsequent In Vitro Activation with Tumor Immune Complexes

Published on: May 31, 2018

11.1K

Related Concept Videos

The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
10.1K
Amplifying Signals via Enzymatic Cascade01:22

Amplifying Signals via Enzymatic Cascade

When a ligand binds to a cell-surface receptor, the receptor's intracellular domain changes shape, which may either activate its enzyme function or allow its binding to other molecules. The initial signal is amplified by most signal transduction pathways. This means that a single ligand molecule can activate multiple molecules of a downstream target. Proteins that relay a signal are most commonly phosphorylated at one or more sites, activating or inactivating the protein. Kinases catalyze...
15.2K
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
The...
7.4K
cAMP-dependent Protein Kinase Pathways01:25

cAMP-dependent Protein Kinase Pathways

Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...
7.3K