The cardioprotective effects of icariin on the isoprenaline-induced takotsubo-like rat model: Involvement of reactive oxygen species and the TLR4/NF-κB signaling pathway.

  title={The cardioprotective effects of icariin on the isoprenaline-induced takotsubo-like rat model: Involvement of reactive oxygen species and the TLR4/NF-$\kappa$B signaling pathway.},
  author={Chunlei Qi and Yangzhen Shao and Xuesong Liu and Daxin Wang and Xueping Li},
  journal={International immunopharmacology},

Icariin Protects H9c2 Rat Cardiomyoblasts from Doxorubicin-Induced Cardiotoxicity: Role of Caveolin-1 Upregulation and Enhanced Autophagic Response

The results suggest that Ica might have beneficial cardioprotective effects in attenuating cardiotoxicity in patients requiring anthracycline chemotherapy through the inhibition of oxidative stress and, in particular, through the modulation of Cav-1 expression levels and the involvement of PDE5a activity, thereby leading to cardiac cell survival.

Takotsubo Syndrome: Translational Implications and Pathomechanisms

The pathophysiological mechanisms related to Takotsubo syndrome; preclinical TTS models and platforms such as animal models, human-induced pluripotent stem cell-derived cardiomyocyte models and their usefulness for TTS studies are reviewed, including exploring and improving the understanding of the pathomechanism of the disease.

Pterostilbene prevents LPS-induced early pulmonary fibrosis by suppressing oxidative stress, inflammation and apoptosis in vivo.

Early pulmonary fibrosis after acute lung injury leads to poor prognosis and high mortality. Pterostilbene (Pts), a bioactive component in blueberries, possesses anti-inflammatory, antioxidative and

Current Knowledge and Future Challenges in Takotsubo Syndrome: Part 1—Pathophysiology and Diagnosis

Beyond clinical presentation, epidemiology, and novel diagnostic biomarkers, this review draws attention to potential pathophysiological mechanisms for the observed reversible myocardial dysfunction such as sympathetic overdrive-mediated multi-vessel epicardial spasms, microvascular dysfunction, the direct toxicity of catecholamines, lipotoxicity, and inflammation.

Research progress on icariin, a traditional Chinese medicine extract, in the treatment of asthma.

Icariin is considered a novel therapy in controlling asthma; however, the mechanism is still worth further investigation.

Protein tyrosine phosphatase receptor-type O expression as a prognostic marker in patients with acute coronary syndrome undergoing percutaneous coronary intervention: A prospective study

PTPRO expression in peripheral blood mononuclear cells after PCI is associated with the prognosis of patients with ACS, with high PTPRO expression indicating a high risk of poor prognosis in patients with ACS.

Hepatic stellate cells specific liposomes with the Toll‐like receptor 4 shRNA attenuates liver fibrosis

The outcome of this study revealed that the VitA‐coupled cationic liposomes delivered the TLR4 shRNA to aHSCs more efficiently, as compared to the uncoupledCationic Liposomes, both in the in vitro and in vivo conditions.



Stress (Takotsubo) cardiomyopathy—a novel pathophysiological hypothesis to explain catecholamine-induced acute myocardial stunning

It is hypothesized that stress cardiomyopathy is a form of myocardial stunning, but with different cellular mechanisms to those seen during transient episodes of ischemia secondary to coronary stenoses, and that high levels of circulating epinephrine trigger a switch in intracellular signal trafficking in ventricular cardiomeocytes, from Gs protein to Gi protein signaling via the β2-adrenoceptor.

S-Propargyl-cysteine (SPRC) attenuated lipopolysaccharide-induced inflammatory response in H9c2 cells involved in a hydrogen sulfide-dependent mechanism

It is concluded that SPRC produced an anti-inflammatory effect in LPS-stimulated H9c2 cells partly through the CSE/H2S pathway by impairing IκBα/NF-κB signaling and by activating PI3K/Akt signaling pathway.

Effects and mechanisms of icariin on atherosclerosis.

Icariin can prevent atherosclerotic lesion and its mechanism may be that it can defend against the oxidation damage to HUVECs, inhibit the adhesion of monocyte to HUVCs, and reduce the secretion and expression of adhesion molecules including ICAM-1, VCAM- 1, E-selectin.