Kaempferol attenuated cisplatin-induced cardiac injury via inhibiting STING/NF-κB-mediated inflammation

Yajun Qi1, Yin Ying2, Jie Zou3

  • 1Department of Pharmacy, The Cancer Hospital of The University of Chinese Academy of Sciences (Zhejiang Cancer Hospital), Institute of Cancer and Basic Medicine (IBMC), Chinese Academy of Sciences Hangzhou 310022, Zhejiang, China.

Insights

Kaempferol (KPF) protects against heart damage from cisplatin chemotherapy. This natural compound reduces cardiac injury and inflammation by modulating the STING/NF-κB pathway, offering potential therapeutic benefits.

Area of Science:

  • Cardiology
  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • Cardiovascular complications are a significant adverse effect of conventional cancer chemotherapy, particularly cisplatin.
  • Cisplatin-induced cardiotoxicity hinders effective cancer treatment.
  • Kaempferol (KPF) is known for its cardioprotective and anti-inflammatory properties.

Purpose of the Study:

  • To investigate the protective effects of kaempferol (KPF) against cisplatin-induced heart injury.
  • To elucidate the molecular mechanisms underlying KPF's cardioprotective action.

Main Methods:

  • In vivo studies to assess KPF's effect on cisplatin-induced cardiac dysfunction and injury.
  • In vitro experiments using H9c2 cells to evaluate KPF's impact on apoptosis and inflammation.
  • Molecular analysis focusing on the STING/NF-κB pathway.

Main Results:

  • Kaempferol (KPF) demonstrated significant protection against cardiac dysfunction and injury induced by cisplatin in vivo.
  • KPF markedly reduced cisplatin-induced apoptosis and inflammatory responses in H9c2 cells.
  • The protective effects were associated with the modulation of the STING/NF-κB signaling pathway.

Conclusions:

  • Kaempferol (KPF) exhibits substantial potential in mitigating cisplatin-induced cardiac injury.
  • Modulation of the STING/NF-κB pathway is a key mechanism for KPF's cardioprotective effects.
  • Natural compounds containing KPF with anti-inflammatory properties warrant further investigation for treating chemotherapy-induced cardiotoxicity.

Related Concept Videos

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
672
Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists01:28

Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists

Neurokinin 1 (NK1) receptors are distributed across the GI tract, vagal afferents, and key CNS regions including the central vomiting center and chemoreceptor trigger zone (CTZ) Chemotherapy agents stimulate enterochromaffin cells in the gastrointestinal (GI) tract to release large amounts of substance P (SP). SP is a neuropeptide released by specific sensory nerves in response to many different stressors, including those in the GI mucosa affected by chemotherapy.  SP binds and activates...
381
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...
8.8K